PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
10804019-12	2000	In contrast, HCTZ induced a dose-dependent increase in cFOS levels (p < 0.002 by ANOVA), a situation prevented by incubation with EGTA.	Hydrochlorothiazide	13-17	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	55-59
10804019-13	2000	These studies indicate that HCTZ inhibits OC mRNA expression independently of an effect on VDR, YY1, or extracellular Ca2+ levels but involves changes in cFOS levels.	Hydrochlorothiazide	28-32	bone gamma-carboxyglutamate protein	Homo sapiens	42-44
10804019-14	2000	As OC retards bone formation/mineralization, the inhibition of OC production by HCTZ could explain its preventive role in bone loss rate.	Hydrochlorothiazide	80-84	bone gamma-carboxyglutamate protein	Homo sapiens	3-5
10713865-1	1999	Five years ago, our in vitro and in vivo studies demonstrated for the first time that diuretic agents such as furosemide, hydrochlorothiazide, amiloride, triamterene and spironolactone inhibit carbonic anhydrase (CA) I, II and renal CA IV by a direct mechanism of action.	Hydrochlorothiazide	122-141	carbonic anhydrase 1	Homo sapiens	193-218
10804019-3	2000	We therefore investigated the role of hydrochlorothiazide (HCTZ) on OC production by the human osteoblast-like cell line MG-63.	Hydrochlorothiazide	38-57	bone gamma-carboxyglutamate protein	Homo sapiens	68-70
10804019-3	2000	We therefore investigated the role of hydrochlorothiazide (HCTZ) on OC production by the human osteoblast-like cell line MG-63.	Hydrochlorothiazide	59-63	bone gamma-carboxyglutamate protein	Homo sapiens	68-70
10804019-4	2000	HCTZ dose-dependently (1-100 microM) inhibited 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]-induced OC release by these cells (maximal effect, -40-50% and p < 0.005 by analysis of variance [ANOVA]) as measured by ELISA.	Hydrochlorothiazide	0-4	bone gamma-carboxyglutamate protein	Homo sapiens	94-96
10804019-5	2000	This effect of HCTZ on OC release was caused by a direct effect on OC gene expression because Northern blot analysis revealed that OC messenger RNA (mRNA) levels were reduced in the presence of increasing doses of the diuretic (-47.2+/-4.0%; p < 0.0001 by paired ANOVA with 100 microM 13.6+/-0.49 pmol/mg protein/15 minutes; p < 0.05) in MG-63 cells.	Hydrochlorothiazide	15-19	bone gamma-carboxyglutamate protein	Homo sapiens	23-25
10804019-5	2000	This effect of HCTZ on OC release was caused by a direct effect on OC gene expression because Northern blot analysis revealed that OC messenger RNA (mRNA) levels were reduced in the presence of increasing doses of the diuretic (-47.2+/-4.0%; p < 0.0001 by paired ANOVA with 100 microM 13.6+/-0.49 pmol/mg protein/15 minutes; p < 0.05) in MG-63 cells.	Hydrochlorothiazide	15-19	bone gamma-carboxyglutamate protein	Homo sapiens	67-69
10804019-5	2000	This effect of HCTZ on OC release was caused by a direct effect on OC gene expression because Northern blot analysis revealed that OC messenger RNA (mRNA) levels were reduced in the presence of increasing doses of the diuretic (-47.2+/-4.0%; p < 0.0001 by paired ANOVA with 100 microM 13.6+/-0.49 pmol/mg protein/15 minutes; p < 0.05) in MG-63 cells.	Hydrochlorothiazide	15-19	bone gamma-carboxyglutamate protein	Homo sapiens	67-69
10804019-7	2000	Because OC production is strictly dependent on the presence of 1,25(OH)2D3 in human osteoblasts, we next evaluated the possible role of HCTZ on vitamin D3 receptors (VDR) at the mRNA and protein levels.	Hydrochlorothiazide	136-140	vitamin D receptor	Homo sapiens	144-164
10579750-7	1999	The author concludes that adding hydrochlorothiazide to any angiotensin II antagonist results in much greater efficacy than switching or increasing doses of the angiotensin II antagonist.	Hydrochlorothiazide	33-52	angiotensinogen	Homo sapiens	60-74
10334975-10	1999	Hydrochlorothiazide (10(-7) mol/l) significantly decreased 11beta-HSD2 activity (P<0.05 compared with control) at 4 h pretreatment.	Hydrochlorothiazide	0-19	hydroxysteroid 11-beta dehydrogenase 2	Homo sapiens	59-70
10090111-7	1999	RESULTS: After 8 weeks on a regimen of hydrochlorothiazide, increases of 3.3 mg/dL (0.09 mmol/L) in total cholesterol and 2.7 mg/dL in apolipoprotein B were significantly different (P< or =.05) from decreases of 9.3 mg/dL in total cholesterol and 5.4 mg/dL in ApoB levels while receiving prazosin but not from placebo.	Hydrochlorothiazide	39-58	apolipoprotein B	Homo sapiens	263-267
10090111-8	1999	Patients achieving positive DBP control using hydrochlorothiazide (responders) showed no adverse changes in PLPPs, whereas nonresponders exhibited increases in triglycerides, total cholesterol, and low-density lipoprotein cholesterol levels.	Hydrochlorothiazide	46-65	D-box binding PAR bZIP transcription factor	Homo sapiens	28-31
10713865-1	1999	Five years ago, our in vitro and in vivo studies demonstrated for the first time that diuretic agents such as furosemide, hydrochlorothiazide, amiloride, triamterene and spironolactone inhibit carbonic anhydrase (CA) I, II and renal CA IV by a direct mechanism of action.	Hydrochlorothiazide	122-141	carbonic anhydrase 4	Homo sapiens	233-238
10456135-6	1998	In the hydrochlorothiazide group, SBP was significantly reduced from 16.4 +/- 19 mmHg to 141 +/- 17 mmHg (P < 0.00001) and DBP from 102 +/- 6 mmHG to 89 +/- 7 mmHg (P < 0.00001) with normalisation rates of 77% and 82% at 4 weeks and 12 weeks respectively.	Hydrochlorothiazide	7-26	selenium binding protein 1	Homo sapiens	34-37
9681711-0	1998	The blunting of the antiproteinuric efficacy of ACE inhibition by high sodium intake can be restored by hydrochlorothiazide.	Hydrochlorothiazide	104-123	angiotensin I converting enzyme	Homo sapiens	48-51
9681711-8	1998	CONCLUSION: Addition of hydrochlorothiazide can overcome the blunting of the therapeutic efficacy of ACE inhibition on proteinuria and blood pressure by a high sodium intake.	Hydrochlorothiazide	24-43	angiotensin I converting enzyme	Homo sapiens	101-104
9607375-9	1998	Ramipril caused a sustained fall in plasma angiotensin II, whereas HCTZ increased angiotensin II levels.	Hydrochlorothiazide	67-71	angiotensinogen	Homo sapiens	82-96
9777817-10	1998	Hydrochlorothiazide and prazosin were best in low- and medium-renin profiles; captopril was best in medium- and high-renin profiles (low-, medium-, and high-renin response rates were 82%, 78%, and 14%, respectively, for hydrochlorothiazide; 88%, 67%, and 40%, respectively, for prazosin; and 51%, 83%, and 100%, respectively, for captopril for patients with baseline DBP of 95-99 mm Hg).	Hydrochlorothiazide	0-19	renin	Homo sapiens	62-67
9715782-5	1998	The primary analysis of ABP data revealed that both lisinopril and HCTZ effectively lowered mean 24-h systolic (SBP) and diastolic (DBP) blood pressure compared with placebo, (mean change from baseline SBP/DBP: -12.0/-8.2, -10.6/-5.5, and -0.3/-0.5 mm Hg, respectively); however, lisinopril lowered DBP better than HCTZ (P < .05).	Hydrochlorothiazide	67-71	selenium binding protein 1	Homo sapiens	112-115
9715782-5	1998	The primary analysis of ABP data revealed that both lisinopril and HCTZ effectively lowered mean 24-h systolic (SBP) and diastolic (DBP) blood pressure compared with placebo, (mean change from baseline SBP/DBP: -12.0/-8.2, -10.6/-5.5, and -0.3/-0.5 mm Hg, respectively); however, lisinopril lowered DBP better than HCTZ (P < .05).	Hydrochlorothiazide	67-71	D-box binding PAR bZIP transcription factor	Homo sapiens	132-135
9715782-5	1998	The primary analysis of ABP data revealed that both lisinopril and HCTZ effectively lowered mean 24-h systolic (SBP) and diastolic (DBP) blood pressure compared with placebo, (mean change from baseline SBP/DBP: -12.0/-8.2, -10.6/-5.5, and -0.3/-0.5 mm Hg, respectively); however, lisinopril lowered DBP better than HCTZ (P < .05).	Hydrochlorothiazide	67-71	selenium binding protein 1	Homo sapiens	202-205
9715782-5	1998	The primary analysis of ABP data revealed that both lisinopril and HCTZ effectively lowered mean 24-h systolic (SBP) and diastolic (DBP) blood pressure compared with placebo, (mean change from baseline SBP/DBP: -12.0/-8.2, -10.6/-5.5, and -0.3/-0.5 mm Hg, respectively); however, lisinopril lowered DBP better than HCTZ (P < .05).	Hydrochlorothiazide	67-71	D-box binding PAR bZIP transcription factor	Homo sapiens	206-209
9715782-5	1998	The primary analysis of ABP data revealed that both lisinopril and HCTZ effectively lowered mean 24-h systolic (SBP) and diastolic (DBP) blood pressure compared with placebo, (mean change from baseline SBP/DBP: -12.0/-8.2, -10.6/-5.5, and -0.3/-0.5 mm Hg, respectively); however, lisinopril lowered DBP better than HCTZ (P < .05).	Hydrochlorothiazide	67-71	D-box binding PAR bZIP transcription factor	Homo sapiens	206-209
9504451-7	1998	A similar potentiation of the antihypertensive effect was seen during coadministration of hydrochlorothiazide (HCTZ) with the angiotensin converting enzyme inhibitor benazeprilat.	Hydrochlorothiazide	90-109	angiotensin I converting enzyme	Rattus norvegicus	126-155
9504451-7	1998	A similar potentiation of the antihypertensive effect was seen during coadministration of hydrochlorothiazide (HCTZ) with the angiotensin converting enzyme inhibitor benazeprilat.	Hydrochlorothiazide	111-115	angiotensin I converting enzyme	Rattus norvegicus	126-155
8986455-12	1996	TCV-116 and HCTZ each caused a significant increase in plasma renin concentration (PRC), and prazosin caused a slight elevation.	Hydrochlorothiazide	12-16	renin	Rattus norvegicus	62-67
9208337-13	1997	We conclude that the combination of hydrochlorothiazide with an ACE inhibitor has a better metabolic profile for the treatment of essential hypertension than the combination with a beta-blocker.	Hydrochlorothiazide	36-55	angiotensin I converting enzyme	Homo sapiens	64-67
18370462-8	1998	A slight but statistically significant increase in fasting triglycerides occurred with FOS/HCTZ compared with HCTZ (+26.1 vs +13.5 mg/dl, respectively; p < 0.05).	Hydrochlorothiazide	91-95	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	87-90
9360571-0	1997	Rapid life-threatening hyperkalemia after addition of amiloride HCl/hydrochlorothiazide to angiotensin-converting enzyme inhibitor therapy.	Hydrochlorothiazide	68-87	angiotensin I converting enzyme	Homo sapiens	91-120
9140801-1	1997	Combination therapy with the new ACE inhibitor moexipril plus hydrochlorothiazide (HCTZ) results in significant blood pressure (BP) reductions.	Hydrochlorothiazide	83-87	angiotensin I converting enzyme	Homo sapiens	33-36
9140801-8	1997	Headache and cough which are the most frequently reported AEs after treatment with ACE inhibitors were seen in 9% and 10% of the patients in the moexipril/HCTZ group compared to 10% and 4% in the metoprolol/HCTZ group.	Hydrochlorothiazide	155-159	angiotensin I converting enzyme	Homo sapiens	83-86
9021525-8	1997	It appears that the early treatment with angiotensin converting enzyme inhibitor, angiotensin II receptor antagonist or reserpine, hydralazine and hydrochlorothiazide (TRX) may prevent glomerular injury in human patients with renal hypertension.	Hydrochlorothiazide	147-166	thioredoxin	Homo sapiens	168-171
8914012-15	1996	In contrast, HCTZ inhibited the response to TNF-alpha alone (P < 0.05), and also reduced the response to a combination of 1,25(OH)2D3 and TNF-alpha (P < 0.01).	Hydrochlorothiazide	13-17	tumor necrosis factor	Homo sapiens	44-53
8914012-15	1996	In contrast, HCTZ inhibited the response to TNF-alpha alone (P < 0.05), and also reduced the response to a combination of 1,25(OH)2D3 and TNF-alpha (P < 0.01).	Hydrochlorothiazide	13-17	tumor necrosis factor	Homo sapiens	141-150
8914012-5	1996	Under similar conditions, HCTZ dose-dependently inhibited 1,25(OH)2D3-induced osteocalcin secretion by these cells (maximal effect, -40 to 50%, P < 0.005).	Hydrochlorothiazide	26-30	bone gamma-carboxyglutamate protein	Homo sapiens	78-89
8876475-5	1996	Additional blood pressure reductions can be attained with concomitant use of once-daily low-dose hydrochlorothiazide or chlorthalidone with an angiotensin-converting enzyme (ACE) inhibitor, a beta blocker, or a calcium antagonist.	Hydrochlorothiazide	97-116	angiotensin I converting enzyme	Homo sapiens	143-172
20065435-1	1996	OBJECTIVE: We have previously shown that in the treatment of mild to moderate hypertension little is gained by increasing the dose of hydrochlorothiazide (HCT) over 12.5 mg when combined with an ACE-inhibitor.	Hydrochlorothiazide	134-153	angiotensin I converting enzyme	Homo sapiens	195-198
8769587-10	1996	At 6 months, mean DBP decreased by 13.0 mm Hg in both groups, and mean SBP decreased by 19.5 mm Hg in hydrochlorothiazide and 16.0 mm Hg in isradipine (P=.002); the difference in SBP between the 2 groups persisted throughout the study but did not explain the increased incidence of vascular events in patients treated with isradipine.	Hydrochlorothiazide	102-121	selenium binding protein 1	Homo sapiens	71-74
8746604-8	1995	In the hydrochlorothiazide group a significant decrease (p < 0.001) in RVR was found.	Hydrochlorothiazide	7-26	nuclear receptor subfamily 1 group D member 2	Homo sapiens	74-77
8722432-8	1996	Both dose combinations of Fos/HCTZ produced significantly greater reductions in the office seated DBP than placebo at all time points tested with a maximum treatment effect (drug effect - placebo effect) of -7.3 mm Hg for the 10/12.5-mg dose and -8.2 mm Hg for the 20/12.5-mg dose after 8 weeks of therapy (P <or= .01).	Hydrochlorothiazide	30-34	D-box binding PAR bZIP transcription factor	Homo sapiens	98-101
8866628-3	1996	RESULTS: The sixteen patients treated with HCTZ showed the expected directional alterations in plasma TG (+31%), HDL2-C (-16%), and CHOL (+7.6%); in contrast TG and CHOL were unchanged after captopril in fourteen patients and their HDL2-C declined (-16%).	Hydrochlorothiazide	43-47	junctophilin 3	Homo sapiens	113-117
8866628-3	1996	RESULTS: The sixteen patients treated with HCTZ showed the expected directional alterations in plasma TG (+31%), HDL2-C (-16%), and CHOL (+7.6%); in contrast TG and CHOL were unchanged after captopril in fourteen patients and their HDL2-C declined (-16%).	Hydrochlorothiazide	43-47	junctophilin 3	Homo sapiens	232-236
8866628-6	1996	CONCLUSION: These findings indicate that HCTZ and CAPT treatment have small, but demonstrable effects on lipoprotein surface lipid composition in patients with EH that are confined to the HDL2 subfraction.	Hydrochlorothiazide	41-45	junctophilin 3	Homo sapiens	188-192
8992496-4	1996	10 day gavage with indapamide, amiloride and cicletanine, as well as angiotensin-converting enzyme (ACE) inhibitor perindopril and calcium channel blockers nifedipine and verapamil decreases capillary permeability, whereas furosemide, hydrochlorothiazide, ACE inhibitor captopril and calcium channel blocker clentiazem do not modify or increase EB extravasation.	Hydrochlorothiazide	235-254	angiotensin I converting enzyme	Rattus norvegicus	100-103
8746604-6	1995	At the end of cilazapril and hydrochlorothiazide administration significant decreases (p < 0.001) in SBP, DBP and MBP vs baseline values were observed.	Hydrochlorothiazide	29-48	selenium binding protein 1	Homo sapiens	104-107
11835060-0	1994	The Interaction of Hydrochlorothiazide with Spirapril: A Novel Ace Inhibitor.	Hydrochlorothiazide	19-38	angiotensin I converting enzyme	Homo sapiens	63-66
8746604-6	1995	At the end of cilazapril and hydrochlorothiazide administration significant decreases (p < 0.001) in SBP, DBP and MBP vs baseline values were observed.	Hydrochlorothiazide	29-48	D-box binding PAR bZIP transcription factor	Homo sapiens	109-112
8746604-6	1995	At the end of cilazapril and hydrochlorothiazide administration significant decreases (p < 0.001) in SBP, DBP and MBP vs baseline values were observed.	Hydrochlorothiazide	29-48	myelin basic protein	Homo sapiens	117-120
7751430-2	1995	Results showed that HCTZ 6.25 mg contributed significantly to the antihypertensive effectiveness of bisoprolol 5 mg. Bisoprolol 5 mg/HCTZ 6.25 mg (B5/H6.25) produced significantly greater mean reductions from baseline in sitting systolic and diastolic blood pressure (-15.8 mm Hg/-12.6 mm Hg) than bisoprolol 5 mg alone (-10.0 mm Hg/-10.5 mm Hg) and HCTZ 25 mg alone (-10.2 mm Hg/-8.5 mm Hg).	Hydrochlorothiazide	133-137	glycoprotein hormone subunit beta 5	Homo sapiens	147-155
7751430-2	1995	Results showed that HCTZ 6.25 mg contributed significantly to the antihypertensive effectiveness of bisoprolol 5 mg. Bisoprolol 5 mg/HCTZ 6.25 mg (B5/H6.25) produced significantly greater mean reductions from baseline in sitting systolic and diastolic blood pressure (-15.8 mm Hg/-12.6 mm Hg) than bisoprolol 5 mg alone (-10.0 mm Hg/-10.5 mm Hg) and HCTZ 25 mg alone (-10.2 mm Hg/-8.5 mm Hg).	Hydrochlorothiazide	133-137	glycoprotein hormone subunit beta 5	Homo sapiens	147-155
7985599-3	1994	The hyperinsulinemic euglycemic clamp method showed that the significant decrease in insulin sensitivity (p < 0.01) induced by treatment with pindolol, propanolol, metoprolol, atenolol, or hydrochlorothiazide after 4 to 6 months persisted after 2 to 3 years of treatment.	Hydrochlorothiazide	192-211	insulin	Homo sapiens	9-16
7810602-6	1994	An NMDG-Cl- dependent NH4(+)-induced fall in pHi was reduced approximately 33% by 10 mM Ba+, approximately 84% by 0.1 mM bumetanide, and 100% by 1.5 mM furosemide, whereas 1 mM hydrochlorothiazide had no effect; inhibition by Ba+ was observed even in the presence of 0.1 mM verapamil added to block both K+ channels and K+/NH4+ antiport.	Hydrochlorothiazide	177-196	glucose-6-phosphate isomerase	Rattus norvegicus	45-48
11835076-4	1994	Mean supine SBP/DBP reductions from baseline for all HCTZ plus perindopril groups were significantly (p less-than-or-equal 0.05) greater than for HCTZ plus placebo.	Hydrochlorothiazide	53-57	selenium binding protein 1	Homo sapiens	12-15
11835076-4	1994	Mean supine SBP/DBP reductions from baseline for all HCTZ plus perindopril groups were significantly (p less-than-or-equal 0.05) greater than for HCTZ plus placebo.	Hydrochlorothiazide	53-57	D-box binding PAR bZIP transcription factor	Homo sapiens	16-19
11835076-6	1994	At the final visit, mean reductions in supine SBP/DBP were 10.3/6.7, 9.6/8.0, and 9.3/6.3 mmHg for HCTZ plus perindopril 2, 4, and 8 mg, respectively, and 1.6/2.0 mmHg for HCTZ plus placebo.	Hydrochlorothiazide	99-103	selenium binding protein 1	Homo sapiens	46-49
11835076-6	1994	At the final visit, mean reductions in supine SBP/DBP were 10.3/6.7, 9.6/8.0, and 9.3/6.3 mmHg for HCTZ plus perindopril 2, 4, and 8 mg, respectively, and 1.6/2.0 mmHg for HCTZ plus placebo.	Hydrochlorothiazide	99-103	D-box binding PAR bZIP transcription factor	Homo sapiens	50-53
11835076-7	1994	Significantly (p less-than-or-equal 0.05) more HCTZ plus perindopril patients (53.2%) than HCTZ plus placebo patients (24.5%) achieved an adequate response to therapy (supine DBP <90 mmHg or decrease by >10 mmHg).	Hydrochlorothiazide	47-51	D-box binding PAR bZIP transcription factor	Homo sapiens	175-178
8720766-7	1994	Serum insulin levels after glucose administration were lower when the patients were treated with felodipine than when taking hydrochlorothiazide.	Hydrochlorothiazide	125-144	insulin	Homo sapiens	6-13
8082049-0	1994	The modulatory effect of endogenous parathyroid hormone on the action of hydrochlorothiazide in pseudohypoparathyroidism type I.	Hydrochlorothiazide	73-92	parathyroid hormone	Homo sapiens	36-55
8082049-4	1994	Serum parathyroid hormone (PTH) in PHP type I decreased (P < 0.02) after HCTZ administration in response to the increase in serum Ca.	Hydrochlorothiazide	76-80	parathyroid hormone	Homo sapiens	6-25
8206564-7	1994	Also, as body mass index increased, participants taking hydrochlorothiazide had a corresponding increase of serum insulin (P < .05).	Hydrochlorothiazide	56-75	insulin	Homo sapiens	114-121
8200305-4	1993	Serum insulin concentration decreased in 10 patients with essential hypertension at 1 and 2 hour postload during OGTT after antihypertensive treatment with captopril or captopril plus hydrochlorothiazide.	Hydrochlorothiazide	184-203	insulin	Homo sapiens	6-13
10147231-6	1994	Secondly, if once-daily administration is used to promote patient compliance, physicians should be aware that, of the frequently prescribed first-line antihypertensive drugs, hydrochlorothiazide, chlorthalidone and atenolol presently have substantially less expensive once-daily dosage forms than other diuretics or beta-blockers, calcium antagonists or ACE inhibitors.	Hydrochlorothiazide	175-194	angiotensin I converting enzyme	Homo sapiens	354-357
7506210-7	1994	The addition of 500 microM hydrochlorothiazide (HCTZ) to the luminal membranes of distal tubules incubated with PTH further enhanced Ca2+ uptake.	Hydrochlorothiazide	27-46	parathyroid hormone	Oryctolagus cuniculus	112-115
7506210-7	1994	The addition of 500 microM hydrochlorothiazide (HCTZ) to the luminal membranes of distal tubules incubated with PTH further enhanced Ca2+ uptake.	Hydrochlorothiazide	48-52	parathyroid hormone	Oryctolagus cuniculus	112-115
8117053-4	1993	L/HCTZ and C/HCTZ significantly lowered SBP and DBP on occasional recordings and on ABPM.	Hydrochlorothiazide	2-6	selenium binding protein 1	Homo sapiens	40-43
8117053-5	1993	The mean fall in blood pressure on ABPM (SBP, DBP, mean of 24-hour recording, diurnal and nocturnal) at 4 weeks was greater with L/HCTZ than with C/HCTZ.	Hydrochlorothiazide	131-135	selenium binding protein 1	Homo sapiens	41-44
8251321-3	1993	While hydrochlorothiazide therapy alone or in combination with prostaglandin inhibitors or amiloride has been successful in children and adolescents, this is the first report of the successful use of hydrochlorothiazide and amiloride in an infant with congenital NDI.	Hydrochlorothiazide	200-219	arginine vasopressin receptor 2	Homo sapiens	263-266
8281530-4	1993	Plasma glucose concentrations remained unchanged, while insulin and C-peptide concentrations were higher in association with hydrochlorothiazide treatment.	Hydrochlorothiazide	125-144	insulin	Homo sapiens	56-63
8396366-1	1993	We have developed a "test-tube" assay to determine the biological activity of synthetic preparations of human calcitonin (hCT).	Hydrochlorothiazide	122-125	calcitonin related polypeptide alpha	Homo sapiens	110-120
8281530-6	1993	The changes in daylong plasma glucose and insulin-stimulated glucose uptake increased after hydrochlorothiazide treatment and decreased following lisinopril.	Hydrochlorothiazide	92-111	insulin	Homo sapiens	42-49
1363127-1	1992	Renin response to nifedipine, verapamil, propranolol and hypothiazide was studied in 133 patients with Stage II hypertensive disease.	Hydrochlorothiazide	57-69	renin	Homo sapiens	0-5
7512473-6	1993	Preliminary results of an ongoing study investigating the effects of trandolapril or the diuretic combination of hydrochlorothiazide and triamterene on serum glucose and insulin levels are presented.	Hydrochlorothiazide	113-132	insulin	Homo sapiens	170-177
8513849-6	1993	The high response rate to low dose cilazapril monotherapy and hydrochlorothiazide combination therapy has important implications for minimising the cost of therapy with ACE inhibitors.	Hydrochlorothiazide	62-81	angiotensin I converting enzyme	Homo sapiens	169-172
1337459-8	1992	Hydrochlorothiazide increased PRA, AII, and aldosterone, and lowered blood pressure mainly through a reduction in cardiac output.	Hydrochlorothiazide	0-19	NLR family pyrin domain containing 3	Homo sapiens	35-38
8223839-5	1993	Controlled-release metoprolol with hydrochlorothiazide combines effective beta 1-adrenoceptor blockade for 24 h without affecting the pharmacokinetics of hydrochlorothiazide.	Hydrochlorothiazide	35-54	adrenoceptor beta 1	Homo sapiens	74-93
1597846-5	1992	DTZ SR/HCTZ (120/12.5 mg) produced statistically significantly greater reductions in supine DBP compared with each monotherapy and placebo.	Hydrochlorothiazide	7-11	D-box binding PAR bZIP transcription factor	Homo sapiens	92-95
1350796-2	1992	Eight weeks" treatment with the combination of ACE inhibitor and beta-blocker or the diuretic and beta-blocker produced falls in blood pressure (lying: -8.4 +/- 15.4/ -7.3 +/- 80 mmHg and -6.1 +/- 15.3/ -5.2 +/- 8.8 mmHg [mean +/- SD] for lisinopril and hydrochlorothiazide respectively; standing: -10.2 +/- 14.2/8.2 +/- 9.2 mmHg and -6.8 +/- 14/ -6.3 +/- 10.3 mmHg for lisinopril and hydrochlorothiazide respectively) which were not statistically significantly different.	Hydrochlorothiazide	254-273	angiotensin I converting enzyme	Homo sapiens	47-50
1350796-2	1992	Eight weeks" treatment with the combination of ACE inhibitor and beta-blocker or the diuretic and beta-blocker produced falls in blood pressure (lying: -8.4 +/- 15.4/ -7.3 +/- 80 mmHg and -6.1 +/- 15.3/ -5.2 +/- 8.8 mmHg [mean +/- SD] for lisinopril and hydrochlorothiazide respectively; standing: -10.2 +/- 14.2/8.2 +/- 9.2 mmHg and -6.8 +/- 14/ -6.3 +/- 10.3 mmHg for lisinopril and hydrochlorothiazide respectively) which were not statistically significantly different.	Hydrochlorothiazide	385-404	angiotensin I converting enzyme	Homo sapiens	47-50
1597846-6	1992	The lower doses of DTZ SR/HCTZ (60/6.25 mg and 90/6.25 mg) produced statistically significantly greater supine DBP reductions compared with DTZ SR monotherapy and placebo, but not compared with HCTZ monotherapy.	Hydrochlorothiazide	26-30	D-box binding PAR bZIP transcription factor	Homo sapiens	111-114
1930859-13	1991	Plasma renin activity (PRA) increased with HCTZ but not with NIF.	Hydrochlorothiazide	43-47	renin	Homo sapiens	7-12
1665178-7	1991	A total of 93.6% of patients on L/HCTZ achieved a fall in DBP of greater than or equal to 10 mm Hg, compared with 86.7% of patients on C/HCTZ (ns).	Hydrochlorothiazide	34-38	D-box binding PAR bZIP transcription factor	Homo sapiens	58-61
1665178-10	1991	In conclusion, L/HCTZ was as well tolerated as C/HCTZ, but produced a greater fall in DBP.	Hydrochlorothiazide	17-21	D-box binding PAR bZIP transcription factor	Homo sapiens	86-89
1665184-3	1991	SBP reduction from baseline in the L/HCTZ group was significantly greater, sitting and standing, compared with both the monotherapy groups.	Hydrochlorothiazide	37-41	selenium binding protein 1	Homo sapiens	0-3
1665184-4	1991	Sitting DBP reduction from baseline in the L/HCTZ group was significantly greater than in the hydrochlorothiazide group.	Hydrochlorothiazide	45-49	D-box binding PAR bZIP transcription factor	Homo sapiens	8-11
1665184-4	1991	Sitting DBP reduction from baseline in the L/HCTZ group was significantly greater than in the hydrochlorothiazide group.	Hydrochlorothiazide	94-113	D-box binding PAR bZIP transcription factor	Homo sapiens	8-11
1312233-10	1992	The LIS + HCTZ association caused a significant reduction of DBP in comparison to the other combined treatment (88.1 +/- 0.7 vs 90.3 +/- 0.7; p = 0.026).	Hydrochlorothiazide	10-14	D-box binding PAR bZIP transcription factor	Homo sapiens	61-64
1312233-12	1992	At the end of the study 79.5% of patients treated with LIS + HCTZ presented normal results (DBP less than or equal to 90 mmHg), whereas the percentage of similar results in the comparison group was 72%.	Hydrochlorothiazide	61-65	D-box binding PAR bZIP transcription factor	Homo sapiens	92-95
1836220-2	1991	The doses were increased to 10 mg of fosinopril or 50 mg of hydrochlorothiazide if DBP remained above 95 mmHg.	Hydrochlorothiazide	60-79	D-box binding PAR bZIP transcription factor	Homo sapiens	83-86
1920817-5	1991	The combination of KET + HCTZ in the acute study reduced significantly systolic (SBP) and diastolic (DBP) blood pressures for up to 10 hrs.	Hydrochlorothiazide	25-29	selenium binding protein 1	Homo sapiens	81-84
1720834-8	1991	On the other hand, 25 mg of HCTZ increased plasma renin and aldosterone, but left catecholamines unchanged.	Hydrochlorothiazide	28-32	renin	Homo sapiens	50-55
1720834-11	1991	HCTZ, in doses as low as 25 mg, is still capable of stimulating the renin-angiotensin-aldosterone system.	Hydrochlorothiazide	0-4	renin	Homo sapiens	68-73
1853956-11	1991	At the doses studied, hydrochlorothiazide was also more potent than furosemide in increasing plasma renin activity, increasing sodium excretion, and decreasing lithium excretion.	Hydrochlorothiazide	22-41	renin	Homo sapiens	100-105
2045762-10	1991	HCTZ exhibited marginal but significant negative effects on fibrinogen, PV and indices of RBC deformability, but not on RBC aggregation.	Hydrochlorothiazide	0-4	fibrinogen beta chain	Homo sapiens	60-70
2024911-4	1991	After 8 weeks of treatment, the E/HCTZ group had the greatest proportion of normotensive patients (65.9 p. cent, DBP less than or equal to 90 mmHg) and of responders (81.8 p. cent, diastolic blood pressure decrease greater than 10 mmHg).	Hydrochlorothiazide	34-38	D-box binding PAR bZIP transcription factor	Homo sapiens	113-116
2396677-2	1990	In the presence of vasopressin, hydrochlorothiazide (0.1 mM) markedly reduced the net rate of Na absorption, Cl absorption, and active fluid absorption but did not significantly change the transepithelial voltage.	Hydrochlorothiazide	32-51	arginine vasopressin	Rattus norvegicus	19-30
1824760-7	1991	Fasting blood glucose (190 +/- 21 versus 152 +/- 15 mg/dl; p less than 0.01), glucose levels, basal and glucose-stimulated insulin levels were significantly higher after hydrochlorothiazide compared with placebo but remained unchanged after calcium antagonist treatment.	Hydrochlorothiazide	170-189	insulin	Homo sapiens	123-130
1824760-8	1991	Basal hepatic glucose production and peripheral insulin resistance were significantly elevated after hydrochlorothiazide compared with placebo or calcium antagonist therapy.	Hydrochlorothiazide	101-120	insulin	Homo sapiens	48-55
2090833-4	1990	During treatment, increases in total cholesterol, low-density lipoprotein cholesterol (LDL-C) and triglycerides following hydrochlorothiazide, and increases of LDL-C and triglycerides and a decrease of high-density lipoprotein cholesterol (HDL-C) following atenolol were observed up to 42 months.	Hydrochlorothiazide	122-141	component of oligomeric golgi complex 2	Homo sapiens	87-92
2090833-5	1990	After 5.2 +/- 1.4 years of randomised antihypertensive treatment, cessation of hydrochlorothiazide led to a decrease of total cholesterol from 6.40 to 5.98 mmol/l and of LDL-C from 4.33 to 3.89 mmol/l.	Hydrochlorothiazide	79-98	component of oligomeric golgi complex 2	Homo sapiens	170-175
2266340-3	1990	Patients on hydrochlorothiazide showed a significant increase (P less than 0.01) in low-density lipoprotein cholesterol (LDL-C) after 3 months of treatment.	Hydrochlorothiazide	12-31	component of oligomeric golgi complex 2	Homo sapiens	121-126
2266340-5	1990	In patients treated with both hydrochlorothiazide and metoprolol, total cholesterol increased after 3 (P less than 0.001) and 6 months (P less than 0.05), triglycerides increased after 6 (P less than 0.01) and 12 months (P less than 0.01), and LDL-C increased after 3 (P less than 0.05), 6 (P less than 0.001) and 12 months (P less than 0.01) of treatment, respectively.	Hydrochlorothiazide	30-49	component of oligomeric golgi complex 2	Homo sapiens	244-249
2225702-4	1990	Hydrochlorothiazide administration resulted in a 1 kg weight loss and stimulation of plasma renin activity from 1.7 +/- 0.4 to 5.3 +/- 1.1 ng angiotensin I/ml/hr.	Hydrochlorothiazide	0-19	renin	Homo sapiens	92-97
2225702-4	1990	Hydrochlorothiazide administration resulted in a 1 kg weight loss and stimulation of plasma renin activity from 1.7 +/- 0.4 to 5.3 +/- 1.1 ng angiotensin I/ml/hr.	Hydrochlorothiazide	0-19	angiotensinogen	Homo sapiens	142-155
2216936-1	1990	The purpose of the study was to evaluate the effect of 6 weeks treatment with hydrochlorothiazide or propranolol on gastric acid and gastrin secretion in essential hypertension.	Hydrochlorothiazide	78-97	gastrin	Homo sapiens	133-140
25636696-0	2015	Assessing pharmacokinetic interactions between the sodium glucose cotransporter 2 inhibitor empagliflozin and hydrochlorothiazide or torasemide in patients with type 2 diabetes mellitus: a randomized, open-label, crossover study.	Hydrochlorothiazide	110-129	solute carrier family 5 member 2	Homo sapiens	51-81
1974505-10	1990	The patients who received carvedilol in combination with HCTZ and were evaluated for efficacy (n = 38) showed a decrease in SBP/DBP from 156/97 at the end of monotherapy to 145/88 mmHg after 10 weeks; the combination of atenolol with HCTZ (n = 44) reduced BP from 162/97 to 147/88.	Hydrochlorothiazide	57-61	selenium binding protein 1	Homo sapiens	124-127
1974505-10	1990	The patients who received carvedilol in combination with HCTZ and were evaluated for efficacy (n = 38) showed a decrease in SBP/DBP from 156/97 at the end of monotherapy to 145/88 mmHg after 10 weeks; the combination of atenolol with HCTZ (n = 44) reduced BP from 162/97 to 147/88.	Hydrochlorothiazide	57-61	D-box binding PAR bZIP transcription factor	Homo sapiens	128-131
1974505-14	1990	significantly reduced both SBP and DBP over 24 h. The addition of HCTZ led to a further increase in antihypertensive efficacy.	Hydrochlorothiazide	66-70	selenium binding protein 1	Homo sapiens	27-30
2076713-5	1990	The significant increase in plasma renin activity produced by perindopril alone was potentiated by concurrent administration of hydrochlorothiazide.	Hydrochlorothiazide	128-147	renin	Homo sapiens	35-40
2274021-2	1990	In patients with reduced circulating levels of vasopressin, chlorpropamide, clofibrate, idroclorotiazide etc., enhance the effect of vasopressin on the renal tubule or induce a release of vasopressin, thus reducing the diuresis.	Hydrochlorothiazide	88-104	arginine vasopressin	Homo sapiens	47-58
2274021-2	1990	In patients with reduced circulating levels of vasopressin, chlorpropamide, clofibrate, idroclorotiazide etc., enhance the effect of vasopressin on the renal tubule or induce a release of vasopressin, thus reducing the diuresis.	Hydrochlorothiazide	88-104	arginine vasopressin	Homo sapiens	133-144
2274021-2	1990	In patients with reduced circulating levels of vasopressin, chlorpropamide, clofibrate, idroclorotiazide etc., enhance the effect of vasopressin on the renal tubule or induce a release of vasopressin, thus reducing the diuresis.	Hydrochlorothiazide	88-104	arginine vasopressin	Homo sapiens	133-144
1694931-6	1990	Hydrochlorothiazide treatment was associated with a decrease in insulin sensitivity and an increase in blood glucose concentrations.	Hydrochlorothiazide	0-19	insulin	Homo sapiens	64-71
24821289-9	2015	After the addition of HCTZ therapy, systolic and diastolic blood pressures (S-BP, D-BP) as well as proteinuria significantly decreased (S-BP: at 6 months, p < 0.05 and 12 months, p < 0.01 vs. 0 month, D-BP: at 12 months, p < 0.05 vs. 0 month, proteinuria: at 6 months, p < 0.05 and 12 months, p < 0.01 vs. 0 month).	Hydrochlorothiazide	22-26	selenium binding protein 1	Homo sapiens	76-80
24821289-9	2015	After the addition of HCTZ therapy, systolic and diastolic blood pressures (S-BP, D-BP) as well as proteinuria significantly decreased (S-BP: at 6 months, p < 0.05 and 12 months, p < 0.01 vs. 0 month, D-BP: at 12 months, p < 0.05 vs. 0 month, proteinuria: at 6 months, p < 0.05 and 12 months, p < 0.01 vs. 0 month).	Hydrochlorothiazide	22-26	D-box binding PAR bZIP transcription factor	Homo sapiens	82-86
24821289-9	2015	After the addition of HCTZ therapy, systolic and diastolic blood pressures (S-BP, D-BP) as well as proteinuria significantly decreased (S-BP: at 6 months, p < 0.05 and 12 months, p < 0.01 vs. 0 month, D-BP: at 12 months, p < 0.05 vs. 0 month, proteinuria: at 6 months, p < 0.05 and 12 months, p < 0.01 vs. 0 month).	Hydrochlorothiazide	22-26	selenium binding protein 1	Homo sapiens	136-140
24821289-9	2015	After the addition of HCTZ therapy, systolic and diastolic blood pressures (S-BP, D-BP) as well as proteinuria significantly decreased (S-BP: at 6 months, p < 0.05 and 12 months, p < 0.01 vs. 0 month, D-BP: at 12 months, p < 0.05 vs. 0 month, proteinuria: at 6 months, p < 0.05 and 12 months, p < 0.01 vs. 0 month).	Hydrochlorothiazide	22-26	D-box binding PAR bZIP transcription factor	Homo sapiens	207-211
35314480-10	2022	During hydrochlorothiazide treatment, plasma copeptin (surrogate for vasopressin) decreased, quality of life improved, and several markers of kidney damage and glucose metabolism improved.	Hydrochlorothiazide	7-26	arginine vasopressin	Homo sapiens	45-53
34623176-8	2021	In the heart, increased levels of the pro-fibrotic proteins Col-I, Col-III and TGF-beta1 and gene expression of pro-remodeling molecules TGF-beta1, CTGF, MCP-1 and PAI-1 and the pro-oxidative molecules gp91phox and p22phox were significantly reduced by HCTZ, fasudil and spironolactone.	Hydrochlorothiazide	253-257	transforming growth factor, beta 1	Rattus norvegicus	79-88
34623176-8	2021	In the heart, increased levels of the pro-fibrotic proteins Col-I, Col-III and TGF-beta1 and gene expression of pro-remodeling molecules TGF-beta1, CTGF, MCP-1 and PAI-1 and the pro-oxidative molecules gp91phox and p22phox were significantly reduced by HCTZ, fasudil and spironolactone.	Hydrochlorothiazide	253-257	transforming growth factor, beta 1	Rattus norvegicus	137-146
34623176-8	2021	In the heart, increased levels of the pro-fibrotic proteins Col-I, Col-III and TGF-beta1 and gene expression of pro-remodeling molecules TGF-beta1, CTGF, MCP-1 and PAI-1 and the pro-oxidative molecules gp91phox and p22phox were significantly reduced by HCTZ, fasudil and spironolactone.	Hydrochlorothiazide	253-257	cellular communication network factor 2	Rattus norvegicus	148-152
34623176-8	2021	In the heart, increased levels of the pro-fibrotic proteins Col-I, Col-III and TGF-beta1 and gene expression of pro-remodeling molecules TGF-beta1, CTGF, MCP-1 and PAI-1 and the pro-oxidative molecules gp91phox and p22phox were significantly reduced by HCTZ, fasudil and spironolactone.	Hydrochlorothiazide	253-257	mast cell protease 1-like 1	Rattus norvegicus	154-159
34623176-8	2021	In the heart, increased levels of the pro-fibrotic proteins Col-I, Col-III and TGF-beta1 and gene expression of pro-remodeling molecules TGF-beta1, CTGF, MCP-1 and PAI-1 and the pro-oxidative molecules gp91phox and p22phox were significantly reduced by HCTZ, fasudil and spironolactone.	Hydrochlorothiazide	253-257	serpin family E member 1	Rattus norvegicus	164-169
34623176-8	2021	In the heart, increased levels of the pro-fibrotic proteins Col-I, Col-III and TGF-beta1 and gene expression of pro-remodeling molecules TGF-beta1, CTGF, MCP-1 and PAI-1 and the pro-oxidative molecules gp91phox and p22phox were significantly reduced by HCTZ, fasudil and spironolactone.	Hydrochlorothiazide	253-257	cytochrome b-245 beta chain	Rattus norvegicus	202-210
34623176-8	2021	In the heart, increased levels of the pro-fibrotic proteins Col-I, Col-III and TGF-beta1 and gene expression of pro-remodeling molecules TGF-beta1, CTGF, MCP-1 and PAI-1 and the pro-oxidative molecules gp91phox and p22phox were significantly reduced by HCTZ, fasudil and spironolactone.	Hydrochlorothiazide	253-257	cytochrome b-245 alpha chain	Rattus norvegicus	215-222
34434485-3	2021	Under acute exposure, therapeutically relevant concentrations of HCTZ (70, 140, and 370 ng/mL) amplified UVA-induced double-strand breaks, oxidative DNA, and protein damage in HaCaT human keratinocytes, and this effect was associated to a defective activity of the DNA repair enzyme, OGG1.	Hydrochlorothiazide	65-69	8-oxoguanine DNA glycosylase	Homo sapiens	284-288
34834341-6	2021	In the case of MET HCl-HTZ (chiMET HCl = 0.66), we observed a slight enhancement in the dissolution properties compared with pure HTZ (1.21-fold).	Hydrochlorothiazide	23-26	SAFB like transcription modulator	Homo sapiens	15-18
34608550-0	2021	Synthesis of 1,2,3,triazole modified analogues of hydrochlorothiazide via click chemistry approach and in-vitro alpha-glucosidase enzyme inhibition studies.	Hydrochlorothiazide	50-69	sucrase isomaltase (alpha-glucosidase)	Mus musculus	112-129
35314480-10	2022	During hydrochlorothiazide treatment, plasma copeptin (surrogate for vasopressin) decreased, quality of life improved, and several markers of kidney damage and glucose metabolism improved.	Hydrochlorothiazide	7-26	arginine vasopressin	Homo sapiens	69-80
35175408-1	2022	BACKGROUND/AIMS: To investigate a possible association between the use of hydrochlorothiazide (HCT) and/or angiotensin-converting enzyme inhibitors (ACE inhibitors) and the occurrence of periocular non-melanoma skin cancer.	Hydrochlorothiazide	74-93	angiotensin I converting enzyme	Homo sapiens	149-152
35175408-1	2022	BACKGROUND/AIMS: To investigate a possible association between the use of hydrochlorothiazide (HCT) and/or angiotensin-converting enzyme inhibitors (ACE inhibitors) and the occurrence of periocular non-melanoma skin cancer.	Hydrochlorothiazide	95-98	angiotensin I converting enzyme	Homo sapiens	149-152
2643413-4	1989	Furthermore, while hydrochlorothiazide lowered serum potassium values (4.2 +/- 0.25 mmol/L to 3.7 +/- 0.35 mmol/L) and stimulated plasma renin activity (1.5 +/- 1.3 ng/mL/h) pretreatment to 3.3 +/- 2.7 ng/mL/h with verapamil), verapamil only modestly elevated renin activity (1.5 +/- 1.3 ng/mL/h pretreatment to 2.7 +/- 2.5 ng/mL/h with verapamil) and did not lower potassium values.	Hydrochlorothiazide	19-38	renin	Homo sapiens	137-142
2586018-0	1989	Interference of different ACE-inhibitors with the diuretic action of furosemide and hydrochlorothiazide.	Hydrochlorothiazide	84-103	angiotensin I converting enzyme	Homo sapiens	26-29
2671740-3	1989	Captopril increased the insulin-mediated disposal of glucose, as compared with placebo, from 5.7 +/- 2.4 to 6.3 +/- 2.5 mg per kilogram of body weight per minute (P less than 0.05), whereas hydrochlorothiazide caused a decrease from 6.4 +/- 2.0 to 5.7 +/- 1.9 (P less than 0.01).	Hydrochlorothiazide	190-209	insulin	Homo sapiens	24-31
2671740-5	1989	Hydrochlorothiazide increased the basal insulin concentration and the late insulin response to glucose.	Hydrochlorothiazide	0-19	insulin	Homo sapiens	40-47
2671740-5	1989	Hydrochlorothiazide increased the basal insulin concentration and the late insulin response to glucose.	Hydrochlorothiazide	0-19	insulin	Homo sapiens	75-82
2565158-1	1989	An attempt was made to establish whether cardioselective beta-blockade could counteract the stimulation by hydrochlorothiazide of the renin-angiotensin and sympathetic nervous systems and to what extent such actions contributed to the antihypertensive effect of bevantolol.	Hydrochlorothiazide	107-126	renin	Homo sapiens	134-139
2643413-4	1989	Furthermore, while hydrochlorothiazide lowered serum potassium values (4.2 +/- 0.25 mmol/L to 3.7 +/- 0.35 mmol/L) and stimulated plasma renin activity (1.5 +/- 1.3 ng/mL/h) pretreatment to 3.3 +/- 2.7 ng/mL/h with verapamil), verapamil only modestly elevated renin activity (1.5 +/- 1.3 ng/mL/h pretreatment to 2.7 +/- 2.5 ng/mL/h with verapamil) and did not lower potassium values.	Hydrochlorothiazide	19-38	renin	Homo sapiens	260-265
2540224-8	1989	Lisinopril alone or in combination with hydrochlorothiazide produces favorable antihypertensive effects in both younger and older predominantly black, low-renin patients with essential hypertension.	Hydrochlorothiazide	40-59	renin	Homo sapiens	155-160
3049338-9	1988	Plasma renin activity was initially higher in whites than in blacks and rose significantly more in blacks and whites requiring the greatest volume losses and the highest dose of hydrochlorothiazide to attain goal BP.	Hydrochlorothiazide	178-197	renin	Homo sapiens	7-12
2708546-8	1989	Clp was significantly less in patients taking hydrochlorothiazide (27 vs. 31 L/hr) and greater in smokers (33 vs. 29 L/hr).	Hydrochlorothiazide	46-65	calmodulin like 3	Homo sapiens	0-3
3281620-4	1988	We hypothesized that black patients with uncontrolled hypertension and low plasma renin activity on usual-dose hydrochlorothiazide therapy (ie, 50 mg/d) would respond better to higher doses of hydrochlorothiazide (ie, 100 to 150 mg/d) than to a usual-dose diuretic and metoprolol.	Hydrochlorothiazide	193-212	renin	Homo sapiens	82-87
2970886-0	1988	Interaction of amiloride and hydrochlorothiazide with atrial natriuretic factor in the medullary collecting duct.	Hydrochlorothiazide	29-48	natriuretic peptide A	Rattus norvegicus	54-79
2970886-5	1988	Atrial natriuretic factor reduced collecting duct sodium reabsorption when added to amiloride or hydrochlorothiazide to 23% and to 41%, respectively, but had no additional effect when given with amiloride and hydrochlorothiazide.	Hydrochlorothiazide	97-116	natriuretic peptide A	Rattus norvegicus	0-25
3281620-4	1988	We hypothesized that black patients with uncontrolled hypertension and low plasma renin activity on usual-dose hydrochlorothiazide therapy (ie, 50 mg/d) would respond better to higher doses of hydrochlorothiazide (ie, 100 to 150 mg/d) than to a usual-dose diuretic and metoprolol.	Hydrochlorothiazide	111-130	renin	Homo sapiens	82-87
2438500-8	1987	Thus, diltiazem and HCTZ were similar in that the depressor response to each drug activated the renin-angiotensin system, which in turn was accompanied by increased production of PGE2-M.	Hydrochlorothiazide	20-24	renin	Homo sapiens	96-101
3383998-11	1988	The anti-hypertensive effect was potentiated significantly in hydrochlorothiazide-pretreated SHR when the plasma renin activity was increased.	Hydrochlorothiazide	62-81	renin	Rattus norvegicus	113-118
3383998-16	1988	Trandolapril produced dose-related (30-1000 micrograms/kg) reductions in BP, total peripheral resistance and heart work in dogs pretreated with hydrochlorothiazide to increase plasma renin activity.	Hydrochlorothiazide	144-163	renin	Canis lupus familiaris	183-188
3286683-1	1988	A colorimetric enzyme amplification system was used to develop an immunoassay for human calcitonin (hCT) with a sensitivity of 6 pmol/l, and intra- and inter-assay CVs of 12% and 11.8% respectively for the low pool, and 10% and 11.2% for the high pool.	Hydrochlorothiazide	100-103	calcitonin related polypeptide alpha	Homo sapiens	88-98
2828800-5	1988	Administration of hydrochlorothiazide or Ro 5-4864 for five days also caused diuresis and increased renal PBR density.	Hydrochlorothiazide	18-37	translocator protein	Rattus norvegicus	106-109
2833190-12	1987	However, the onset of the hypotension effect was more rapid for both ACE inhibitors in HCTZ-pretreated dogs.	Hydrochlorothiazide	87-91	angiotensin I converting enzyme	Canis lupus familiaris	69-72
2832575-10	1987	Both hydrochlorothiazide and atenolol increased plasma atrial natriuretic peptide (ANP) concentrations (P less than 0.01), suggesting that ANP could contribute to the hypotensive effects of these two drug classes.	Hydrochlorothiazide	5-24	natriuretic peptide A	Homo sapiens	55-81
2832575-10	1987	Both hydrochlorothiazide and atenolol increased plasma atrial natriuretic peptide (ANP) concentrations (P less than 0.01), suggesting that ANP could contribute to the hypotensive effects of these two drug classes.	Hydrochlorothiazide	5-24	natriuretic peptide A	Homo sapiens	83-86
2832575-10	1987	Both hydrochlorothiazide and atenolol increased plasma atrial natriuretic peptide (ANP) concentrations (P less than 0.01), suggesting that ANP could contribute to the hypotensive effects of these two drug classes.	Hydrochlorothiazide	5-24	natriuretic peptide A	Homo sapiens	139-142
3623734-5	1987	Statistically, serum insulin decreased significantly with verapamil (13.4 +/- 4.3 U/ml, m +/- SD) when compared with both the wash-out (16.2 +/- 5.7 U/ml) and hydrochlorothiazide (17.1 +/- 6.5 ml) periods.	Hydrochlorothiazide	159-178	insulin	Homo sapiens	21-28
3320720-8	1987	Hydrochlorothiazide patients had increases in serum uric acid, serum globulin, CO2 content, and plasma renin activity.	Hydrochlorothiazide	0-19	renin	Homo sapiens	103-108
3617754-0	1987	[Evaluation of the effect of long-term treatment with hydrochlorothiazide on the activity of the renin-angiotensin-aldosterone system, sodium metabolism and renal function in patients with primary arterial hypertension].	Hydrochlorothiazide	54-73	renin	Homo sapiens	97-102
3024863-5	1987	Similar results were obtained in normotensive rats treated with hydrochlorothiazide; the increase in coronary flow after captopril correlated significantly with the control plasma renin activity.	Hydrochlorothiazide	64-83	renin	Rattus norvegicus	180-185
3517076-4	1986	Mean basal plasma renin activity rose significantly from 0.45 +/- 0.44 to 1.42 +/- 1.31 ng/mL/hr and from 0.67 +/- 0.46 to 1.27 +/- 0.83 ng/mL/hr in patients receiving hydrochlorothiazide and combination therapy, respectively, but there was no change in those administered pindolol.	Hydrochlorothiazide	168-187	renin	Homo sapiens	18-23
3551335-0	1986	[Effect of long-term hydrochlorothiazide treatment on blood pressure and plasma volume in patients with normal and low-renin arterial hypertension].	Hydrochlorothiazide	21-40	renin	Homo sapiens	119-124
3007351-6	1986	Patients receiving enalapril and hydrochlorothiazide showed stimulation of plasma renin activity and suppression of plasma angiotensin II, although the initial degree of suppression was not sustained in all patients during prolonged therapy.	Hydrochlorothiazide	33-52	renin	Homo sapiens	82-87
3007351-6	1986	Patients receiving enalapril and hydrochlorothiazide showed stimulation of plasma renin activity and suppression of plasma angiotensin II, although the initial degree of suppression was not sustained in all patients during prolonged therapy.	Hydrochlorothiazide	33-52	angiotensinogen	Homo sapiens	123-137
3026294-6	1986	Enalapril increased plasma renin activity (PRA), reduced plasma angiotensin II (AII) and aldosterone concentrations, and reduced ACE activity, whereas hydrochlorothiazide increased PRA, plasma AII, and aldosterone concentrations without altering ACE activity.	Hydrochlorothiazide	151-170	angiotensinogen	Homo sapiens	193-196
3710315-10	1986	Plasma renin activities measured after 17 weeks treatment of the drugs indicated that the renin-angiotensin system was activated by hydrochlorothiazide.	Hydrochlorothiazide	132-151	renin	Rattus norvegicus	7-12
3710315-10	1986	Plasma renin activities measured after 17 weeks treatment of the drugs indicated that the renin-angiotensin system was activated by hydrochlorothiazide.	Hydrochlorothiazide	132-151	renin	Rattus norvegicus	90-95
3532044-0	1986	[Effect of hydrochlorothiazide treatment on the secretion of insulin, glucagon and pancreatic polypeptide in patients with arterial hypertension].	Hydrochlorothiazide	11-30	insulin	Homo sapiens	61-68
3710315-11	1986	These results suggest that the antihypertensive effect of long-term administration of SA446 in SHR is enhanced by the combined administration of diuretics such as hydrochlorothiazide, which activates the renin-angiotensin system.	Hydrochlorothiazide	163-182	renin	Rattus norvegicus	204-209
4008611-5	1985	Treatment with hydrochlorothiazide (50 mg/day) produced a decline in fasting urinary Ca (to 0.07 +/- 0.02 mg/100 ml GF; P less than 0.01), serum PTH (from 39 +/- 19 to 21 +/- 1 microliters eq/ml; P less than 0.05), and urinary cAMP excretion (from 5.30 +/- 0.57 to 3.57 +/- 0.59 nmol/100 ml GF; P less than 0.0025).	Hydrochlorothiazide	15-34	parathyroid hormone	Homo sapiens	145-148
4008611-9	1985	That these abnormalities may reflect PTH-dependent osteoclastic resorption and bone turnover was supported by the reduction of these indices after correction of secondary hyperparathyroidism with hydrochlorothiazide therapy.	Hydrochlorothiazide	196-215	parathyroid hormone	Homo sapiens	37-40
4068453-0	1985	[Change in the spectrum of lipids and apoproteins A1 and B as affected by hypothiazide and pratsiol in patients with hypertension].	Hydrochlorothiazide	74-86	BCL2 related protein A1	Homo sapiens	50-58
2985406-1	1985	The long-term effect of hydrochlorothiazide on beta 2-adrenoceptor density on mononuclear cells was investigated in 10 male patients with essential hypertension.	Hydrochlorothiazide	24-43	adrenoceptor beta 2	Homo sapiens	47-66
3156993-0	1985	Novel photoaffinity label for the dopamine D2 receptor: synthesis of 4-azido-5-iodo-2-methoxy-N-[1-(phenylmethyl)-4-piperidinyl] benzamide (iodoazidoclebopride, IAC) and the corresponding 125I-labeled analogue (125IAC).	Hydrochlorothiazide	161-164	dopamine receptor D2	Homo sapiens	34-54
4068453-2	1985	Hydrochlorothiazide caused a significant increase in total cholesterol (CH), LDL cholesterol, apo-A1 and apo-B, and a decrease in cholesterol load of HDL particles as compared to placebo effects.	Hydrochlorothiazide	0-19	apolipoprotein A1	Homo sapiens	94-100
4068453-2	1985	Hydrochlorothiazide caused a significant increase in total cholesterol (CH), LDL cholesterol, apo-A1 and apo-B, and a decrease in cholesterol load of HDL particles as compared to placebo effects.	Hydrochlorothiazide	0-19	apolipoprotein B	Homo sapiens	105-110
3873891-1	1985	Photosensitive eruptions with clinical and histologic features of subacute cutaneous lupus erythematosus and antibodies to SS-A(Ro) antigen occurred in five patients taking hydrochlorothiazide.	Hydrochlorothiazide	173-192	tripartite motif containing 21	Homo sapiens	123-130
2994988-7	1985	Patients on enalapril/hydrochlorothiazide demonstrated stimulation of plasma renin activity with inhibition of plasma angiotensin II, indicating adherence with therapy.	Hydrochlorothiazide	22-41	renin	Homo sapiens	77-82
4094841-4	1985	Hydrochlorothiazide and binazine treatment decreased systolic and diastolic blood pressure, the total electromechanical systolic time index (QS2I) and the left ventricular ejection time index (LVETI), and increased the PEP/LVET index at rest and after exercise.	Hydrochlorothiazide	0-19	progestagen associated endometrial protein	Homo sapiens	219-222
2994988-7	1985	Patients on enalapril/hydrochlorothiazide demonstrated stimulation of plasma renin activity with inhibition of plasma angiotensin II, indicating adherence with therapy.	Hydrochlorothiazide	22-41	angiotensinogen	Homo sapiens	118-132
6337951-0	1983	Synergistic effect of captopril with hydrochlorothiazide for the treatment of low-renin hypertensive black patients.	Hydrochlorothiazide	37-56	renin	Homo sapiens	82-87
6384279-9	1984	In the eight patients requiring diuretic, plasma renin activity remained constant after captopril monotherapy, but rose threefold after hydrochlorothiazide was added.	Hydrochlorothiazide	136-155	renin	Homo sapiens	49-54
6620141-1	1983	VIII: Dissolution survey of marketed hydrochlorothiazide tablets.	Hydrochlorothiazide	37-56	cytochrome c oxidase subunit 8A	Homo sapiens	0-4
6344619-3	1983	In this study, the relation between renin activity and therapeutic response to hydrochlorothiazide or propranolol was studied.	Hydrochlorothiazide	79-98	renin	Homo sapiens	36-41
6344619-12	1983	In comparing therapeutic response, patients with a low renin profile had a better response to hydrochlorothiazide, and propranolol was more effective in patients with a high renin profile.	Hydrochlorothiazide	94-113	renin	Homo sapiens	55-60
6369882-5	1984	Hydrochlorothiazide and amiloride, often used in combination, both have a t 1/2 of about 10 h. Canrenone, an active metabolite of spironolactone, has a t 1/2 of 15-20 h. Chlorthalidone is eliminated very slowly with a t 1/2 of about two days.	Hydrochlorothiazide	0-19	interleukin 1 receptor like 1	Homo sapiens	74-77
6369882-5	1984	Hydrochlorothiazide and amiloride, often used in combination, both have a t 1/2 of about 10 h. Canrenone, an active metabolite of spironolactone, has a t 1/2 of 15-20 h. Chlorthalidone is eliminated very slowly with a t 1/2 of about two days.	Hydrochlorothiazide	0-19	interleukin 1 receptor like 1	Homo sapiens	87-90
6084124-1	1984	The effect of antihypertensive therapy with guanabenz or hydrochlorothiazide (HCTZ) on the secretion of growth hormone, prolactin, insulin, and glucagon was evaluated in double-blind fashion in 45 patients.	Hydrochlorothiazide	78-82	insulin	Homo sapiens	131-138
6756696-0	1982	Plasma active and inactive renin and urinary kallikrein in normal subjects in response to hydrochlorothiazide, spironolactone or aldosterone administration.	Hydrochlorothiazide	90-109	kallikrein related peptidase 4	Homo sapiens	45-55
6338348-0	1983	The effects of hydrochlorothiazide on the renin-aldosterone system.	Hydrochlorothiazide	15-34	renin	Homo sapiens	42-47
6757152-8	1982	In 71% of patients on mepindolol plus hydrochlorothiazide a particularly more marked decrease in DAP was observed.	Hydrochlorothiazide	38-57	death associated protein	Homo sapiens	97-100
6284411-3	1982	HCTZ plus captopril inhibited serum ACE 95.2%; increased PRA 38-fold and reduced MABP 47.5 mm Hg.	Hydrochlorothiazide	0-4	angiotensin I converting enzyme	Rattus norvegicus	36-39
6284411-6	1982	These results suggest that the potentiating effect of HCTZ is due to some mechanism that shifts the animal"s blood pressure maintenance system to a renin-dependent state and is not due to changes in vascular reactivity.	Hydrochlorothiazide	54-58	renin	Rattus norvegicus	148-153
6183482-2	1982	This possibility was investigated by studying the influence of hydrochlorothiazide on blood pressure and urinary kallikrein excretion in patients with essential hypertension.	Hydrochlorothiazide	63-82	kallikrein related peptidase 4	Homo sapiens	113-123
7047003-7	1982	Captopril and HCTZ increased plasma renin activity (PRA) but only the combination of captopril and HCTZ produced a greater and longer lasting increase of PRA.	Hydrochlorothiazide	14-18	renin	Rattus norvegicus	36-41
7047003-8	1982	It is concluded that the mechanism for the synergism is the renin dependency, created by the combination of HCTZ and captopril, resulting in a greater role of the renin system in blood pressure control and increased responsiveness to angiotensin converting enzyme inhibition by captopril.	Hydrochlorothiazide	108-112	renin	Rattus norvegicus	60-65
7047003-8	1982	It is concluded that the mechanism for the synergism is the renin dependency, created by the combination of HCTZ and captopril, resulting in a greater role of the renin system in blood pressure control and increased responsiveness to angiotensin converting enzyme inhibition by captopril.	Hydrochlorothiazide	108-112	renin	Rattus norvegicus	163-168
6280212-1	1982	The effects of diazoxide and hydrochlorothiazide on vasopressin-induced increments in osmotic water flow and sodium transport across the frog bladder were studied.	Hydrochlorothiazide	29-48	arginine vasopressin	Homo sapiens	52-63
7028060-1	1981	1 Chronic treatment with a constant dose of hydrochlorothiazide or tienilic acid increases plasma renin activity (PRA) acutely to reach a maximum within the first week.	Hydrochlorothiazide	44-63	renin	Homo sapiens	98-103
7028060-3	1981	3 A significant (P less than 0.01) correlation (r = 0.74) between changes in plasma angiotensin II and renin activity provoked by chronic treatment for 3 months with hydrochlorothiazide and tienilic acid was found.	Hydrochlorothiazide	166-185	angiotensinogen	Homo sapiens	84-98
7028060-3	1981	3 A significant (P less than 0.01) correlation (r = 0.74) between changes in plasma angiotensin II and renin activity provoked by chronic treatment for 3 months with hydrochlorothiazide and tienilic acid was found.	Hydrochlorothiazide	166-185	renin	Homo sapiens	103-108
7028060-4	1981	4 The increase in plasma aldosterone during chronic treatment with hydrochlorothiazide and tienilic acid (1000 mg) is related (r = 0.68; P less than 0.01) to the rise in plasma angiotensin II.	Hydrochlorothiazide	67-86	angiotensinogen	Homo sapiens	177-191
7004877-5	1980	In a second child with renin-induced hypertension since the firth month of life, treatment wiht hydralazine, clonidine and hydrochlorothiazide was in part effective, but failure to thrive was progressive.	Hydrochlorothiazide	123-142	renin	Homo sapiens	23-28
7016928-0	1981	Effect of guanabenz and hydrochlorothiazide on blood pressure and plasma renin activity.	Hydrochlorothiazide	24-43	renin	Homo sapiens	73-78
7024946-0	1981	[Levels of cholesterol, triglycerides, uric acid and glucose following prolonged treatment of hypertension with low and normal renin activity with hydrochlorothiazide].	Hydrochlorothiazide	147-166	renin	Homo sapiens	127-132
7018804-4	1981	On captopril and hydrochlorothiazide the plasma concentrations of renin substrate and angiotensin II decreased markedly, while renin and angiotensin I levels were increased.	Hydrochlorothiazide	17-36	renin	Homo sapiens	66-71
7018804-4	1981	On captopril and hydrochlorothiazide the plasma concentrations of renin substrate and angiotensin II decreased markedly, while renin and angiotensin I levels were increased.	Hydrochlorothiazide	17-36	angiotensinogen	Homo sapiens	86-100
7018804-4	1981	On captopril and hydrochlorothiazide the plasma concentrations of renin substrate and angiotensin II decreased markedly, while renin and angiotensin I levels were increased.	Hydrochlorothiazide	17-36	renin	Homo sapiens	127-132
7018804-4	1981	On captopril and hydrochlorothiazide the plasma concentrations of renin substrate and angiotensin II decreased markedly, while renin and angiotensin I levels were increased.	Hydrochlorothiazide	17-36	angiotensinogen	Homo sapiens	86-99
7047914-0	1981	The secretion of insulin in patients with arterial hypertension, treated with hydrochlorothiazide.	Hydrochlorothiazide	78-97	insulin	Homo sapiens	17-24
518220-3	1979	Renin status was categorized by (1) the intravenous furosemide test, (2) ambulation during placebo, and (3) ambulation during spironolactone and hydrochlorothiazide treatment.	Hydrochlorothiazide	145-164	renin	Homo sapiens	0-5
518220-5	1979	No method identified a low renin subgroup that was more responsive to either spironolactone or hydrochlorothiazide.	Hydrochlorothiazide	95-114	renin	Homo sapiens	27-32
282043-0	1978	Acid-activated renin responses to hydrochlorothiazide, propranol and indomethacin.	Hydrochlorothiazide	34-53	renin	Homo sapiens	15-20
744063-1	1978	The anatomical distribution of a biologically active and biologically inactive preparation of radioiodinated human calcitonin (hCT) was studied in rats.	Hydrochlorothiazide	127-130	calcitonin related polypeptide alpha	Homo sapiens	115-125
730416-0	1978	Renin-aldosterone system and urinary electrolytes after amiloride, hydrochlorothiazide and the combination.	Hydrochlorothiazide	67-86	renin	Homo sapiens	0-5
883759-0	1977	Plasma renin activity in pregnant women with oedema treated with hydrochlorothiazide.	Hydrochlorothiazide	65-84	renin	Homo sapiens	7-12
696414-0	1978	Influence of sodium intake on hydrochlorothiazide-induced changes in blood pressure, serum electrolytes, renin and aldosterone in essential hypertension.	Hydrochlorothiazide	30-49	renin	Homo sapiens	105-110
318952-0	1977	Spironolactone and hydrochlorothiazide in normal-renin and low-renin essential hypertension.	Hydrochlorothiazide	19-38	renin	Homo sapiens	49-54
318952-0	1977	Spironolactone and hydrochlorothiazide in normal-renin and low-renin essential hypertension.	Hydrochlorothiazide	19-38	renin	Homo sapiens	63-68
799560-0	1976	Quantitative effects of timolol and hydrochlorothiazide on blood pressure, heart rate and plasma renin activity: results of a double-blind factorial trial in patients with essential hypertension.	Hydrochlorothiazide	36-55	renin	Homo sapiens	97-102
60566-0	1976	Effects of timolol and hydrochlorothiazide on blood-pressure and plasma renin activity.	Hydrochlorothiazide	23-42	renin	Homo sapiens	72-77
4318270-0	1970	Effect of furosemide and hydrochlorothiazide on plasma renin activity in man.	Hydrochlorothiazide	25-44	renin	Homo sapiens	55-60
1002400-0	1976	Stimulation of renin secretion by various methods: optional results with hydrochlorothiazide.	Hydrochlorothiazide	73-92	renin	Homo sapiens	15-20
49892-3	1975	Stimulation of the renin-angiotensin system by the salt-free diet, hydrochlorthiazide and by placing the body into orthostatic position caused a relatively weaker increase in the renin activity in comparison with such in healthy individuals.	Hydrochlorothiazide	67-85	renin	Homo sapiens	19-24
234821-6	1975	Plasma renin activity, which did not change during treatment with timolol, was substantially elevated during treatment with hydrochlorothiazide.	Hydrochlorothiazide	124-143	renin	Canis lupus familiaris	7-12
234821-8	1975	When timolol was administered concomitantly with hydrochlorothiazide, plasma renin activity was suppressed and blood pressure was significantly lowered.	Hydrochlorothiazide	49-68	renin	Canis lupus familiaris	77-82
234821-10	1975	These observations suggest that compensatory activation of the renin-angiotensin system limits the antihypertensive activity of hydrochlorothiazide in renal hypertensive dogs and suppression of diuretic-induced renin release by timolol unmasks the antihypertensive effect of the diuretic.	Hydrochlorothiazide	128-147	renin	Canis lupus familiaris	63-68
1100752-4	1975	It is thought that insulin helps the selective action of hydrochlorothiazide on the beta cells by removing the protective glucose barrier.	Hydrochlorothiazide	57-76	insulin	Oryctolagus cuniculus	19-26
4456598-0	1974	[Effects of combined treatment with hydrochlorothiazide and oxprenolol on arterial pressure and activity of plasma renin.	Hydrochlorothiazide	36-55	renin	Homo sapiens	115-120
5537102-0	1970	[Effects of extended application of hydrochlorothiazide on the plasma renin activity and electrolyte balance in adrenalectomized patients].	Hydrochlorothiazide	36-55	renin	Homo sapiens	70-75
33390050-8	2021	We determined NCC activity by standard 50 mg HCTZ sensitivity test (day 11).	Hydrochlorothiazide	45-49	solute carrier family 12 member 3	Homo sapiens	14-17
4313054-0	1969	[Effect of prolonged hydrochlorothiazide administration on the plasma renin activity and aldosterone excretion rate in normal persons].	Hydrochlorothiazide	21-40	renin	Homo sapiens	70-75
14222759-0	1964	[EFFECTS OF OUABAIN, MERCAPTOMERIN AND HYDROCHLOROTHIAZIDE ON ATPASE ACTIVITY OF HUMAN ERYTHROCYTE MEMBRANE].	Hydrochlorothiazide	39-58	dynein axonemal heavy chain 8	Homo sapiens	62-68
13997901-0	1962	[Inbitition of vasopressin antidiures is by hydrochlorothiazide].	Hydrochlorothiazide	44-63	arginine vasopressin	Homo sapiens	15-26
33420690-0	2021	UV-Vis LED-assisted photo-Fenton process for mineralization of losartan and hydrochlorothiazide: optimization using desirability function.	Hydrochlorothiazide	76-95	small integral membrane protein 10 like 2A	Homo sapiens	7-10
33420690-1	2021	This study presents the results obtained for the optimization of the mineralization of losartan (LOS) and hydrochlorothiazide (HCTZ) using the photo-Fenton process with a UV-Vis LED.	Hydrochlorothiazide	106-125	small integral membrane protein 10 like 2A	Homo sapiens	178-181
33420690-1	2021	This study presents the results obtained for the optimization of the mineralization of losartan (LOS) and hydrochlorothiazide (HCTZ) using the photo-Fenton process with a UV-Vis LED.	Hydrochlorothiazide	127-131	small integral membrane protein 10 like 2A	Homo sapiens	178-181
33420690-5	2021	The energy consumption calculated for mineralization of LOS and HCTZ at a concentration of 20 mg L-1 using the UV-Vis LED-assisted photo-Fenton process, at 60 min, was 130 kWh m-3.	Hydrochlorothiazide	64-68	small integral membrane protein 10 like 2A	Homo sapiens	118-121
33727808-14	2021	Conclusion: These findings demonstrated a promising detection specificity and treatment efficacy for our system (SiNPs-TZ, 1:8 Hc-TZ), encouraging its potential use as a new theranostic agent for HER2-positive BC lesions.	Hydrochlorothiazide	127-132	erb-b2 receptor tyrosine kinase 2	Homo sapiens	196-200
33029806-3	2021	HCTZ is excreted in the kidney via organic anion transporters 1 and 3 (OAT1 and OAT3).	Hydrochlorothiazide	0-4	solute carrier family 22 member 6	Homo sapiens	35-69
33029806-3	2021	HCTZ is excreted in the kidney via organic anion transporters 1 and 3 (OAT1 and OAT3).	Hydrochlorothiazide	0-4	solute carrier family 22 member 6	Homo sapiens	71-75
33029806-3	2021	HCTZ is excreted in the kidney via organic anion transporters 1 and 3 (OAT1 and OAT3).	Hydrochlorothiazide	0-4	solute carrier family 22 member 8	Homo sapiens	80-84
33609289-8	2021	RESULTS: Long-term use of HCTZ increased absolute and relative risks of SCC (PS-weighted IRR, 1.95; 95% CI, 1.87-2.02; RD per 100 000 person-years, 87.4), but not of BCC or CMM.	Hydrochlorothiazide	26-30	insulin receptor related receptor	Homo sapiens	89-92
5791574-0	1969	[Effect of dimethylbiguanide on sensitivity to exogenous insulin in nondiabetic subjects treated by hydrochlorothiazide].	Hydrochlorothiazide	100-119	insulin	Homo sapiens	57-64
34020248-7	2021	Interestingly, the chronic administration of a combination of firibastat with [Enalapril+HCTZ] reduced plasma arginine-vasopressin levels by 62% relative to those measured in DOCA-salt rats receiving bitherapy.	Hydrochlorothiazide	89-93	arginine vasopressin	Rattus norvegicus	119-130
34020248-8	2021	Our data show that tritherapy with firibastat, enalapril and HCTZ improves BP control and arginine-vasopressin release in an experimental salt-dependent model of hypertension, paving the way for the development of new treatments for patients with currently difficult-to-treat or resistant hypertension.	Hydrochlorothiazide	61-65	arginine vasopressin	Homo sapiens	99-110
32791082-2	2021	OBJECTIVES: To characterize the association between HCTZ use and invasive SCC, SCC in situ (SCCis) and basal cell carcinoma (BCC).	Hydrochlorothiazide	52-56	serpin family B member 3	Homo sapiens	74-77
32791082-5	2021	RESULTS: A cumulative HCTZ dose above 37,500 mg was associated with increased risk of invasive SCC (OR=1.69, 95% CI: 1.04 - 2.74).	Hydrochlorothiazide	22-26	serpin family B member 3	Homo sapiens	95-98
32791082-8	2021	CONCLUSION: High cumulative exposure to HCTZ is associated with the development of keratinocyte carcinoma and, most importantly, invasive SCC.	Hydrochlorothiazide	40-44	serpin family B member 3	Homo sapiens	138-141
33434556-4	2021	RESULTS: Mean systolic/diastolic blood pressure (SBP/DBP) reduction with HCTZ vs chlorthalidone: 8+-8/4+-5 vs 12+-9/7+-5 mmHg in whites (p<10-6 SBP and DBP); 12+-10/7+-6 vs 15+-10/9+-6 in blacks (p=0.008 SBP, p=0.054 DBP).	Hydrochlorothiazide	73-77	selenium binding protein 1	Homo sapiens	49-52
32956652-3	2021	NHA2 knock-out mice displayed reduced blood pressure, normocalcemic hypocalciuria and an attenuated response to the thiazide diuretic hydrochlorothiazide.	Hydrochlorothiazide	134-153	solute carrier family 9, subfamily B (NHA2, cation proton antiporter 2), member 2	Mus musculus	0-4
33434556-4	2021	RESULTS: Mean systolic/diastolic blood pressure (SBP/DBP) reduction with HCTZ vs chlorthalidone: 8+-8/4+-5 vs 12+-9/7+-5 mmHg in whites (p<10-6 SBP and DBP); 12+-10/7+-6 vs 15+-10/9+-6 in blacks (p=0.008 SBP, p=0.054 DBP).	Hydrochlorothiazide	73-77	D-box binding PAR bZIP transcription factor	Homo sapiens	53-56
33434556-4	2021	RESULTS: Mean systolic/diastolic blood pressure (SBP/DBP) reduction with HCTZ vs chlorthalidone: 8+-8/4+-5 vs 12+-9/7+-5 mmHg in whites (p<10-6 SBP and DBP); 12+-10/7+-6 vs 15+-10/9+-6 in blacks (p=0.008 SBP, p=0.054 DBP).	Hydrochlorothiazide	73-77	selenium binding protein 1	Homo sapiens	144-147
33434556-4	2021	RESULTS: Mean systolic/diastolic blood pressure (SBP/DBP) reduction with HCTZ vs chlorthalidone: 8+-8/4+-5 vs 12+-9/7+-5 mmHg in whites (p<10-6 SBP and DBP); 12+-10/7+-6 vs 15+-10/9+-6 in blacks (p=0.008 SBP, p=0.054 DBP).	Hydrochlorothiazide	73-77	D-box binding PAR bZIP transcription factor	Homo sapiens	152-155
33434556-4	2021	RESULTS: Mean systolic/diastolic blood pressure (SBP/DBP) reduction with HCTZ vs chlorthalidone: 8+-8/4+-5 vs 12+-9/7+-5 mmHg in whites (p<10-6 SBP and DBP); 12+-10/7+-6 vs 15+-10/9+-6 in blacks (p=0.008 SBP, p=0.054 DBP).	Hydrochlorothiazide	73-77	selenium binding protein 1	Homo sapiens	144-147
33434556-4	2021	RESULTS: Mean systolic/diastolic blood pressure (SBP/DBP) reduction with HCTZ vs chlorthalidone: 8+-8/4+-5 vs 12+-9/7+-5 mmHg in whites (p<10-6 SBP and DBP); 12+-10/7+-6 vs 15+-10/9+-6 in blacks (p=0.008 SBP, p=0.054 DBP).	Hydrochlorothiazide	73-77	D-box binding PAR bZIP transcription factor	Homo sapiens	152-155
33434556-5	2021	Treatment with HCTZ vs CTD in whites resulted in significantly fewer patients acheiving target-BP (<140/90 mmHg) (44% vs 57%, p=0.018) or clinical response rate (>=10 mmHg DBP reduction); and significantly higher non-response rate (<6 mmHg DBP reduction); but no significant differences in rates among blacks (e.g. target-BP rate: 56% vs 63%, p=0.31).	Hydrochlorothiazide	15-19	D-box binding PAR bZIP transcription factor	Homo sapiens	172-175
33434556-5	2021	Treatment with HCTZ vs CTD in whites resulted in significantly fewer patients acheiving target-BP (<140/90 mmHg) (44% vs 57%, p=0.018) or clinical response rate (>=10 mmHg DBP reduction); and significantly higher non-response rate (<6 mmHg DBP reduction); but no significant differences in rates among blacks (e.g. target-BP rate: 56% vs 63%, p=0.31).	Hydrochlorothiazide	15-19	D-box binding PAR bZIP transcription factor	Homo sapiens	240-243
32293069-7	2020	Among HT African-Americans, three of the 12 single nucleotide polymorphisms interrogated for the SNX1 gene were associated with a decrease in systolic BP in response to hydrochlorothiazide (HCTZ).	Hydrochlorothiazide	169-188	sorting nexin 1	Mus musculus	97-101
32592815-7	2020	An increase in natriuresis was observed after treatment with hydrochlorothiazide, but not amiloride, a change observed in parallel with increased phosphorylated sodium-chloride cotransporter (NCC).	Hydrochlorothiazide	61-80	solute carrier family 12 member 3	Rattus norvegicus	192-195
32293069-7	2020	Among HT African-Americans, three of the 12 single nucleotide polymorphisms interrogated for the SNX1 gene were associated with a decrease in systolic BP in response to hydrochlorothiazide (HCTZ).	Hydrochlorothiazide	190-194	sorting nexin 1	Mus musculus	97-101
31743708-4	2020	Therefore the present work targets the amyloid inhibiting potential of diuretics (a class of antihypertensive drugs) - Indapamide (INDP) and Hydrochlorothiazide (HCTZ) against human serum albumin (HSA) and human lysozyme (HL) fibrillogenesis.	Hydrochlorothiazide	141-160	albumin	Homo sapiens	182-195
31743708-4	2020	Therefore the present work targets the amyloid inhibiting potential of diuretics (a class of antihypertensive drugs) - Indapamide (INDP) and Hydrochlorothiazide (HCTZ) against human serum albumin (HSA) and human lysozyme (HL) fibrillogenesis.	Hydrochlorothiazide	162-166	albumin	Homo sapiens	182-195
32148128-5	2020	This protective pathway involves activation of PVN Galphai2 signaling pathways, which mediate sympathoinhibition to the blood vessels and kidneys (renal norepinephrine [pg/mg] 8% NaCl; SCR oligodeoxynucleotide 375+-39 versus Galphai2 oligodeoxynucleotide 850+-27; P<0.05) and suppression of the activity of the sodium chloride cotransporter assessed as peak natriuresis to hydrochlorothiazide.	Hydrochlorothiazide	373-392	G protein subunit alpha i2	Rattus norvegicus	51-59
31322418-9	2019	However, strong in vivo inhibitors of hOAT1/3 may alter renal secretion of HCTZ.	Hydrochlorothiazide	75-79	solute carrier family 22 member 6	Homo sapiens	38-43
31373922-1	2019	OBJECTIVES: The aim of this study was to identify associations between the smoothness index of central SBP (CSBP) and changes of ambulatory carotid femoral pulse wave velocity in response to 20-week treatments with losartan and amlodipine vs. losartan and hydrochlorthiazide combinations.	Hydrochlorothiazide	256-274	selenium binding protein 1	Homo sapiens	103-106
32104886-6	2020	In IL-17A-infused mice, treatment with hydralazine and hydrochlorothiazide diminished blood pressure elevation, without modifying mechanical and structural properties of small mesenteric artery, suggesting a direct vascular effect of IL-17A.	Hydrochlorothiazide	55-74	interleukin 17A	Mus musculus	3-9
31322418-0	2019	Renal secretion of hydrochlorothiazide involves organic anion transporter 1/3, organic cation transporter 2, and multidrug and toxin extrusion protein 2-K. Hydrochlorothiazide (HCTZ) is the most widely used thiazide diuretic for the treatment of hypertension either alone or in combination with other antihypertensives.	Hydrochlorothiazide	19-38	solute carrier family 22 member 2	Homo sapiens	48-107
31327267-6	2019	A relatively small number of gene variants related to loci associated with drug-signaling pathways (KCNK3, SULT1C3, AMH, PDE3A, PLCE1, PRKAG2) with large effect size (-3.5 to +3.5 mm Hg difference in response per allele) and differing allele frequencies in black versus white individuals explained a large proportion of the difference in response to candesartan and hydrochlorothiazide between these groups.	Hydrochlorothiazide	366-385	potassium two pore domain channel subfamily K member 3	Homo sapiens	100-105
31322418-0	2019	Renal secretion of hydrochlorothiazide involves organic anion transporter 1/3, organic cation transporter 2, and multidrug and toxin extrusion protein 2-K. Hydrochlorothiazide (HCTZ) is the most widely used thiazide diuretic for the treatment of hypertension either alone or in combination with other antihypertensives.	Hydrochlorothiazide	19-38	solute carrier family 47 member 1	Homo sapiens	113-122
31322418-0	2019	Renal secretion of hydrochlorothiazide involves organic anion transporter 1/3, organic cation transporter 2, and multidrug and toxin extrusion protein 2-K. Hydrochlorothiazide (HCTZ) is the most widely used thiazide diuretic for the treatment of hypertension either alone or in combination with other antihypertensives.	Hydrochlorothiazide	156-175	solute carrier family 22 member 2	Homo sapiens	48-107
31322418-0	2019	Renal secretion of hydrochlorothiazide involves organic anion transporter 1/3, organic cation transporter 2, and multidrug and toxin extrusion protein 2-K. Hydrochlorothiazide (HCTZ) is the most widely used thiazide diuretic for the treatment of hypertension either alone or in combination with other antihypertensives.	Hydrochlorothiazide	156-175	solute carrier family 47 member 1	Homo sapiens	113-122
31322418-0	2019	Renal secretion of hydrochlorothiazide involves organic anion transporter 1/3, organic cation transporter 2, and multidrug and toxin extrusion protein 2-K. Hydrochlorothiazide (HCTZ) is the most widely used thiazide diuretic for the treatment of hypertension either alone or in combination with other antihypertensives.	Hydrochlorothiazide	177-181	solute carrier family 22 member 2	Homo sapiens	48-107
31322418-3	2019	Uptake experiments further showed that HCTZ is transported by hOAT1, hOAT3, hOCT2, and hMATE2-K but not by hMATE1.	Hydrochlorothiazide	39-43	solute carrier family 22 member 6	Homo sapiens	62-67
31322418-3	2019	Uptake experiments further showed that HCTZ is transported by hOAT1, hOAT3, hOCT2, and hMATE2-K but not by hMATE1.	Hydrochlorothiazide	39-43	solute carrier family 22 member 8	Homo sapiens	69-74
31322418-3	2019	Uptake experiments further showed that HCTZ is transported by hOAT1, hOAT3, hOCT2, and hMATE2-K but not by hMATE1.	Hydrochlorothiazide	39-43	solute carrier family 22 member 2	Homo sapiens	76-81
31322418-3	2019	Uptake experiments further showed that HCTZ is transported by hOAT1, hOAT3, hOCT2, and hMATE2-K but not by hMATE1.	Hydrochlorothiazide	39-43	solute carrier family 47 member 2	Homo sapiens	87-93
31322418-4	2019	Detailed kinetic analysis coupled with quantification of membrane transporter proteins by targeted proteomics revealed that HCTZ is an excellent substrate for hOAT1 and hOAT3.	Hydrochlorothiazide	124-128	solute carrier family 22 member 6	Homo sapiens	159-164
31322418-4	2019	Detailed kinetic analysis coupled with quantification of membrane transporter proteins by targeted proteomics revealed that HCTZ is an excellent substrate for hOAT1 and hOAT3.	Hydrochlorothiazide	124-128	solute carrier family 22 member 8	Homo sapiens	169-174
31322418-6	2019	On the other hand, hOCT2 and hMATE2-K showed much lower affinity for HCTZ.	Hydrochlorothiazide	69-73	solute carrier family 22 member 2	Homo sapiens	19-24
31322418-6	2019	On the other hand, hOCT2 and hMATE2-K showed much lower affinity for HCTZ.	Hydrochlorothiazide	69-73	solute carrier family 47 member 2	Homo sapiens	29-35
31322418-7	2019	The calculated transport efficiency (kcat/Km) at the single transporter level followed the rank order of hOAT1&gt; hOAT3 &gt; hOCT2 and hMATE2-K, suggesting a major role of organic anion transporters in tubular secretion of HCTZ.	Hydrochlorothiazide	224-228	solute carrier family 22 member 6	Homo sapiens	105-110
31322418-7	2019	The calculated transport efficiency (kcat/Km) at the single transporter level followed the rank order of hOAT1&gt; hOAT3 &gt; hOCT2 and hMATE2-K, suggesting a major role of organic anion transporters in tubular secretion of HCTZ.	Hydrochlorothiazide	224-228	solute carrier family 22 member 8	Homo sapiens	115-120
31322418-7	2019	The calculated transport efficiency (kcat/Km) at the single transporter level followed the rank order of hOAT1&gt; hOAT3 &gt; hOCT2 and hMATE2-K, suggesting a major role of organic anion transporters in tubular secretion of HCTZ.	Hydrochlorothiazide	224-228	solute carrier family 22 member 2	Homo sapiens	126-131
31322418-7	2019	The calculated transport efficiency (kcat/Km) at the single transporter level followed the rank order of hOAT1&gt; hOAT3 &gt; hOCT2 and hMATE2-K, suggesting a major role of organic anion transporters in tubular secretion of HCTZ.	Hydrochlorothiazide	224-228	solute carrier family 47 member 2	Homo sapiens	136-144
31327267-6	2019	A relatively small number of gene variants related to loci associated with drug-signaling pathways (KCNK3, SULT1C3, AMH, PDE3A, PLCE1, PRKAG2) with large effect size (-3.5 to +3.5 mm Hg difference in response per allele) and differing allele frequencies in black versus white individuals explained a large proportion of the difference in response to candesartan and hydrochlorothiazide between these groups.	Hydrochlorothiazide	366-385	protein kinase AMP-activated non-catalytic subunit gamma 2	Homo sapiens	135-141
30805791-6	2019	These cases suggest that a combination of lithium with ACE inhibitors is possible when sufficient hydration is ensured and a combination with hydrochlorothiazide is avoided.	Hydrochlorothiazide	142-161	angiotensin I converting enzyme	Homo sapiens	55-58
31055826-0	2019	[Association of STK39 gene polymorphism with response to hydrochlorothiazide among ethnic Han Chinese with essential hypertension].	Hydrochlorothiazide	57-76	serine/threonine kinase 39	Homo sapiens	16-21
31055826-1	2019	OBJECTIVE: To assess the association of single nucleotide polymorphisms (SNPs) of STK39 gene with response to hydrochlorothiazide among ethnic Han Chinese patients with essential hypertension.	Hydrochlorothiazide	110-129	serine/threonine kinase 39	Homo sapiens	82-87
31055826-9	2019	Relative risk analysis showed that STK39 rs3754777 was significantly associated with BP response to hydrochlorothiazide (OR=0.416, 95%CI=0.189-0.918, P&lt;0.05).	Hydrochlorothiazide	100-119	serine/threonine kinase 39	Homo sapiens	35-40
31055826-10	2019	CONCLUSION: Polymorphisms of STK39 rs3754777 may be associated with BP response to hydrochlorothiazide among ethnic Han Chinese with essential hypertension.	Hydrochlorothiazide	83-102	serine/threonine kinase 39	Homo sapiens	29-34
30894383-0	2019	Ambulatory Blood Pressure Reduction With SGLT-2 Inhibitors: Dose-Response Meta-analysis and Comparative Evaluation With Low-Dose Hydrochlorothiazide.	Hydrochlorothiazide	129-148	solute carrier family 5 member 2	Homo sapiens	41-47
30426292-0	2019	Hydrochlorothiazide ameliorates polyuria caused by tolvaptan treatment of polycystic kidney disease in PCK rats.	Hydrochlorothiazide	0-19	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	103-106
30426292-8	2019	Notably, aquaporin 2 redistribution from the apical to intracellular domains was observed in tolvaptan-treated rats and was partially reversed in the tolvaptan + HCTZ group.	Hydrochlorothiazide	162-166	aquaporin 2	Rattus norvegicus	9-20
30605394-7	2019	SS Kcnj16-/- rats chronically treated with bicarbonate or the carbonic anhydrase inhibitor hydrochlorothiazide had partial restoration of arterial pH, but there was a further reduction in the ventilatory response to hypercapnic acidosis.	Hydrochlorothiazide	91-110	potassium inwardly-rectifying channel, subfamily J, member 16	Rattus norvegicus	3-9
29907477-9	2018	CONCLUSION: Our case demonstrates the efficacy of hydrochlorothiazide in the prophylactic treatment of normoKPP caused by the SCN4A mutation of p.Thr704Met, the most frequent mutation of hyperKPP.	Hydrochlorothiazide	50-69	sodium voltage-gated channel alpha subunit 4	Homo sapiens	126-131
30218717-0	2019	Hydrochlorothiazide binding to human serum albumin induces some compactness in the molecular structure of the protein: A multi-spectroscopic and computational study.	Hydrochlorothiazide	0-19	albumin	Homo sapiens	37-50
30218717-1	2019	The interaction between hydrochlorothiazide (HCTZ), a diuretic drug, with human serum albumin (HSA) was investigated by different biophysical approaches such as UV absorption, circular dichroism (CD), Fourier transform infrared (FT-IR), and fluorescence spectroscopy in 50 mM sodium phosphate buffer, pH 7.4.	Hydrochlorothiazide	24-43	albumin	Homo sapiens	80-93
30218717-1	2019	The interaction between hydrochlorothiazide (HCTZ), a diuretic drug, with human serum albumin (HSA) was investigated by different biophysical approaches such as UV absorption, circular dichroism (CD), Fourier transform infrared (FT-IR), and fluorescence spectroscopy in 50 mM sodium phosphate buffer, pH 7.4.	Hydrochlorothiazide	45-49	albumin	Homo sapiens	80-93
30360726-7	2019	Thus, some preliminary evidence exists to support that relatively long-term treatment with the angiotensin converting enzyme inhibitor zofenopril alone or combined with hydrochlorothiazide is effective in controlling blood pressure and may confer some kidney protection due to ACE inhibition properties.	Hydrochlorothiazide	169-188	angiotensin I converting enzyme	Homo sapiens	277-280
30539654-4	2019	WT, UT-A3 KO, and UT-A1/A3 KO acutely respond to hydrochlorothiazide and furosemide; however, UT-A1/A3 KO fail to show a diuretic or natriuretic response following amiloride administration, indicating that baseline epithelial Na+ channel (ENaC) activity is impaired.	Hydrochlorothiazide	49-68	solute carrier family 14 (urea transporter), member 2	Mus musculus	18-29
31336455-10	2019	Drugs that had more interaction with insulin were: acetylsalicylic acid (40%), enalapril (18%), losartan (32%) and hydrochlorothiazide (23%).	Hydrochlorothiazide	115-134	insulin	Homo sapiens	37-44
29737520-14	2018	By contrast, hydrochlorothiazide (HCTZ)-induced natriuresis decreased gradually over 7 days, consistent with increased ability of ENaC activity to compensate for decreased Na+ reabsorption in the distal convoluted tubule.	Hydrochlorothiazide	13-32	sodium channel epithelial 1 subunit gamma	Rattus norvegicus	130-134
29968917-3	2018	To assess the effects of photosensitizing drugs voriconazole and hydrochlorothiazide (HCTZ) on the enhancement of UV-induced inflammatory responses and UV-induced tumorigenesis, we utilized Xpa-knockout mice, which is DNA repair-deficient and more susceptible to UV-induced inflammation and tumor development than wild-type mice.	Hydrochlorothiazide	86-90	xeroderma pigmentosum, complementation group A	Mus musculus	190-193
29737520-14	2018	By contrast, hydrochlorothiazide (HCTZ)-induced natriuresis decreased gradually over 7 days, consistent with increased ability of ENaC activity to compensate for decreased Na+ reabsorption in the distal convoluted tubule.	Hydrochlorothiazide	34-38	sodium channel epithelial 1 subunit gamma	Rattus norvegicus	130-134
29631358-9	2018	NCC inhibition with hydrochlorothiazide attenuated interleukin-17A protein expression along with the phosphorylation of NCC in Aldo/NaCl rats.	Hydrochlorothiazide	20-39	interleukin 17A	Rattus norvegicus	51-66
29753906-3	2018	Within this study, drug-free and hydrochlorothiazide (HCT) containing ODFs should be imprinted in-line with enalapril maleate (EM) ink during continuous ODF production.	Hydrochlorothiazide	33-52	outer dense fiber of sperm tails 1	Homo sapiens	70-73
29753906-3	2018	Within this study, drug-free and hydrochlorothiazide (HCT) containing ODFs should be imprinted in-line with enalapril maleate (EM) ink during continuous ODF production.	Hydrochlorothiazide	54-57	outer dense fiber of sperm tails 1	Homo sapiens	70-73
29970015-6	2018	CONCLUSIONS: This case report indicates that while addition of hydrochlorothiazide may improve tolerability of vasopressin V2 receptor antagonists, co-prescription should only be used with great scrutiny as it may decrease tolvaptan effect on rate of ADPKD disease progression.	Hydrochlorothiazide	63-82	arginine vasopressin receptor 2	Homo sapiens	111-134
30050451-3	2018	Hypothesis: Pre-treatment with probenecid down-regulates pendrin; therefore, leaving NCC as the main salt absorbing transporter in the distal nephron, and hence enhances the hydrochlorothiazide (HCTZ)-induced diuresis.	Hydrochlorothiazide	174-193	solute carrier family 26 member 4	Rattus norvegicus	57-64
30050451-3	2018	Hypothesis: Pre-treatment with probenecid down-regulates pendrin; therefore, leaving NCC as the main salt absorbing transporter in the distal nephron, and hence enhances the hydrochlorothiazide (HCTZ)-induced diuresis.	Hydrochlorothiazide	195-199	solute carrier family 26 member 4	Rattus norvegicus	57-64
30030908-4	2018	In this model, DCT1-specific expression of a constitutively active mutant form of the NCC-phosphorylating kinase, SPAK (CA-SPAK), increases NCC activity and hydrochlorothiazide (HCTZ)-sensitive Na+ reabsorption.	Hydrochlorothiazide	178-182	serine/threonine kinase 39	Mus musculus	114-118
30030908-4	2018	In this model, DCT1-specific expression of a constitutively active mutant form of the NCC-phosphorylating kinase, SPAK (CA-SPAK), increases NCC activity and hydrochlorothiazide (HCTZ)-sensitive Na+ reabsorption.	Hydrochlorothiazide	178-182	serine/threonine kinase 39	Mus musculus	120-127
30030908-4	2018	In this model, DCT1-specific expression of a constitutively active mutant form of the NCC-phosphorylating kinase, SPAK (CA-SPAK), increases NCC activity and hydrochlorothiazide (HCTZ)-sensitive Na+ reabsorption.	Hydrochlorothiazide	157-176	solute carrier family 11 (proton-coupled divalent metal ion transporters), member 2	Mus musculus	15-19
30030908-4	2018	In this model, DCT1-specific expression of a constitutively active mutant form of the NCC-phosphorylating kinase, SPAK (CA-SPAK), increases NCC activity and hydrochlorothiazide (HCTZ)-sensitive Na+ reabsorption.	Hydrochlorothiazide	157-176	serine/threonine kinase 39	Mus musculus	114-118
30030908-4	2018	In this model, DCT1-specific expression of a constitutively active mutant form of the NCC-phosphorylating kinase, SPAK (CA-SPAK), increases NCC activity and hydrochlorothiazide (HCTZ)-sensitive Na+ reabsorption.	Hydrochlorothiazide	157-176	serine/threonine kinase 39	Mus musculus	120-127
30030908-4	2018	In this model, DCT1-specific expression of a constitutively active mutant form of the NCC-phosphorylating kinase, SPAK (CA-SPAK), increases NCC activity and hydrochlorothiazide (HCTZ)-sensitive Na+ reabsorption.	Hydrochlorothiazide	178-182	solute carrier family 11 (proton-coupled divalent metal ion transporters), member 2	Mus musculus	15-19
30030908-5	2018	These mice were normomagnesemic and HCTZ administration comparably reduced plasma Mg2+ levels in CA-SPAK mice and control littermates.	Hydrochlorothiazide	36-40	serine/threonine kinase 39	Mus musculus	97-104
30030908-6	2018	As inferred by the initial response to HCTZ, CA-SPAK mice exhibited greater NCC-dependent Na+ reabsorption together with decreased Mg2+ reabsorption, compared to controls.	Hydrochlorothiazide	39-43	serine/threonine kinase 39	Mus musculus	45-52
30030908-7	2018	Following prolonged HCTZ administration (4 days), CA-SPAK mice exhibited higher urinary Mg2+ excretion, while urinary Na+ excretion decreased to levels observed in control animals.	Hydrochlorothiazide	20-24	serine/threonine kinase 39	Mus musculus	50-57
29217346-2	2018	OBJECTIVE: To examine the association between hydrochlorothiazide use and the risk of basal cell carcinoma (BCC) and squamous cell carcinoma (SCC).	Hydrochlorothiazide	46-65	serpin family B member 3	Homo sapiens	142-145
29226589-7	2018	Mice received either HCT (1 mg mL-1 ) or vehicle.	Hydrochlorothiazide	21-24	L1 cell adhesion molecule	Mus musculus	31-35
29483157-5	2018	Correcting the hyperkalemia by treatment with hydrochlorothiazide corrected the metabolic acidosis, increased ammonia excretion, and normalized ammoniagenic enzyme and Rhcg expression in DCT-CA-SPAK mice.	Hydrochlorothiazide	46-65	Rhesus blood group-associated C glycoprotein	Mus musculus	168-172
29483157-5	2018	Correcting the hyperkalemia by treatment with hydrochlorothiazide corrected the metabolic acidosis, increased ammonia excretion, and normalized ammoniagenic enzyme and Rhcg expression in DCT-CA-SPAK mice.	Hydrochlorothiazide	46-65	serine/threonine kinase 39	Mus musculus	194-198
29217346-6	2018	Using conditional logistic regression, we calculated odds ratios (ORs) for BCC and SCC associated with hydrochlorothiazide use.	Hydrochlorothiazide	103-122	serpin family B member 3	Homo sapiens	83-86
29217346-7	2018	RESULTS: High use of hydrochlorothiazide (&gt;=50,000 mg) was associated with ORs of 1.29 (95% confidence interval [CI], 1.23-1.35) for BCC and 3.98 (95% CI, 3.68-4.31) for SCC.	Hydrochlorothiazide	21-40	serpin family B member 3	Homo sapiens	173-176
29217346-8	2018	We found clear dose-response relationships between hydrochlorothiazide use and both BCC and SCC; the highest cumulative dose category (&gt;=200,000 mg of HCTZ) had ORs of 1.54 (95% CI, 1.38-1.71) and 7.38 (95% CI, 6.32-8.60) for BCC and SCC, respectively.	Hydrochlorothiazide	51-70	serpin family B member 3	Homo sapiens	92-95
29217346-8	2018	We found clear dose-response relationships between hydrochlorothiazide use and both BCC and SCC; the highest cumulative dose category (&gt;=200,000 mg of HCTZ) had ORs of 1.54 (95% CI, 1.38-1.71) and 7.38 (95% CI, 6.32-8.60) for BCC and SCC, respectively.	Hydrochlorothiazide	51-70	serpin family B member 3	Homo sapiens	237-240
29217346-8	2018	We found clear dose-response relationships between hydrochlorothiazide use and both BCC and SCC; the highest cumulative dose category (&gt;=200,000 mg of HCTZ) had ORs of 1.54 (95% CI, 1.38-1.71) and 7.38 (95% CI, 6.32-8.60) for BCC and SCC, respectively.	Hydrochlorothiazide	154-158	serpin family B member 3	Homo sapiens	92-95
29217346-8	2018	We found clear dose-response relationships between hydrochlorothiazide use and both BCC and SCC; the highest cumulative dose category (&gt;=200,000 mg of HCTZ) had ORs of 1.54 (95% CI, 1.38-1.71) and 7.38 (95% CI, 6.32-8.60) for BCC and SCC, respectively.	Hydrochlorothiazide	154-158	serpin family B member 3	Homo sapiens	237-240
29217346-11	2018	CONCLUSIONS: Hydrochlorothiazide use is associated with a substantially increased risk of NMSC, especially SCC.	Hydrochlorothiazide	13-32	serpin family B member 3	Homo sapiens	107-110
29580174-4	2018	RESULTS: In GENRES, we identified 31 loci associated with hydrochlorothiazide-induced change in SUA at p &lt; 5 x 10-5. rs1002976 near VEGFC associated with the change in GENRES and in LIFE.	Hydrochlorothiazide	58-77	vascular endothelial growth factor C	Homo sapiens	135-140
29310825-8	2018	Disruption of Kir4.1 significantly increased basal urinary sodium excretion but it abolished the natriuretic effect of hydrochlorothiazide.	Hydrochlorothiazide	119-138	potassium inwardly-rectifying channel, subfamily J, member 10	Mus musculus	14-20
29334491-6	2018	At 8 weeks, both AZL-M/CTD FDCs reduced 24-h SBP more than OLM/HCTZ (-26.4 and -27.9 versus -20.7 mmHg; both P &lt; 0.001), and higher proportions in both AZL-M/CTD groups achieved target BP compared with the OLM/HCTZ group (69.4 and 68.9 versus 54.7%, both P &lt; 0.001).	Hydrochlorothiazide	213-217	CTD	Homo sapiens	17-26
29523524-11	2018	CONCLUSIONS: These results suggest that HMGCS2 is a promising candidate gene involved in chlorthalidone and Hydrochlorothiazide (HCTZ)-induced glucose change.	Hydrochlorothiazide	108-127	3-hydroxy-3-methylglutaryl-CoA synthase 2	Homo sapiens	40-46
29523524-11	2018	CONCLUSIONS: These results suggest that HMGCS2 is a promising candidate gene involved in chlorthalidone and Hydrochlorothiazide (HCTZ)-induced glucose change.	Hydrochlorothiazide	129-133	3-hydroxy-3-methylglutaryl-CoA synthase 2	Homo sapiens	40-46
28509725-7	2017	SBP reduction was positively related to increasing urinary sodium and PP levels for patients in both groups but increased faster with increasing PP in HCTZ than in telmisartan (P = 0.0238 for group x PP).	Hydrochlorothiazide	151-155	selenium binding protein 1	Homo sapiens	0-3
29288159-10	2017	CONCLUSIONS: This study provides insight into potential pharmacometabolomic and genetic mechanisms underlying HCTZ BP response and suggests that SPTLC3 is a potential determinant of the BP response to HCTZ.	Hydrochlorothiazide	201-205	serine palmitoyltransferase long chain base subunit 3	Homo sapiens	145-151
29085669-8	2017	Systolic BP response to HCTZ is positively related to heart rate and negatively to renin levels.	Hydrochlorothiazide	24-28	renin	Homo sapiens	83-88
29251736-10	2018	Amiloride (ENaC) and hydrochlorothiazide (pendrin inhibitor) equally attenuated the effect of PGE2 on sodium transport.	Hydrochlorothiazide	21-40	solute carrier family 26, member 4	Mus musculus	42-49
28967043-7	2018	Particularly, decreased ethyl cellulose to copovidone K28 weight ratio was found to suppress the crystallization of hydrochlorothiazide and to increase the release rate of the dispensed drugs.	Hydrochlorothiazide	116-135	keratin 28	Homo sapiens	54-57
29288159-6	2017	Testing 78 variants, within 14 genes involved in the sphingolipid metabolic canonical pathway, with the BP response to HCTZ identified variant rs6078905, within the SPTLC3 gene, as a novel biomarker significantly associated with the BP response to HCTZ in whites (n=228).	Hydrochlorothiazide	119-123	serine palmitoyltransferase long chain base subunit 3	Homo sapiens	165-171
29288159-6	2017	Testing 78 variants, within 14 genes involved in the sphingolipid metabolic canonical pathway, with the BP response to HCTZ identified variant rs6078905, within the SPTLC3 gene, as a novel biomarker significantly associated with the BP response to HCTZ in whites (n=228).	Hydrochlorothiazide	248-252	serine palmitoyltransferase long chain base subunit 3	Homo sapiens	165-171
29288159-7	2017	We found that rs6078905 C-allele carriers had a better BP response to HCTZ versus noncarriers ( SBP/ DBP: -11.4/-6.9 versus -6.8/-3.5 mm Hg;  SBP P=6.7E-04;  DBP P=4.8E-04).	Hydrochlorothiazide	70-74	selenium binding protein 1	Homo sapiens	96-99
29288159-7	2017	We found that rs6078905 C-allele carriers had a better BP response to HCTZ versus noncarriers ( SBP/ DBP: -11.4/-6.9 versus -6.8/-3.5 mm Hg;  SBP P=6.7E-04;  DBP P=4.8E-04).	Hydrochlorothiazide	70-74	D-box binding PAR bZIP transcription factor	Homo sapiens	101-104
29288159-7	2017	We found that rs6078905 C-allele carriers had a better BP response to HCTZ versus noncarriers ( SBP/ DBP: -11.4/-6.9 versus -6.8/-3.5 mm Hg;  SBP P=6.7E-04;  DBP P=4.8E-04).	Hydrochlorothiazide	70-74	selenium binding protein 1	Homo sapiens	142-145
29288159-7	2017	We found that rs6078905 C-allele carriers had a better BP response to HCTZ versus noncarriers ( SBP/ DBP: -11.4/-6.9 versus -6.8/-3.5 mm Hg;  SBP P=6.7E-04;  DBP P=4.8E-04).	Hydrochlorothiazide	70-74	D-box binding PAR bZIP transcription factor	Homo sapiens	158-161
29288159-8	2017	Additionally, in blacks (n=148), we found genetic signals in the SPTLC3 genomic region significantly associated with the BP response to HCTZ (P&lt;0.05).	Hydrochlorothiazide	136-140	serine palmitoyltransferase long chain base subunit 3	Homo sapiens	65-71
29288159-10	2017	CONCLUSIONS: This study provides insight into potential pharmacometabolomic and genetic mechanisms underlying HCTZ BP response and suggests that SPTLC3 is a potential determinant of the BP response to HCTZ.	Hydrochlorothiazide	110-114	serine palmitoyltransferase long chain base subunit 3	Homo sapiens	145-151
28343298-1	2017	We evaluated the effect of hydrochlorothiazide in a sample of anuric patients on hemodialysis and found an increase in serum calcium, which occurred only in those with parathyroid hormone &gt;300 pg/ml.	Hydrochlorothiazide	27-46	parathyroid hormone	Homo sapiens	168-187
28274929-8	2017	This study highlights that NCC1/2, NCC1-3, and pNCC1-3-T55/T60 are upregulated by hydrochlorothiazide, and the increase in NCC abundance in uEVs of essential hypertensive patients correlates with the blood pressure response to hydrochlorothiazide.	Hydrochlorothiazide	82-101	C-C motif chemokine ligand 13	Homo sapiens	27-33
28587581-3	2017	METHODS: The ACE phenotype was determined in plasma of 14 patients with hypertension treated chronically for 4 weeks with 40 mg enalapril (E) or 20 mg E + 16 mg candesartan (EC) and in 20 patients with hypertension treated acutely with a single dose (20 mg) of E with or without pretreatment with hydrochlorothiazide.	Hydrochlorothiazide	297-316	angiotensin I converting enzyme	Homo sapiens	13-16
28274929-7	2017	Despite the inhibitory action of hydrochlorothiazide on NCC activity, immunoblot analysis of uEVs showed significantly increased abundance of NCC isoforms 1 and 2 (NCC1/2), total NCC (NCC1-3), and the phosphorylated form of total NCC (pNCC1-3-T55/T60) in essential hypertensive patients treated with hydrochlorothiazide but not with valsartan.	Hydrochlorothiazide	33-52	solute carrier family 12 member 3	Homo sapiens	56-59
28274929-8	2017	This study highlights that NCC1/2, NCC1-3, and pNCC1-3-T55/T60 are upregulated by hydrochlorothiazide, and the increase in NCC abundance in uEVs of essential hypertensive patients correlates with the blood pressure response to hydrochlorothiazide.	Hydrochlorothiazide	82-101	solute carrier family 12 member 3	Homo sapiens	35-41
28274929-8	2017	This study highlights that NCC1/2, NCC1-3, and pNCC1-3-T55/T60 are upregulated by hydrochlorothiazide, and the increase in NCC abundance in uEVs of essential hypertensive patients correlates with the blood pressure response to hydrochlorothiazide.	Hydrochlorothiazide	82-101	solute carrier family 12 member 3	Homo sapiens	27-30
28274929-8	2017	This study highlights that NCC1/2, NCC1-3, and pNCC1-3-T55/T60 are upregulated by hydrochlorothiazide, and the increase in NCC abundance in uEVs of essential hypertensive patients correlates with the blood pressure response to hydrochlorothiazide.	Hydrochlorothiazide	227-246	C-C motif chemokine ligand 13	Homo sapiens	27-33
28274929-8	2017	This study highlights that NCC1/2, NCC1-3, and pNCC1-3-T55/T60 are upregulated by hydrochlorothiazide, and the increase in NCC abundance in uEVs of essential hypertensive patients correlates with the blood pressure response to hydrochlorothiazide.	Hydrochlorothiazide	227-246	solute carrier family 12 member 3	Homo sapiens	27-30
28039944-0	2017	Hydrochlorothiazide modulates ischemic heart failure-induced cardiac remodeling via inhibiting angiotensin II type 1 receptor pathway in rats.	Hydrochlorothiazide	0-19	angiotensin II receptor, type 1b	Rattus norvegicus	95-125
28039944-8	2017	Furthermore, hydrochlorothiazide inhibited angiotensin II-induced TGF-beta1 and Smad2 protein expression in the neonatal rat ventricular fibroblasts.	Hydrochlorothiazide	13-32	SMAD family member 2	Rattus norvegicus	80-85
28039944-1	2017	AIMS: Our previous study indicates that hydrochlorothiazide inhibits transforming growth factor (TGF)-beta/Smad signaling pathway, improves cardiac function and reduces fibrosis.	Hydrochlorothiazide	40-59	transforming growth factor, beta 1	Rattus norvegicus	97-106
28039944-10	2017	Hydrochlorothiazide may reduce the left ventricular wall stress and angiotensin II signaling pathway to provide these beneficial effects.	Hydrochlorothiazide	0-19	angiotensinogen	Rattus norvegicus	68-82
28039944-7	2017	In addition, hydrochlorothiazide reduced plasma angiotensin II and aldosterone levels.	Hydrochlorothiazide	13-32	angiotensinogen	Rattus norvegicus	48-62
28039944-8	2017	Furthermore, hydrochlorothiazide inhibited angiotensin II-induced TGF-beta1 and Smad2 protein expression in the neonatal rat ventricular fibroblasts.	Hydrochlorothiazide	13-32	angiotensinogen	Rattus norvegicus	43-57
28039944-8	2017	Furthermore, hydrochlorothiazide inhibited angiotensin II-induced TGF-beta1 and Smad2 protein expression in the neonatal rat ventricular fibroblasts.	Hydrochlorothiazide	13-32	transforming growth factor, beta 1	Rattus norvegicus	66-75
28153413-4	2017	Exposure potential given by the ratio amount of the drug exported to the sea/amount emitted to the environment was higher than 50% for 7 drugs (Piperacillin, Lorazepam, Metformin, Hydroxycarbamide, Hydrochlorothiazide, Furosemide and Cetirizine), implying that a high proportion of them will reach the sea, and below 10% for 27 drugs, implying high catchment attenuation.	Hydrochlorothiazide	198-217	S13 erythroblastosis (avian) oncogene homolog	Homo sapiens	73-76
28115488-10	2017	Moreover, baseline expression of the VASP mRNA was significantly higher in 25 good responders to hydrochlorothiazide compared with 25 poor responders (P=0.01).	Hydrochlorothiazide	97-116	vasodilator stimulated phosphoprotein	Homo sapiens	37-41
28706401-0	2017	Influence of West African Ethnicity and Gender on Beta-Cell Function and Insulin Sensitivity in Essential Hypertensives Treated with Hydrochlorothiazide and Hydrochlorothiazide-lisinopril Combination.	Hydrochlorothiazide	133-152	insulin	Homo sapiens	73-80
28706401-0	2017	Influence of West African Ethnicity and Gender on Beta-Cell Function and Insulin Sensitivity in Essential Hypertensives Treated with Hydrochlorothiazide and Hydrochlorothiazide-lisinopril Combination.	Hydrochlorothiazide	157-176	insulin	Homo sapiens	73-80
28750403-0	2017	Ablation of the Cl-/HCO3- Exchanger Pendrin Enhances Hydrochlorothiazide-Induced Diuresis.	Hydrochlorothiazide	53-72	solute carrier family 26, member 4	Mus musculus	36-43
28750403-2	2017	We hypothesized that deletion of pendrin leaves NCC as the major salt absorbing transporter in the distal nephron and therefore enhances salt excretion by hydrochlorothiazide (HCTZ).	Hydrochlorothiazide	155-174	solute carrier family 26, member 4	Mus musculus	33-40
28750403-2	2017	We hypothesized that deletion of pendrin leaves NCC as the major salt absorbing transporter in the distal nephron and therefore enhances salt excretion by hydrochlorothiazide (HCTZ).	Hydrochlorothiazide	176-180	solute carrier family 26, member 4	Mus musculus	33-40
28750403-6	2017	Urine output and water intake increased significantly only in pendrin KO mice in response to HCTZ, but not in WT or NCC KO mice.	Hydrochlorothiazide	93-97	solute carrier family 26, member 4	Mus musculus	62-69
28750403-7	2017	Sodium and chloride excretion increased in HCTZ-treated pendrin KO mice, but they remained unchanged in WT or NCC KO mice.	Hydrochlorothiazide	43-47	solute carrier family 26, member 4	Mus musculus	56-63
28750403-8	2017	Pendrin KO mice treated with HCTZ developed volume depletion, as determined by increased expression of renin mRNA and protein.	Hydrochlorothiazide	29-33	solute carrier family 26, member 4	Mus musculus	0-7
28750403-9	2017	The expression of ENaC and pendrin increased in HCTZ-treated WT mice.	Hydrochlorothiazide	48-52	sodium channel, nonvoltage-gated 1 alpha	Mus musculus	18-22
28750403-9	2017	The expression of ENaC and pendrin increased in HCTZ-treated WT mice.	Hydrochlorothiazide	48-52	solute carrier family 26, member 4	Mus musculus	27-34
28750403-11	2017	CONCLUSION: The ablation of the Cl-/HCO3- exchanger Pendrin enhances the magnitude of salt wasting by HCTZ.	Hydrochlorothiazide	102-106	solute carrier family 26, member 4	Mus musculus	52-59
26584406-7	2016	In patients with SDH (n = 39) or IDH (n = 40), hydrochlorothiazide treatment significantly increased serum adiponectin (P = 0 001 and 0 007, respectively) and reduced asymmetric dimethylarginine levels (P &lt; 0 001, in both groups).	Hydrochlorothiazide	47-66	adiponectin, C1Q and collagen domain containing	Homo sapiens	107-118
26982381-1	2016	OBJECTIVE: Experiments were carried out to investigate whether diuretics (hydrochlorothiazide + furosemide) impact on the effects of a sodium-dependent glucose cotransporter 2 (SGLT2) inhibitor on glucose metabolism and blood pressure (BP) in metabolic syndrome SHR/NDmcr-cp(+/+) rats (SHRcp).	Hydrochlorothiazide	74-93	solute carrier family 5 member 2	Rattus norvegicus	135-175
26963391-19	2016	Despite being considered mild agents individually, we propose that the combination of acetazolamide and amiloride in the setting of NCC inhibition (i.e., hydrochlorothiazide) will be a powerful diuretic regimen.	Hydrochlorothiazide	154-173	solute carrier family 12, member 3	Mus musculus	132-135
27231243-3	2016	We sought to investigate, in CKD patients not on dialysis, the influence of either hydrochlorothiazide (Hydro) or furosemide (Furo) on circulating parathyroid hormone (PTH) and whether such actions are determined by the effects of these compounds on calcium excretion.	Hydrochlorothiazide	83-102	parathyroid hormone	Homo sapiens	147-166
27231243-3	2016	We sought to investigate, in CKD patients not on dialysis, the influence of either hydrochlorothiazide (Hydro) or furosemide (Furo) on circulating parathyroid hormone (PTH) and whether such actions are determined by the effects of these compounds on calcium excretion.	Hydrochlorothiazide	83-102	parathyroid hormone	Homo sapiens	168-171
27231243-3	2016	We sought to investigate, in CKD patients not on dialysis, the influence of either hydrochlorothiazide (Hydro) or furosemide (Furo) on circulating parathyroid hormone (PTH) and whether such actions are determined by the effects of these compounds on calcium excretion.	Hydrochlorothiazide	104-109	parathyroid hormone	Homo sapiens	147-166
27666126-8	2016	Plasma renin and serum aldosterone levels were unaltered with empagliflozin or torasemide alone, but tended to increase with hydrochlorothiazide alone, and tended to increase when empagliflozin was co-administered with a diuretic compared with either diuretic alone.	Hydrochlorothiazide	125-144	renin	Homo sapiens	7-12
27006319-16	2016	A 40% decrease in Rock1 expression also was observed after long-term treatment with hydrochlorothiazide plus amiloride.	Hydrochlorothiazide	84-103	Rho-associated coiled-coil containing protein kinase 1	Mus musculus	18-23
26142561-1	2015	The application of capillary electrophoresis-frontal analysis for comparative evaluation of the binding interaction between antihypertensive drug captopril and human serum albumin in the absence and presence of diuretic drug hydrochlorothiazide was presented in this work.	Hydrochlorothiazide	225-244	albumin	Homo sapiens	166-179
26308670-1	2015	The addition of spironolactone or hydrochlorothiazide enhances the antialbuminuric effect of renin-angiotensin blockers.	Hydrochlorothiazide	34-53	renin	Homo sapiens	93-98
26176708-5	2016	The addition of HCTZ 25 mg significantly reduced SeDBP (-2.8 mm Hg; P&lt;.0001), lowered seated systolic BP (SeSBP) and ambulatory DBP and SBP, and improved BP goal rates.	Hydrochlorothiazide	16-20	selenium binding protein 1	Homo sapiens	111-114
26425837-4	2015	RESULTS: In whites, two polymorphisms near the gene PTPRD (rs12346562 and rs1104514) were associated with DBP response to atenolol (P = 3.2 x 10 and P = 5.9 x 10, respectively) with directionally opposite association for response to hydrochlorothiazide in another group of 228 whites (P = 0.0018 and P = 0.00012).	Hydrochlorothiazide	233-252	protein tyrosine phosphatase receptor type D	Homo sapiens	52-57
26425837-4	2015	RESULTS: In whites, two polymorphisms near the gene PTPRD (rs12346562 and rs1104514) were associated with DBP response to atenolol (P = 3.2 x 10 and P = 5.9 x 10, respectively) with directionally opposite association for response to hydrochlorothiazide in another group of 228 whites (P = 0.0018 and P = 0.00012).	Hydrochlorothiazide	233-252	D-box binding PAR bZIP transcription factor	Homo sapiens	106-109
25862792-7	2015	Treatment with antihypertensive therapy (hydrochlorothiazide and reserpine) from 6 to 12 weeks of age to attenuate age-related increases in BP abolished the sex difference in NOS activity and NOS1 expression between sexually mature SHR males and females.	Hydrochlorothiazide	41-60	nitric oxide synthase 1	Rattus norvegicus	192-196
26049382-5	2015	Despite lower risks of metabolic side-effects, meta-analysis of clinical trials showed that, for any given difference in achieved clinic SBP, HCTZ therapy was associated with 18% higher adverse cardiovascular events when compared with CTD.	Hydrochlorothiazide	142-146	selenium binding protein 1	Homo sapiens	137-140
25695618-0	2015	TET2 and CSMD1 genes affect SBP response to hydrochlorothiazide in never-treated essential hypertensives.	Hydrochlorothiazide	44-63	tet methylcytosine dioxygenase 2	Homo sapiens	0-4
25695618-0	2015	TET2 and CSMD1 genes affect SBP response to hydrochlorothiazide in never-treated essential hypertensives.	Hydrochlorothiazide	44-63	CUB and Sushi multiple domains 1	Homo sapiens	9-14
25695618-0	2015	TET2 and CSMD1 genes affect SBP response to hydrochlorothiazide in never-treated essential hypertensives.	Hydrochlorothiazide	44-63	selenium binding protein 1	Homo sapiens	28-31
25695618-5	2015	TET2 and CSMD1 as plausible candidate genes to affect SBP response to hydrochlorothiazide were identified.	Hydrochlorothiazide	70-89	tet methylcytosine dioxygenase 2	Homo sapiens	0-4
25695618-5	2015	TET2 and CSMD1 as plausible candidate genes to affect SBP response to hydrochlorothiazide were identified.	Hydrochlorothiazide	70-89	CUB and Sushi multiple domains 1	Homo sapiens	9-14
25695618-5	2015	TET2 and CSMD1 as plausible candidate genes to affect SBP response to hydrochlorothiazide were identified.	Hydrochlorothiazide	70-89	selenium binding protein 1	Homo sapiens	54-57
25695618-9	2015	CONCLUSION: This exploratory study reports two plausible loci associated with SBP response to hydrochlorothiazide: TET2, an aldosterone-responsive mediator of alphaENaC gene transcription; and CSMD1, previously described as associated with hypertension in a case-control study.	Hydrochlorothiazide	94-113	selenium binding protein 1	Homo sapiens	78-81
25695618-9	2015	CONCLUSION: This exploratory study reports two plausible loci associated with SBP response to hydrochlorothiazide: TET2, an aldosterone-responsive mediator of alphaENaC gene transcription; and CSMD1, previously described as associated with hypertension in a case-control study.	Hydrochlorothiazide	94-113	tet methylcytosine dioxygenase 2	Homo sapiens	115-119
25695618-9	2015	CONCLUSION: This exploratory study reports two plausible loci associated with SBP response to hydrochlorothiazide: TET2, an aldosterone-responsive mediator of alphaENaC gene transcription; and CSMD1, previously described as associated with hypertension in a case-control study.	Hydrochlorothiazide	94-113	CUB and Sushi multiple domains 1	Homo sapiens	193-198
25816110-7	2015	The rates of achievement of SBP &lt; 135 mmHg both in the morning and evening were: 81.8% and 21.4% in Los/HCTZ- and High-Los-treated isolated morning hypertension (p = 0.003), respectively; and 61.4% and 36.6% in Los/HCTX- and High-Los-treated sustained hypertension (p = 0.022), respectively.	Hydrochlorothiazide	107-111	selenium binding protein 1	Homo sapiens	28-31
25216597-15	2015	Hydrochlorothiazide decreased RPF and increased plasma insulin and uric acid concentrations in hypertensive subjects whom were not receiving estrogen plus progestin therapy.	Hydrochlorothiazide	0-19	insulin	Homo sapiens	55-62
24786779-11	2014	The combination treatment lercanidipine + enalapril seems to be more effective than lercanidipine + hydrochlorothiazide in activating insulin signalling in human lympho-monocytes.	Hydrochlorothiazide	100-119	insulin	Homo sapiens	134-141
25918454-0	2015	Assessment of glomerular filtration rate based on alterations of serum brain-derived neurotrophic factor in type 2 diabetic subjects treated with amlodipine/benazepril or valsartan/hydrochlorothiazide.	Hydrochlorothiazide	181-200	brain derived neurotrophic factor	Homo sapiens	71-104
25918454-6	2015	RESULTS: Of the 153 enrolled subjects, the changes in eGFR were significantly and inversely correlated with those in BDNF in the 76 subjects treated with valsartan/hydrochlorothiazide (r = -0.264, P = 0.021) but not in the 77 subjects treated with benazepril/amlodipine (r = -0.025, P = 0.862).	Hydrochlorothiazide	164-183	epidermal growth factor receptor	Homo sapiens	54-58
25918454-6	2015	RESULTS: Of the 153 enrolled subjects, the changes in eGFR were significantly and inversely correlated with those in BDNF in the 76 subjects treated with valsartan/hydrochlorothiazide (r = -0.264, P = 0.021) but not in the 77 subjects treated with benazepril/amlodipine (r = -0.025, P = 0.862).	Hydrochlorothiazide	164-183	brain derived neurotrophic factor	Homo sapiens	117-121
25918454-7	2015	The 45 subjects with increased BDNF following valsartan/hydrochlorothiazide treatment exhibited a significantly reduced eGFR (-8.8 +- 14.9 mL/min/1.73 m(2); P &lt; 0.001).	Hydrochlorothiazide	56-75	brain derived neurotrophic factor	Homo sapiens	31-35
25918454-7	2015	The 45 subjects with increased BDNF following valsartan/hydrochlorothiazide treatment exhibited a significantly reduced eGFR (-8.8 +- 14.9 mL/min/1.73 m(2); P &lt; 0.001).	Hydrochlorothiazide	56-75	epidermal growth factor receptor	Homo sapiens	120-124
25918454-7	2015	The 45 subjects with increased BDNF following valsartan/hydrochlorothiazide treatment exhibited a significantly reduced eGFR (-8.8 +- 14.9 mL/min/1.73 m(2); P &lt; 0.001).	Hydrochlorothiazide	56-75	CD59 molecule (CD59 blood group)	Homo sapiens	142-147
25918454-9	2015	CONCLUSIONS: Increased serum BDNF is associated with reduced eGFR in type 2 diabetic subjects treated with valsartan/hydrochlorothiazide but not with amlodipine/benazepril.	Hydrochlorothiazide	117-136	brain derived neurotrophic factor	Homo sapiens	29-33
25918454-9	2015	CONCLUSIONS: Increased serum BDNF is associated with reduced eGFR in type 2 diabetic subjects treated with valsartan/hydrochlorothiazide but not with amlodipine/benazepril.	Hydrochlorothiazide	117-136	epidermal growth factor receptor	Homo sapiens	61-65
25002871-9	2014	RESULTS: The mean change in sNa per day with hydrochlorothiazide and low renal solute feed was 2.5 - 3 mmol/L; on desmopressin treatment, the mean change in sNa was 6.8-7.9 mmol/L.	Hydrochlorothiazide	45-64	snail family transcriptional repressor 1	Homo sapiens	28-31
24694645-14	2014	In conclusion, the baseline potassium level and the WNK1 rs4980973 polymorphism were independent predictors of decreases in serum potassium after short-term hydrochlorothiazide treatment in nondiabetic hypertensive patients.	Hydrochlorothiazide	157-176	WNK lysine deficient protein kinase 1	Homo sapiens	52-56
24352504-5	2014	In polarized mouse cortical collecting duct (mpkCCD) cells, HCTZ treatment attenuated the Li-induced downregulation of aquaporin-2 (AQP2) water channel abundance.	Hydrochlorothiazide	60-64	aquaporin 2	Mus musculus	119-130
24352504-5	2014	In polarized mouse cortical collecting duct (mpkCCD) cells, HCTZ treatment attenuated the Li-induced downregulation of aquaporin-2 (AQP2) water channel abundance.	Hydrochlorothiazide	60-64	aquaporin 2	Mus musculus	132-136
24352504-8	2014	HCTZ increased AQP2 abundance on top of that of amiloride and did not affect the ENaC-mediated transcellular voltage.	Hydrochlorothiazide	0-4	aquaporin 2	Mus musculus	15-19
24352504-10	2014	These data indicated that in mpkCCD cells, HCTZ attenuated lithium-induced downregulation of AQP2 independently of NCC and ENaC.	Hydrochlorothiazide	43-47	aquaporin 2	Mus musculus	93-97
24352504-11	2014	Treatment of Li-NDI NCC knockout mice with HCTZ revealed a significantly reduced urine volume, unchanged urine osmolality, and increased cortical AQP2 abundance compared with Li-treated NCC knockout mice.	Hydrochlorothiazide	43-47	aquaporin 2	Mus musculus	146-150
24402096-6	2014	We tested this using renal clearance methodology in anesthetized mice, by the administration of hydrochlorothiazide (HCTZ) and/or benzamil (BZM) to exert specific blockade of NCC and ENaC, respectively.	Hydrochlorothiazide	96-115	sodium channel, nonvoltage-gated 1 alpha	Mus musculus	183-187
24402096-6	2014	We tested this using renal clearance methodology in anesthetized mice, by the administration of hydrochlorothiazide (HCTZ) and/or benzamil (BZM) to exert specific blockade of NCC and ENaC, respectively.	Hydrochlorothiazide	117-121	sodium channel, nonvoltage-gated 1 alpha	Mus musculus	183-187
24958603-2	2014	Here we determined whether renin-angiotensin system (RAS) phenotyping, i.e., the measurement of renin or ACE, can predict the individual response to RAS blockade, either chronically (enalapril vs. enalapril + candesartan) or acutely (enalapril +- hydrochlorothiazide, HCT).	Hydrochlorothiazide	268-271	renin	Homo sapiens	27-32
23400010-0	2014	Genome-wide association analyses suggest NELL1 influences adverse metabolic response to HCTZ in African Americans.	Hydrochlorothiazide	88-92	neural EGFL like 1	Homo sapiens	41-46
24260196-9	2013	The increased urine output in ACTZ/HCTZ treated rats was associated with a significant reduction in urine osmolality and reduced membrane localization of AQP-2 (aquaporin2).	Hydrochlorothiazide	35-39	aquaporin 2	Rattus norvegicus	154-159
24126713-8	2013	Nebivolol/HCTZ lowered central SBP by 15.8 +- 14.9 mmHg and DBP 10.5 +- 8.4 mmHg, and with metoprolol/HCTZ by 13.5 +- 12.3 mmHg for SBP and 9.5 +- 6.8 mmHg for DBP (all P &lt; 0.001).	Hydrochlorothiazide	10-14	selenium binding protein 1	Homo sapiens	31-34
24126713-8	2013	Nebivolol/HCTZ lowered central SBP by 15.8 +- 14.9 mmHg and DBP 10.5 +- 8.4 mmHg, and with metoprolol/HCTZ by 13.5 +- 12.3 mmHg for SBP and 9.5 +- 6.8 mmHg for DBP (all P &lt; 0.001).	Hydrochlorothiazide	10-14	selenium binding protein 1	Homo sapiens	132-135
24128935-0	2013	Impact of TCF7L2 single nucleotide polymorphisms on hydrochlorothiazide-induced diabetes.	Hydrochlorothiazide	52-71	transcription factor 7 like 2	Homo sapiens	10-16
24260196-9	2013	The increased urine output in ACTZ/HCTZ treated rats was associated with a significant reduction in urine osmolality and reduced membrane localization of AQP-2 (aquaporin2).	Hydrochlorothiazide	35-39	aquaporin 2	Rattus norvegicus	161-171
22907731-2	2013	KCNJ1 encodes a potassium channel and one study observed that a KCNJ1 single-nucleotide polymorphism (SNP) was associated with changes in fasting glucose (FG) during hydrochlorothiazide (HCTZ) treatment.	Hydrochlorothiazide	166-185	potassium inwardly rectifying channel subfamily J member 1	Homo sapiens	0-5
22907731-0	2013	Association of KCNJ1 variation with change in fasting glucose and new onset diabetes during HCTZ treatment.	Hydrochlorothiazide	92-96	potassium inwardly rectifying channel subfamily J member 1	Homo sapiens	15-20
22907731-2	2013	KCNJ1 encodes a potassium channel and one study observed that a KCNJ1 single-nucleotide polymorphism (SNP) was associated with changes in fasting glucose (FG) during hydrochlorothiazide (HCTZ) treatment.	Hydrochlorothiazide	166-185	potassium inwardly rectifying channel subfamily J member 1	Homo sapiens	64-69
22907731-2	2013	KCNJ1 encodes a potassium channel and one study observed that a KCNJ1 single-nucleotide polymorphism (SNP) was associated with changes in fasting glucose (FG) during hydrochlorothiazide (HCTZ) treatment.	Hydrochlorothiazide	187-191	potassium inwardly rectifying channel subfamily J member 1	Homo sapiens	0-5
22907731-2	2013	KCNJ1 encodes a potassium channel and one study observed that a KCNJ1 single-nucleotide polymorphism (SNP) was associated with changes in fasting glucose (FG) during hydrochlorothiazide (HCTZ) treatment.	Hydrochlorothiazide	187-191	potassium inwardly rectifying channel subfamily J member 1	Homo sapiens	64-69
22907731-3	2013	We used linear regression to test association of KCNJ1 SNPs and haplotypes with FG changes during HCTZ treatment in the Pharmacogenomic Evaluation of Antihypertensive Responses (PEAR) study.	Hydrochlorothiazide	98-102	potassium inwardly rectifying channel subfamily J member 1	Homo sapiens	49-54
22907731-4	2013	We used logistic regression to test association of KCNJ1 variation with NOD in HCTZ-treated patients from the International Verapamil SR Trandolapril Study (INVEST).	Hydrochlorothiazide	79-83	potassium inwardly rectifying channel subfamily J member 1	Homo sapiens	51-56
22907731-6	2013	In PEAR blacks, a KCNJ1 SNP was associated with increased FG during HCTZ treatment (beta=8.47, P(FDR)=0.009).	Hydrochlorothiazide	68-72	potassium inwardly rectifying channel subfamily J member 1	Homo sapiens	18-23
22907731-8	2013	Our findings support that KCNJ1 variation is associated with HCTZ-induced dysglycemia and NOD.	Hydrochlorothiazide	61-65	potassium inwardly rectifying channel subfamily J member 1	Homo sapiens	26-31
23863317-0	2013	Effects of ACE and ADD1 gene polymorphisms on blood pressure response to hydrochlorothiazide: a meta-analysis.	Hydrochlorothiazide	73-92	angiotensin I converting enzyme	Homo sapiens	11-14
23863317-0	2013	Effects of ACE and ADD1 gene polymorphisms on blood pressure response to hydrochlorothiazide: a meta-analysis.	Hydrochlorothiazide	73-92	adducin 1	Homo sapiens	19-23
23863317-3	2013	A meta-analysis of published data was conducted to evaluate the pharmacogenetic associations of ACE I/D and ADD1 Gly460Trp polymorphisms with blood pressure changes during HCTZ therapy.	Hydrochlorothiazide	172-176	angiotensin I converting enzyme	Homo sapiens	96-99
23863317-3	2013	A meta-analysis of published data was conducted to evaluate the pharmacogenetic associations of ACE I/D and ADD1 Gly460Trp polymorphisms with blood pressure changes during HCTZ therapy.	Hydrochlorothiazide	172-176	adducin 1	Homo sapiens	108-112
23863317-8	2013	This study is the first meta-analysis to evaluate the influences of ACE and ADD1 polymorphisms on blood pressure responses to HCTZ to combine the inconsistent results of previous studies.	Hydrochlorothiazide	126-130	angiotensin I converting enzyme	Homo sapiens	68-71
23863317-8	2013	This study is the first meta-analysis to evaluate the influences of ACE and ADD1 polymorphisms on blood pressure responses to HCTZ to combine the inconsistent results of previous studies.	Hydrochlorothiazide	126-130	adducin 1	Homo sapiens	76-80
23837919-7	2013	The elevation of hepatic TG levels after HCTZ treatment was additionally accompanied by a reduction in insulin sensitivity:  SI HCTZ = -1.14.	Hydrochlorothiazide	41-45	insulin	Homo sapiens	103-110
23707192-6	2013	Lipid peroxidation, protein carbonyl formation, vitamin C level and catalase activity decreased after HFD, HCTZ or HFD plus HCTZ ingestion.	Hydrochlorothiazide	107-111	catalase	Rattus norvegicus	56-76
23707192-6	2013	Lipid peroxidation, protein carbonyl formation, vitamin C level and catalase activity decreased after HFD, HCTZ or HFD plus HCTZ ingestion.	Hydrochlorothiazide	124-128	catalase	Rattus norvegicus	56-76
23837919-7	2013	The elevation of hepatic TG levels after HCTZ treatment was additionally accompanied by a reduction in insulin sensitivity:  SI HCTZ = -1.14.	Hydrochlorothiazide	128-132	insulin	Homo sapiens	103-110
23837919-15	2013	HCTZ treatment worsened hepatic steatosis measured as hepatic triglyceride content and reduced insulin sensitivity.	Hydrochlorothiazide	0-4	insulin	Homo sapiens	95-102
22350108-0	2013	Association of chromosome 12 locus with antihypertensive response to hydrochlorothiazide may involve differential YEATS4 expression.	Hydrochlorothiazide	69-88	YEATS domain containing 4	Homo sapiens	114-120
23680668-6	2013	NEB reduced plasma angiotensin II concentration, which was increased in SHR and after HCTZ treatment.	Hydrochlorothiazide	86-90	angiotensinogen	Rattus norvegicus	19-33
22350108-6	2013	Expression analyses in HCTZ-treated African-Americans showed differential pre-treatment leukocyte YEATS4 expression between rs7297610 genotype groups (P=0.024), and reduced post-treatment expression in C/C genotypes (P=0.009), but not in T-carriers.	Hydrochlorothiazide	23-27	YEATS domain containing 4	Homo sapiens	98-104
22350108-7	2013	Our data confirm previous genome-wide findings at 12q15 and suggest differential YEATS4 expression could underpin rs7297610-associated HCTZ response variability, which may have future implications for guiding thiazide treatment.	Hydrochlorothiazide	135-139	YEATS domain containing 4	Homo sapiens	81-87
23353631-6	2013	RESULTS: Significant associations or trends were found between rs4149601, rs292449, rs75982813 and rs1008899 and decreases in blood pressure in whites on hydrochlorothiazide, and a significant association was observed with increasing copies of the GC rs4149601-rs292449 haplotype and greater blood pressure response to hydrochlorothiazide in whites (P = 0.0006 and 0.006, SBP and DBP, respectively).	Hydrochlorothiazide	319-338	selenium binding protein 1	Homo sapiens	372-375
23427142-9	2013	The upregulation of pSPAK/OSR1, pNKCC2, and pNCC in WNK3-/- mice relative to the levels in WT mice when fed a low-salt diet was paralleled by an increased diuresis in response to hydrochlorothiazide.	Hydrochlorothiazide	179-198	WNK lysine deficient protein kinase 3	Mus musculus	52-56
23353631-6	2013	RESULTS: Significant associations or trends were found between rs4149601, rs292449, rs75982813 and rs1008899 and decreases in blood pressure in whites on hydrochlorothiazide, and a significant association was observed with increasing copies of the GC rs4149601-rs292449 haplotype and greater blood pressure response to hydrochlorothiazide in whites (P = 0.0006 and 0.006, SBP and DBP, respectively).	Hydrochlorothiazide	319-338	D-box binding PAR bZIP transcription factor	Homo sapiens	380-383
23353631-8	2013	CONCLUSION: NEDD4L rs4149601, rs292449 and rs75982813 may be predictors for blood pressure response to hydrochlorothiazide in whites, and NEDD4L rs4149601 may be a predictor for adverse cardiovascular outcomes in whites not treated with hydrochlorothiazide.	Hydrochlorothiazide	103-122	NEDD4 like E3 ubiquitin protein ligase	Homo sapiens	12-18
23353631-8	2013	CONCLUSION: NEDD4L rs4149601, rs292449 and rs75982813 may be predictors for blood pressure response to hydrochlorothiazide in whites, and NEDD4L rs4149601 may be a predictor for adverse cardiovascular outcomes in whites not treated with hydrochlorothiazide.	Hydrochlorothiazide	237-256	NEDD4 like E3 ubiquitin protein ligase	Homo sapiens	12-18
22773432-0	2012	Efficacy and effect on plasma B-type natriuretic peptide concentration of losartan-hydrochlorothiazide for hypertension uncontrolled by losartan-based therapy: subanalysis of a Multicentre Prospective Observational Study.	Hydrochlorothiazide	83-102	natriuretic peptide B	Homo sapiens	30-56
22952039-2	2013	After patients were observed with hydrochlorothiazide (HCTZ)-associated CTCL, HCTZ was examined as a putative chronic antigen in a cohort of prospectively staged patients.	Hydrochlorothiazide	34-53	TSPY like 2	Homo sapiens	72-76
22952039-2	2013	After patients were observed with hydrochlorothiazide (HCTZ)-associated CTCL, HCTZ was examined as a putative chronic antigen in a cohort of prospectively staged patients.	Hydrochlorothiazide	55-59	TSPY like 2	Homo sapiens	72-76
24082785-7	2013	The T/A SPC is associated with a lower incidence of edema than amlodipine monotherapy, and the T/H SPC with a lower incidence of hypokalemia than hydrochlorothiazide monotherapy.	Hydrochlorothiazide	146-165	proline rich protein gene cluster	Homo sapiens	99-102
23235349-8	2013	In comparison to the valsartan/HCTZ cohort, the irbesartan/HCTZ group was associated with significant reductions in both systolic BP (SBP; -9 vs. -2 mm Hg; p = 0.021) and diastolic BP (DBP; -5 vs. 0 mm Hg; p = 0.022).	Hydrochlorothiazide	59-63	DEAD-box helicase 19B	Homo sapiens	171-192
22747613-1	2012	The authors previously reported that addition of valsartan ameliorated the negative metabolic effects of hydrochlorothiazide in obese hypertensive patients through an enhanced postprandial insulin response.	Hydrochlorothiazide	105-124	insulin	Homo sapiens	189-196
24250503-2	2012	The selected ACE inhibitors had sufficiently different structures which can indicate the method suitability for their lipophilicity evaluation as the model substances in comparison with HCTZ.	Hydrochlorothiazide	186-190	angiotensin I converting enzyme	Homo sapiens	13-16
22747613-2	2012	In this secondary analysis, the authors tested whether this enhanced insulin response to valsartan/hydrochlorothiazide was influenced by serum potassium levels, which were reduced to a lesser extent, when compared with amlodipine/hydrochlorothiazide.	Hydrochlorothiazide	99-118	insulin	Homo sapiens	69-76
22747613-3	2012	Results showed that the early insulin response with valsartan plus hydrochlorothiazide occurred regardless of serum potassium levels.	Hydrochlorothiazide	67-86	insulin	Homo sapiens	30-37
22747613-6	2012	Thus, the metabolic response to hydrochlorothiazide was improved with addition of valsartan through an enhanced insulin response that was not greatly affected by changes in potassium levels.	Hydrochlorothiazide	32-51	insulin	Homo sapiens	112-119
22278145-1	2012	OBJECTIVES: The aim of this study was to compare the single-dose effects of thiazide-type diuretics cicletanine and hydrochlorothiazide (HCTZ), on natriuresis and kaliuresis in prehypertensive and treatment-naive, stage 1 hypertensive patients and to explore the impact of GRK4 gene polymorphisms on thiazide-induced urinary electrolyte excretion.	Hydrochlorothiazide	116-135	G protein-coupled receptor kinase 4	Homo sapiens	273-277
22311004-7	2012	At Week 4, V/HCTZ was more effective than HCTZ or V at reducing mean sitting systolic BP (MSSBP), independent of baseline PRA, with reductions of -16.9, -12.6, and -9.5 mmHg, respectively, in low-renin subjects and -19.4, -11.5, and -8.6 mmHg in normal-high renin subjects.	Hydrochlorothiazide	13-17	renin	Homo sapiens	196-201
22311004-7	2012	At Week 4, V/HCTZ was more effective than HCTZ or V at reducing mean sitting systolic BP (MSSBP), independent of baseline PRA, with reductions of -16.9, -12.6, and -9.5 mmHg, respectively, in low-renin subjects and -19.4, -11.5, and -8.6 mmHg in normal-high renin subjects.	Hydrochlorothiazide	13-17	renin	Homo sapiens	258-263
23098346-7	2012	As a result of treatment (41 to 53% of patients received losartan only or in combination with HCTZ) SBP decrease in the groups ranged from 20 to 38 mm Hg, DBP - from 10 to 17 mm Hg, the target blood pressure is achieved in 29-66% of patients.	Hydrochlorothiazide	94-98	selenium binding protein 1	Homo sapiens	100-103
22438773-0	2012	The Last Nail in Hydrochlorothiazide"s Coffin?	Hydrochlorothiazide	17-36	CD244 molecule	Homo sapiens	9-13
22440088-9	2012	RESULTS: In one cohort, a polymorphism in DOT1L (rs2269879) was strongly associated with greater systolic (P = 0.0002) and diastolic (P = 0.0016) blood pressure response to hydrochlorothiazide in Caucasians.	Hydrochlorothiazide	173-192	DOT1 like histone lysine methyltransferase	Homo sapiens	42-47
22440088-14	2012	However, a possibility exists that rs2269879 in DOT1L could be associated with HCTZ response in Caucasians.	Hydrochlorothiazide	79-83	DOT1 like histone lysine methyltransferase	Homo sapiens	48-53
21746766-0	2012	Effect of fixed-dose losartan/hydrochlorothiazide on brain natriuretic peptide in patients with hypertension.	Hydrochlorothiazide	30-49	natriuretic peptide B	Homo sapiens	53-78
22311496-1	2012	OBJECTIVE: To evaluate the effect of CYP11B2 gene -344T/C polymorphism on renin-angiotensin-aldosterone system (RAAS) activity and blood pressure in response to hydrochlorothiazide (HCTZ) treatment in Han Chinese patients with essential hypertension.	Hydrochlorothiazide	161-180	cytochrome P450 family 11 subfamily B member 2	Homo sapiens	37-44
22311496-13	2012	CONCLUSION: In males, the -344T/C polymorphism of CYP11B2 gene is associated with aldosterone level, and the change of aldosterone level was greater, the blood pressure response was weaker after HCTZ treatment.	Hydrochlorothiazide	195-199	cytochrome P450 family 11 subfamily B member 2	Homo sapiens	50-57
22188593-0	2012	Antihypertensive efficacy of the losartan/hydrochlorothiazide combination and its effect on plasma B-type natriuretic peptide in hypertensive patients uncontrolled by angiotensin II type 1 receptor antagonist-based therapy: a multicentre prospective observational study.	Hydrochlorothiazide	42-61	natriuretic peptide B	Homo sapiens	99-125
22188593-13	2012	CONCLUSION: Antihypertensive treatment using two types of drugs (LOS/HCTZ) with different mechanisms yielded potent antihypertensive efficacy with safety and decreased plasma BNP levels.	Hydrochlorothiazide	69-73	natriuretic peptide B	Homo sapiens	175-178
22844584-5	2012	Treatment with telmisartan-HCTZ induced significantly greater reductions in BP (-31.1/-18.3 mm Hg) than valsartan-HCTZ (-28.4/-16.3 mm Hg; SBP P = 0.0265, diastolic BP P = 0.0041).	Hydrochlorothiazide	27-31	selenium binding protein 1	Homo sapiens	139-142
22035463-3	2011	The volume reduction with these agents stimulates the renin-angiotensin system (RAS), making RAS inhibitors such as the direct renin inhibitor aliskiren a logical choice for combination therapy with HCTZ.	Hydrochlorothiazide	199-203	renin	Homo sapiens	54-59
21647824-0	2011	Gender-specific association between ACE gene I/D polymorphism and blood pressure response to hydrochlorothiazide in Han Chinese hypertensive patients.	Hydrochlorothiazide	93-112	angiotensin I converting enzyme	Homo sapiens	36-39
21647824-1	2011	To evaluate the interaction between the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and gender with individual blood pressure response to hydrochlorothiazide (HCTZ) in hypertensives, we enrolled 829 mild-moderate hypertensive patients.	Hydrochlorothiazide	173-192	angiotensin I converting enzyme	Homo sapiens	71-74
21647824-1	2011	To evaluate the interaction between the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and gender with individual blood pressure response to hydrochlorothiazide (HCTZ) in hypertensives, we enrolled 829 mild-moderate hypertensive patients.	Hydrochlorothiazide	194-198	angiotensin I converting enzyme	Homo sapiens	40-69
21647824-1	2011	To evaluate the interaction between the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and gender with individual blood pressure response to hydrochlorothiazide (HCTZ) in hypertensives, we enrolled 829 mild-moderate hypertensive patients.	Hydrochlorothiazide	194-198	angiotensin I converting enzyme	Homo sapiens	71-74
21647824-5	2011	Moreover, in each gender, the genotype that was associated with the greatest blood pressure response to HCTZ (DD homozygotes in men and II homozygotes in women) was also associated with the greatest increase in serum ACE activity in response to HCTZ.	Hydrochlorothiazide	104-108	angiotensin I converting enzyme	Homo sapiens	217-220
21647824-5	2011	Moreover, in each gender, the genotype that was associated with the greatest blood pressure response to HCTZ (DD homozygotes in men and II homozygotes in women) was also associated with the greatest increase in serum ACE activity in response to HCTZ.	Hydrochlorothiazide	245-249	angiotensin I converting enzyme	Homo sapiens	217-220
21343376-10	2011	Coumarins, quinolones, antiepileptics, and hydrochlorothiazide were frequently part of a PDI.	Hydrochlorothiazide	43-62	peptidyl arginine deiminase 1	Homo sapiens	89-92
22050062-6	2011	NEB plus HCTZ was associated with reduced oxidative stress in terms of glutathione availability, lower angiotensin I levels as index of plasma renin activity and reduced clearance of urinary sodium compared with HCTZ alone.	Hydrochlorothiazide	9-13	renin	Rattus norvegicus	143-148
21261619-9	2011	CONCLUSIONS: In addition to PRA, renin rs11240688 CC polymorphism may also independently predict the effect of HCTZ.	Hydrochlorothiazide	111-115	renin	Homo sapiens	33-38
21796332-0	2011	Hydrochlorothiazide versus calcium channel blockers: what is the best add-on to a renin-angiotensin system blocker for treating hypertension in patients with renal disease?	Hydrochlorothiazide	0-19	renin	Homo sapiens	82-87
21703256-12	2011	These results suggest that hydrochlorothiazide improves cardiac remodeling as effectively as spironolactone by reducing proinflammatory cytokine levels and inhibiting the TGF-beta signaling pathway in post-myocardial infarction congestive heart failure.	Hydrochlorothiazide	27-46	transforming growth factor, beta 1	Rattus norvegicus	171-179
21633011-6	2011	Furthermore, chronic treatment with hydrochlorothiazide normalized urinary excretion of Na(+) and Ca(2+), and abolished acidosis in Kir5.1(-/-) mice.	Hydrochlorothiazide	36-55	potassium inwardly-rectifying channel, subfamily J, member 16	Mus musculus	132-138
22258466-0	2011	Central Pressure and Biomarker Responses to Renin Inhibition with Hydrochlorothiazide and Ramipril in Obese Hypertensives: The ATTAIN Study.	Hydrochlorothiazide	66-85	renin	Homo sapiens	44-49
21164499-3	2011	We hypothesized that intergenic polymorphisms between OAT1 and OAT3 might be associated with adult hypertension and the antihypertensive effects of hydrochlorothiazide (HCTZ).	Hydrochlorothiazide	148-167	solute carrier family 22 member 6	Homo sapiens	54-58
21164499-3	2011	We hypothesized that intergenic polymorphisms between OAT1 and OAT3 might be associated with adult hypertension and the antihypertensive effects of hydrochlorothiazide (HCTZ).	Hydrochlorothiazide	148-167	solute carrier family 22 member 8	Homo sapiens	63-67
21164499-3	2011	We hypothesized that intergenic polymorphisms between OAT1 and OAT3 might be associated with adult hypertension and the antihypertensive effects of hydrochlorothiazide (HCTZ).	Hydrochlorothiazide	169-173	solute carrier family 22 member 6	Homo sapiens	54-58
21164499-3	2011	We hypothesized that intergenic polymorphisms between OAT1 and OAT3 might be associated with adult hypertension and the antihypertensive effects of hydrochlorothiazide (HCTZ).	Hydrochlorothiazide	169-173	solute carrier family 22 member 8	Homo sapiens	63-67
21164499-8	2011	CONCLUSIONS: Intergenic polymorphism rs10792367 between OAT1 and OAT3 is not associated with hypertension, but appears to be involved in between-individual variations in antihypertensive responses to HCTZ.	Hydrochlorothiazide	200-204	solute carrier family 22 member 6	Homo sapiens	56-60
21164499-8	2011	CONCLUSIONS: Intergenic polymorphism rs10792367 between OAT1 and OAT3 is not associated with hypertension, but appears to be involved in between-individual variations in antihypertensive responses to HCTZ.	Hydrochlorothiazide	200-204	solute carrier family 22 member 8	Homo sapiens	65-69
21039412-1	2011	The initial appearance of subacute cutaneous lupus erythematosus (SCLE) skin lesions in conjunction with Ro/SS-A autoantibodies occurring as an adverse reaction to hydrochlorothiazide [i.e. drug-induced SCLE (DI-SCLE)] was first reported in 1985.	Hydrochlorothiazide	164-183	tripartite motif containing 21	Homo sapiens	105-112
21714597-3	2011	The renoprotective effects of the ACE inhibitor, benazepril, independent of blood pressure control, have been demonstrated, as monotherapy or in combination with amlodipine or hydrochlorothiazide, in large clinical trials: Avoiding Cardiovascular Events through Combination Therapy in Patients Living with Systolic Hypertension (ACCOMPLISH) and Gauging Albuminuria Reduction with Lotrel in Diabetic Patients with Hypertension (GUARD) in patients with mild-to-severe chronic kidney disease.	Hydrochlorothiazide	176-195	angiotensin I converting enzyme	Homo sapiens	34-37
21332024-0	2011	Hydrochlorothiazide compared to candesartan treatment increases adipose tissue gene expression and circulating levels of serum amyloid A in hypertensive patients.	Hydrochlorothiazide	0-19	serum amyloid A1 cluster	Homo sapiens	121-136
21332024-5	2011	Adipose tissue gene expression of serum amyloid A (SAA) was higher after hydrochlorothiazide treatment compared to candesartan (p=0.036), and this was in accordance with our previous finding on circulating SAA levels.	Hydrochlorothiazide	73-92	serum amyloid A1 cluster	Homo sapiens	34-49
21332024-5	2011	Adipose tissue gene expression of serum amyloid A (SAA) was higher after hydrochlorothiazide treatment compared to candesartan (p=0.036), and this was in accordance with our previous finding on circulating SAA levels.	Hydrochlorothiazide	73-92	serum amyloid A1 cluster	Homo sapiens	51-54
21332024-5	2011	Adipose tissue gene expression of serum amyloid A (SAA) was higher after hydrochlorothiazide treatment compared to candesartan (p=0.036), and this was in accordance with our previous finding on circulating SAA levels.	Hydrochlorothiazide	73-92	serum amyloid A1 cluster	Homo sapiens	206-209
21332024-8	2011	In comparison to candesartan, hydrochlorothiazide raised the adipose tissue gene expression of SAA and the serum level of SAA as well as E selectin in hypertensive patients.	Hydrochlorothiazide	30-49	serum amyloid A1 cluster	Homo sapiens	95-98
21332024-8	2011	In comparison to candesartan, hydrochlorothiazide raised the adipose tissue gene expression of SAA and the serum level of SAA as well as E selectin in hypertensive patients.	Hydrochlorothiazide	30-49	serum amyloid A1 cluster	Homo sapiens	122-125
21406342-7	2011	The standard error of prediction (SEP) for valsartan and hydrochlorothiazide was 0.020 and 0.038 mug mL-1, respectively.	Hydrochlorothiazide	57-76	L1 cell adhesion molecule	Mus musculus	101-105
21123038-0	2011	Micelles from PEO-PPO-PEO block copolymers as nanocontainers for solubilization of a poorly water soluble drug hydrochlorothiazide.	Hydrochlorothiazide	111-130	protoporphyrinogen oxidase	Homo sapiens	18-21
20725057-7	2010	Higher plasma renin activity was consistently associated with greater blood pressure responses to atenolol and lesser responses to hydrochlorothiazide.	Hydrochlorothiazide	131-150	renin	Homo sapiens	14-19
21309738-2	2011	Lipopolysaccharide-induced secretion of IL-1beta by PMNs from 15 hypertensive and 15 normotensive subjects after incubation with losartan, captopril, amlodipine, atenolol, and hydrochlorothiazide were assessed.	Hydrochlorothiazide	176-195	interleukin 1 beta	Homo sapiens	40-48
21127457-5	2011	BP response to atenolol and hydrochlorothiazide by ADRBK1 SNPs and GRK5 Gln41Leu was tested in 418 patients from the Pharmacogenomic Evaluation of Antihypertensive Responses Study using linear regression.	Hydrochlorothiazide	28-47	G protein-coupled receptor kinase 2	Homo sapiens	51-57
21269061-0	2011	Interaction of ACE and CYP11B2 genes on blood pressure response to hydrochlorothiazide in Han Chinese hypertensive patients.	Hydrochlorothiazide	67-86	angiotensin I converting enzyme	Homo sapiens	15-18
21269061-0	2011	Interaction of ACE and CYP11B2 genes on blood pressure response to hydrochlorothiazide in Han Chinese hypertensive patients.	Hydrochlorothiazide	67-86	cytochrome P450 family 11 subfamily B member 2	Homo sapiens	23-30
21269061-3	2011	After 6 weeks, the results showed that the ACE I/D polymorphism, not the CYP11B2 -344T/C polymorphism, was associated with systolic blood pressure (SBP) response to HCTZ (P = 0.009) in the Han Chinese population with essential hypertension, with no interaction.	Hydrochlorothiazide	165-169	angiotensin I converting enzyme	Homo sapiens	43-46
20725057-9	2010	CONCLUSIONS: Plasma renin activity and pretreatment blood pressure level predict blood pressure responses to atenolol and hydrochlorothiazide administered as mono- and as add-on therapy in men and women &lt; or =65 years of age.	Hydrochlorothiazide	122-141	renin	Homo sapiens	20-25
20673201-15	2010	A similar trend was observed in the subgroup analyses comparing SPC of valsartan/amlodipine vs. FCs of ARB + CCB and SPC of valsartan/HCTZ vs. FCs of ARB + HCTZ.	Hydrochlorothiazide	134-138	proline rich protein gene cluster	Homo sapiens	117-120
20556561-9	2010	However, the mean 24-hour ABPM SBP significantly decreased by 16.7 mmHg with eprosartan/HCTZ and 20.3 mmHg with losartan/HCTZ (P&lt;0.001 vs. baseline).	Hydrochlorothiazide	88-92	selenium binding protein 1	Homo sapiens	31-34
20808673-7	2010	Protein abundance of NHE3, SGLT1, and NKCC2 decreased in the hypercalciuric rats, and only SGLT1 protein abundance was increased by HCTZ in the hypercalciuric rats.	Hydrochlorothiazide	132-136	solute carrier family 5 member 1	Rattus norvegicus	91-96
20808673-9	2010	This attenuation seems to have resulted from the lack of HCTZ"s effect on protein abundance of TRPV5 in severe hypercalciuric condition induced by high calcium and vitamin D.	Hydrochlorothiazide	57-61	transient receptor potential cation channel, subfamily V, member 5	Rattus norvegicus	95-100
21134851-4	2010	The linearity range was found to be 8-40, 1-5 and 3-15 mug mL-1 for losartan potassium, amlodipine besilate and hydrochlorothiazide, respectively.	Hydrochlorothiazide	112-131	L1 cell adhesion molecule	Mus musculus	59-63
20498618-10	2010	CONCLUSION: The novel observation of this investigation was that the combination of valsartan and hydrochlorothiazide was associated with greater glucose-stimulated insulin secretory and lesser glycemic excursion responses than the amlodipine combination group.	Hydrochlorothiazide	98-117	insulin	Homo sapiens	165-172
20716842-0	2010	Fixed-dose telmisartan/hydrochlorothiazide in comparison with losartan/hydrochlorothiazide in decreasing serum hepatocyte growth factor and improving endothelial dysfunction in hypertensive patients.	Hydrochlorothiazide	23-42	hepatocyte growth factor	Homo sapiens	111-135
20716842-0	2010	Fixed-dose telmisartan/hydrochlorothiazide in comparison with losartan/hydrochlorothiazide in decreasing serum hepatocyte growth factor and improving endothelial dysfunction in hypertensive patients.	Hydrochlorothiazide	71-90	hepatocyte growth factor	Homo sapiens	111-135
20556561-9	2010	However, the mean 24-hour ABPM SBP significantly decreased by 16.7 mmHg with eprosartan/HCTZ and 20.3 mmHg with losartan/HCTZ (P&lt;0.001 vs. baseline).	Hydrochlorothiazide	121-125	selenium binding protein 1	Homo sapiens	31-34
20331602-0	2010	Spironolactone and hydrochlorothiazide exert antioxidant effects and reduce vascular matrix metalloproteinase-2 activity and expression in a model of renovascular hypertension.	Hydrochlorothiazide	19-38	matrix metallopeptidase 2	Rattus norvegicus	85-111
20331602-13	2010	CONCLUSIONS AND IMPLICATIONS: SPRL or HCTZ, alone or combined, exerted antioxidant effects, and decreased renovascular hypertension-induced MMP-2 up-regulation, thus improving the vascular dysfunction and remodelling found in this model of hypertension.	Hydrochlorothiazide	38-42	matrix metallopeptidase 2	Rattus norvegicus	140-145
20407632-4	2010	Based on these considerations, addition of hydrochlorothiazide to the combination of an antagonist of the renin-angiotensin system with a calcium channel blocker would constitute a logical approach.	Hydrochlorothiazide	43-62	renin	Homo sapiens	106-111
19730415-7	2009	Conversely, hydrochlorothiazide, 0.1 micromol/l, reduced adiponectin by 37% (P &lt; 0.01).	Hydrochlorothiazide	12-31	adiponectin, C1Q and collagen domain containing	Homo sapiens	57-68
20104189-6	2010	RESULTS: The blood pressure response to Ang II was blocked by more than 90% with irbesartan alone or in association with HCTZ and with olmesartan/HCTZ and by nearly 60% with valsartan/HCTZ and losartan/HCTZ (P &lt; 0.05).	Hydrochlorothiazide	121-125	angiogenin	Homo sapiens	40-43
20104189-6	2010	RESULTS: The blood pressure response to Ang II was blocked by more than 90% with irbesartan alone or in association with HCTZ and with olmesartan/HCTZ and by nearly 60% with valsartan/HCTZ and losartan/HCTZ (P &lt; 0.05).	Hydrochlorothiazide	146-150	angiogenin	Homo sapiens	40-43
20104189-6	2010	RESULTS: The blood pressure response to Ang II was blocked by more than 90% with irbesartan alone or in association with HCTZ and with olmesartan/HCTZ and by nearly 60% with valsartan/HCTZ and losartan/HCTZ (P &lt; 0.05).	Hydrochlorothiazide	146-150	angiogenin	Homo sapiens	40-43
20104189-6	2010	RESULTS: The blood pressure response to Ang II was blocked by more than 90% with irbesartan alone or in association with HCTZ and with olmesartan/HCTZ and by nearly 60% with valsartan/HCTZ and losartan/HCTZ (P &lt; 0.05).	Hydrochlorothiazide	146-150	angiogenin	Homo sapiens	40-43
20104189-8	2010	Irbesartan +/- HCTZ and olmesartan/HCTZ blocked the renal hemodynamic response to Ang II nearly completely, whereas valsartan/HCTZ and losartan/HCTZ only blunted this effect by 34 and 45%, respectively.	Hydrochlorothiazide	15-19	angiogenin	Homo sapiens	82-85
20104189-8	2010	Irbesartan +/- HCTZ and olmesartan/HCTZ blocked the renal hemodynamic response to Ang II nearly completely, whereas valsartan/HCTZ and losartan/HCTZ only blunted this effect by 34 and 45%, respectively.	Hydrochlorothiazide	35-39	angiogenin	Homo sapiens	82-85
20104189-8	2010	Irbesartan +/- HCTZ and olmesartan/HCTZ blocked the renal hemodynamic response to Ang II nearly completely, whereas valsartan/HCTZ and losartan/HCTZ only blunted this effect by 34 and 45%, respectively.	Hydrochlorothiazide	35-39	angiogenin	Homo sapiens	82-85
20104189-8	2010	Irbesartan +/- HCTZ and olmesartan/HCTZ blocked the renal hemodynamic response to Ang II nearly completely, whereas valsartan/HCTZ and losartan/HCTZ only blunted this effect by 34 and 45%, respectively.	Hydrochlorothiazide	35-39	angiogenin	Homo sapiens	82-85
21949632-7	2010	From a pathophysiologic perspective, it can be combined with hydrochlorothiazide successfully, because it can block the diuretic-induced increase in plasma renin activity.	Hydrochlorothiazide	61-80	renin	Homo sapiens	156-161
19929980-3	2010	METHODS: i-RESPOND, a randomised, controlled, multicentre, double-blind study evaluated the effect of 16 weeks of irbesartan vs. hydrochlorothiazide (HCTZ) on insulin resistance as well as on lipid and inflammatory parameters in hypertensive subjects with metabolic syndrome.	Hydrochlorothiazide	150-154	insulin	Homo sapiens	159-166
19730415-9	2009	Gene expression of adiponectin correlated with these results: with telmisartan, it increased by 27%, and with hydrochlorothiazide it decreased by 38% (P &lt; 0.05 for both compared to the control).	Hydrochlorothiazide	110-129	adiponectin, C1Q and collagen domain containing	Homo sapiens	19-30
19640361-10	2009	We accordingly propose that a low dose of hydrochlorothiazide should be administered to those patients in whom the blood pressure is not well controlled by intensive renin-angiotensin system inhibition therapy using the maximum recommended doses of angiotensin II Type I receptor blockers and angiotensin I-converting enzyme inhibitors.	Hydrochlorothiazide	42-61	renin	Homo sapiens	166-171
19640361-10	2009	We accordingly propose that a low dose of hydrochlorothiazide should be administered to those patients in whom the blood pressure is not well controlled by intensive renin-angiotensin system inhibition therapy using the maximum recommended doses of angiotensin II Type I receptor blockers and angiotensin I-converting enzyme inhibitors.	Hydrochlorothiazide	42-61	angiotensin I converting enzyme	Homo sapiens	293-324
19194547-2	2009	We assessed the effects of hydrochlorothiazide (HCTZ) on the expression of TRPV5, calbindin-D(28K), and several sodium transporters in hypercalciuric rats.	Hydrochlorothiazide	27-46	transient receptor potential cation channel, subfamily V, member 5	Rattus norvegicus	75-80
19591299-5	2009	Losartan/HCTZ combination tablets effectively reduce BP when switched from the usual dose of ARB or ACE inhibitors.	Hydrochlorothiazide	9-13	angiotensin I converting enzyme	Homo sapiens	100-103
19247266-8	2009	Although homozygous ACE GG subjects and ACE C allele carriers both had an increased risk of diabetes associated with thiazide use, this risk was more increased for ACE GG subjects (SI 1.70 (95% CI: 1.08-2.66)), particularly at doses &gt; or =1 daily defined dose (DDD) (=25 mg hydrochlorothiazide)/day (SI 2.0 (95% CI: 1.20-3.32)).	Hydrochlorothiazide	277-296	angiotensin I converting enzyme	Homo sapiens	20-23
19655819-1	2009	BACKGROUND: The combination of olmesartan medoxomil and hydrochlorothiazide (HCTZ) [olmesartan medoxomil/HCTZ] has previously been shown to produce significantly greater SBP/DBP reductions than monotherapy with either agent alone in a randomized, double-blind, factorial study in patients with stage 2 hypertension.	Hydrochlorothiazide	56-75	selenium binding protein 1	Homo sapiens	170-173
19655819-1	2009	BACKGROUND: The combination of olmesartan medoxomil and hydrochlorothiazide (HCTZ) [olmesartan medoxomil/HCTZ] has previously been shown to produce significantly greater SBP/DBP reductions than monotherapy with either agent alone in a randomized, double-blind, factorial study in patients with stage 2 hypertension.	Hydrochlorothiazide	56-75	D-box binding PAR bZIP transcription factor	Homo sapiens	174-177
19655819-1	2009	BACKGROUND: The combination of olmesartan medoxomil and hydrochlorothiazide (HCTZ) [olmesartan medoxomil/HCTZ] has previously been shown to produce significantly greater SBP/DBP reductions than monotherapy with either agent alone in a randomized, double-blind, factorial study in patients with stage 2 hypertension.	Hydrochlorothiazide	77-81	selenium binding protein 1	Homo sapiens	170-173
19655819-1	2009	BACKGROUND: The combination of olmesartan medoxomil and hydrochlorothiazide (HCTZ) [olmesartan medoxomil/HCTZ] has previously been shown to produce significantly greater SBP/DBP reductions than monotherapy with either agent alone in a randomized, double-blind, factorial study in patients with stage 2 hypertension.	Hydrochlorothiazide	77-81	D-box binding PAR bZIP transcription factor	Homo sapiens	174-177
19655819-1	2009	BACKGROUND: The combination of olmesartan medoxomil and hydrochlorothiazide (HCTZ) [olmesartan medoxomil/HCTZ] has previously been shown to produce significantly greater SBP/DBP reductions than monotherapy with either agent alone in a randomized, double-blind, factorial study in patients with stage 2 hypertension.	Hydrochlorothiazide	105-109	selenium binding protein 1	Homo sapiens	170-173
19655819-1	2009	BACKGROUND: The combination of olmesartan medoxomil and hydrochlorothiazide (HCTZ) [olmesartan medoxomil/HCTZ] has previously been shown to produce significantly greater SBP/DBP reductions than monotherapy with either agent alone in a randomized, double-blind, factorial study in patients with stage 2 hypertension.	Hydrochlorothiazide	105-109	D-box binding PAR bZIP transcription factor	Homo sapiens	174-177
19084001-0	2009	Adverse renal effects of hydrochlorothiazide in rats with myocardial infarction treated with an ACE inhibitor.	Hydrochlorothiazide	25-44	angiotensin I converting enzyme	Rattus norvegicus	96-99
19844087-7	2009	The natriuretic response to hydrochlorothiazide supported an increase in activity of NCC with Ang II in aged mice only.	Hydrochlorothiazide	28-47	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	94-100
19194547-6	2009	TRPV5 protein abundance decreased in all hypercalciuric rats, and restored by HCTZ in both high salt with HCTZ and high Ca with HCTZ group.	Hydrochlorothiazide	78-82	transient receptor potential cation channel, subfamily V, member 5	Rattus norvegicus	0-5
19194547-6	2009	TRPV5 protein abundance decreased in all hypercalciuric rats, and restored by HCTZ in both high salt with HCTZ and high Ca with HCTZ group.	Hydrochlorothiazide	106-110	transient receptor potential cation channel, subfamily V, member 5	Rattus norvegicus	0-5
19194547-6	2009	TRPV5 protein abundance decreased in all hypercalciuric rats, and restored by HCTZ in both high salt with HCTZ and high Ca with HCTZ group.	Hydrochlorothiazide	106-110	transient receptor potential cation channel, subfamily V, member 5	Rattus norvegicus	0-5
19194547-8	2009	Protein abundance of NHE3 and NKCC2 decreased in all hypercalciuric rats, and were restored by HCTZ in only high Ca-induced hypercalciuric rats.	Hydrochlorothiazide	95-99	solute carrier family 9 member A3	Rattus norvegicus	21-25
19194547-10	2009	The hypocalciuric effect of HCTZ is associated with increased protein abundance of TRPV5 in high salt or calcium diet-induced hypercalciuric rats.	Hydrochlorothiazide	28-32	transient receptor potential cation channel, subfamily V, member 5	Rattus norvegicus	83-88
19194547-2	2009	We assessed the effects of hydrochlorothiazide (HCTZ) on the expression of TRPV5, calbindin-D(28K), and several sodium transporters in hypercalciuric rats.	Hydrochlorothiazide	48-52	transient receptor potential cation channel, subfamily V, member 5	Rattus norvegicus	75-80
18504326-7	2008	Antihypertensive medication consistent of hydrochlorothiazide, hydralazine, and reserpine ameliorated the histopathologic changes and attenuated p16(INK4a) expression in kidneys of deoxycorticosterone acetate-salt-treated rats.	Hydrochlorothiazide	42-61	cyclin-dependent kinase inhibitor 2A	Rattus norvegicus	145-148
18976849-10	2008	RESULTS: A greater HCTZ dose increased renin, aldosterone, and plasma protein concentrations.	Hydrochlorothiazide	19-23	renin	Homo sapiens	39-44
18981327-0	2008	Hydrochlorothiazide, but not Candesartan, aggravates insulin resistance and causes visceral and hepatic fat accumulation: the mechanisms for the diabetes preventing effect of Candesartan (MEDICA) Study.	Hydrochlorothiazide	0-19	insulin	Homo sapiens	53-60
18981327-10	2008	Blood pressure was reduced similarly by C and H versus P. In conclusion, visceral fat redistribution, liver fat accumulation, low-grade inflammation, and aggravated insulin resistance were demonstrated after hydrochlorothiazide but not candesartan treatment.	Hydrochlorothiazide	208-227	insulin	Homo sapiens	165-172
18584987-7	2008	Under the optimized chemical and physical variables, the detection limit for hydrochlorothiazide and losartan potassium calculated as 3Syx/b was 0.07 and 0.09 mgL(-1), respectively, for a sample loading volume of 1.0 mL.	Hydrochlorothiazide	77-96	pleckstrin homology and RhoGEF domain containing G5	Homo sapiens	135-138
18584987-7	2008	Under the optimized chemical and physical variables, the detection limit for hydrochlorothiazide and losartan potassium calculated as 3Syx/b was 0.07 and 0.09 mgL(-1), respectively, for a sample loading volume of 1.0 mL.	Hydrochlorothiazide	77-96	LLGL scribble cell polarity complex component 1	Homo sapiens	159-165
19120715-6	2008	HCTZ also increased plasma aldosterone and C-reactive protein levels.	Hydrochlorothiazide	0-4	C-reactive protein	Homo sapiens	43-61
18813314-8	2008	We found an increased risk of SCC (IRR of 1.79 (95% confidence interval (CI): 1.45-2.21)) and MM (IRR of 1.43 (95% CI: 1.09-1.88)) among users of combined amiloride and hydrochlorothiazide therapy.	Hydrochlorothiazide	169-188	serpin family B member 3	Homo sapiens	30-33
18504326-7	2008	Antihypertensive medication consistent of hydrochlorothiazide, hydralazine, and reserpine ameliorated the histopathologic changes and attenuated p16(INK4a) expression in kidneys of deoxycorticosterone acetate-salt-treated rats.	Hydrochlorothiazide	42-61	cyclin-dependent kinase inhibitor 2A	Rattus norvegicus	149-154
19343087-6	2008	HCTZ significantly increased the plasma concentrations of angiotensin I (Ang I) and angiotensin II (Ang II) in both WKY and SHR while reducing angiotensin converting enzyme (ACE) activity and the Ang II/Ang I ratio (17.1 +/- 2.9 before versus 10.3 +/- 2.9 after, p < 0.05) only in SHR.	Hydrochlorothiazide	0-4	angiotensinogen	Rattus norvegicus	100-106
18385266-7	2008	In contrast, hydrochlorothiazide produced an exaggerated natriuresis in Romk(-/-) mice, indicating upregulation of salt absorption by the DCT.	Hydrochlorothiazide	13-32	potassium inwardly-rectifying channel, subfamily J, member 1	Mus musculus	72-76
18385266-9	2008	Moreover, hydrochlorothiazide increased the fractional K(+) excretion rate in Romk(-/-) mice, confirming our recent observation that maxi-K channels contribute to distal K(+) secretion in the absence of ROMK.	Hydrochlorothiazide	10-29	potassium inwardly-rectifying channel, subfamily J, member 1	Mus musculus	78-82
18475165-8	2008	Plasma renin activity was positively correlated with blood pressure responses to losartan (P values 0.001-0.005) and bisoprolol (P values 0.03-0.17), and negatively with blood pressure responses to hydrochlorothiazide (P values 0.01-0.07).	Hydrochlorothiazide	198-217	renin	Homo sapiens	7-12
18681815-6	2008	RESULTS: Treatment with irbesartan/HCTZ was associated with significant mean reductions in BP (intent-to-treat population, n = 370; SBP/DBP: -22.9/-10.3 +/- 14.7/8.8 mm Hg).	Hydrochlorothiazide	35-39	selenium binding protein 1	Homo sapiens	132-135
18305093-5	2008	Obese rats had significantly greater net natriuretic response to single injections of hydrochlorothiazide and benzamil, suggesting increased activity of NCC and ENaC, respectively; however, only the response to benzamil was reduced by CAN.	Hydrochlorothiazide	86-105	sodium channel epithelial 1 subunit gamma	Rattus norvegicus	161-165
18059056-0	2008	Interaction of glycyrrhetinic acid, furosemide and hydrochlorothiazide with bovine serum albumin and their displacement interactions: capillary electrophoresis and fluorescence quenching study.	Hydrochlorothiazide	51-70	albumin	Homo sapiens	83-96
18059056-3	2008	In this work, capillary electrophoresis-frontal analysis (CE-FA) was applied to study the binding of bovine serum albumin with GA and two diuretics: furosemide (FU) and hydrochlorothiazide (HZ).	Hydrochlorothiazide	169-188	albumin	Homo sapiens	108-121
19343087-6	2008	HCTZ significantly increased the plasma concentrations of angiotensin I (Ang I) and angiotensin II (Ang II) in both WKY and SHR while reducing angiotensin converting enzyme (ACE) activity and the Ang II/Ang I ratio (17.1 +/- 2.9 before versus 10.3 +/- 2.9 after, p < 0.05) only in SHR.	Hydrochlorothiazide	0-4	angiotensin I converting enzyme	Rattus norvegicus	143-172
19343087-6	2008	HCTZ significantly increased the plasma concentrations of angiotensin I (Ang I) and angiotensin II (Ang II) in both WKY and SHR while reducing angiotensin converting enzyme (ACE) activity and the Ang II/Ang I ratio (17.1 +/- 2.9 before versus 10.3 +/- 2.9 after, p < 0.05) only in SHR.	Hydrochlorothiazide	0-4	angiotensin I converting enzyme	Rattus norvegicus	174-177
19343087-7	2008	HCTZ increased cardiac ACE2 mRNA and activity, and neprilysin mRNA in WKY, but not SHR.	Hydrochlorothiazide	0-4	angiotensin I converting enzyme 2	Rattus norvegicus	23-27
19337534-0	2008	Renin inhibition with aliskiren in hypertension: focus on aliskiren/hydrochlorothiazide combination therapy.	Hydrochlorothiazide	68-87	renin	Homo sapiens	0-5
18310964-0	2008	Effect of delapril/manidipine vs olmesartan/ hydrochlorothiazide combination on insulin sensitivity and fibrinogen in obese hypertensive patients.	Hydrochlorothiazide	45-64	insulin	Homo sapiens	80-87
18310964-1	2008	OBJECTIVE: To compare the effect of delapril/manidipine vs olmesartan/hydrochlorothiazide (HCTZ) combination on insulin sensitivity and plasma fibrinogen in obese hypertensive patients.	Hydrochlorothiazide	70-89	insulin	Homo sapiens	112-119
18310964-1	2008	OBJECTIVE: To compare the effect of delapril/manidipine vs olmesartan/hydrochlorothiazide (HCTZ) combination on insulin sensitivity and plasma fibrinogen in obese hypertensive patients.	Hydrochlorothiazide	91-95	insulin	Homo sapiens	112-119
19337534-6	2008	Hydrochlorothiazide (HCTZ) together with an agent blocking the RAAS such as an angiotensin converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) are widely used effective anti-hypertensive therapy.	Hydrochlorothiazide	0-19	angiotensin I converting enzyme	Homo sapiens	79-108
19337534-6	2008	Hydrochlorothiazide (HCTZ) together with an agent blocking the RAAS such as an angiotensin converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) are widely used effective anti-hypertensive therapy.	Hydrochlorothiazide	0-19	angiotensin I converting enzyme	Homo sapiens	110-113
19337534-6	2008	Hydrochlorothiazide (HCTZ) together with an agent blocking the RAAS such as an angiotensin converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) are widely used effective anti-hypertensive therapy.	Hydrochlorothiazide	21-25	angiotensin I converting enzyme	Homo sapiens	110-113
17910747-8	2007	T/HCTZ also produced significantly greater reductions than V/HCTZ in 24-hour mean ABP (differences in favour of T/HCTZ: SBP 3.0 mm Hg, p = 0.0002; DBP 1.6 mm Hg, p = 0.0006) and during the morning, daytime and night-time periods (p &lt; 0.003).	Hydrochlorothiazide	2-6	D-box binding PAR bZIP transcription factor	Homo sapiens	147-150
18188985-0	2007	Possible association of ACE gene I/D polymorphism with blood pressure--lowering response to hydrochlorothiazide.	Hydrochlorothiazide	92-111	angiotensin I converting enzyme	Homo sapiens	24-27
18188985-1	2007	OBJECTIVE: To explore the association between polymorphism in the ACE I/D gene and blood pressure-lowering response to hydrochlorothiazide (HCTZ) in 829 patients.	Hydrochlorothiazide	119-138	angiotensin I converting enzyme	Homo sapiens	66-69
18188985-1	2007	OBJECTIVE: To explore the association between polymorphism in the ACE I/D gene and blood pressure-lowering response to hydrochlorothiazide (HCTZ) in 829 patients.	Hydrochlorothiazide	140-144	angiotensin I converting enzyme	Homo sapiens	66-69
18188985-10	2007	CONCLUSION: ACE genotyping is associated with blood pressure-lowering response to HCTZ.	Hydrochlorothiazide	82-86	angiotensin I converting enzyme	Homo sapiens	12-15
17229912-8	2007	hOAT4 facilitates substantial uptake of [(14)C]urate, which was elevated 2.6-fold by intracellular HCTZ.	Hydrochlorothiazide	99-103	solute carrier family 22 member 11	Homo sapiens	0-5
17703139-9	2007	At 24 hours postdose, plasma renin activity was increased after furosemide or HCTZ administered alone or with tolvaptan, but it was unchanged after tolvaptan alone.	Hydrochlorothiazide	78-82	renin	Homo sapiens	29-34
17563829-13	2007	BP reduction with renin-angiotensin system blocker and hydrochlorothiazide therapy reduces LVH while lowering CRP level.	Hydrochlorothiazide	55-74	C-reactive protein	Homo sapiens	110-113
17584643-0	2007	[Effects of furosemide, antisterone and hydrochlorothiazide on expression of kidney aquaporin-2 gene and urine aquaporin-2 excretion in rats].	Hydrochlorothiazide	40-59	aquaporin 2	Rattus norvegicus	84-95
17584643-0	2007	[Effects of furosemide, antisterone and hydrochlorothiazide on expression of kidney aquaporin-2 gene and urine aquaporin-2 excretion in rats].	Hydrochlorothiazide	40-59	aquaporin 2	Rattus norvegicus	111-122
17584643-1	2007	OBJECTIVE: To investigate effects of the furosemide, antisterone and hydrochlorothiazide on expression of kidney aquaporin-2 (AQP(2)) gene and urine aquaporin-2 excretion in rats.	Hydrochlorothiazide	69-88	aquaporin 2	Rattus norvegicus	113-124
17584643-1	2007	OBJECTIVE: To investigate effects of the furosemide, antisterone and hydrochlorothiazide on expression of kidney aquaporin-2 (AQP(2)) gene and urine aquaporin-2 excretion in rats.	Hydrochlorothiazide	69-88	aquaporin 2	Rattus norvegicus	126-132
17584643-1	2007	OBJECTIVE: To investigate effects of the furosemide, antisterone and hydrochlorothiazide on expression of kidney aquaporin-2 (AQP(2)) gene and urine aquaporin-2 excretion in rats.	Hydrochlorothiazide	69-88	aquaporin 2	Rattus norvegicus	149-160
17584643-12	2007	Hydrochlorothiazide reduces kidney AQP(2) mRNA and protein expression, while furosemide increased kidney AQP(2) gene expression.	Hydrochlorothiazide	0-19	aquaporin 2	Rattus norvegicus	35-41
17531119-9	2007	CONCLUSIONS: AGT-6G allele, CYP11B2 -344CC genotype and its combination with ACE D allele are associated with BP response to hydrochlorothiazide treatment.	Hydrochlorothiazide	125-144	cytochrome P450 family 11 subfamily B member 2	Homo sapiens	28-35
17531119-9	2007	CONCLUSIONS: AGT-6G allele, CYP11B2 -344CC genotype and its combination with ACE D allele are associated with BP response to hydrochlorothiazide treatment.	Hydrochlorothiazide	125-144	angiotensin I converting enzyme	Homo sapiens	77-80
17906162-7	2007	In the HCTZ + DRSP/E2 group, serum potassium, aldosterone, and plasma renin activity all increased in a manner marginally consistent with a beneficial antialdosterone effect, counteracting the HCTZ-induced potassium loss and lowering both systolic and diastolic blood pressure.	Hydrochlorothiazide	7-11	renin	Homo sapiens	70-75
17906162-7	2007	In the HCTZ + DRSP/E2 group, serum potassium, aldosterone, and plasma renin activity all increased in a manner marginally consistent with a beneficial antialdosterone effect, counteracting the HCTZ-induced potassium loss and lowering both systolic and diastolic blood pressure.	Hydrochlorothiazide	193-197	renin	Homo sapiens	70-75
17229912-9	2007	Thus, hOAT4 is the long-postulated, low-affinity apical urate anion exchanger that facilitates HCTZ-associated hyperuricemia.	Hydrochlorothiazide	95-99	solute carrier family 22 member 11	Homo sapiens	6-11
17135398-0	2007	Multidrug resistance-associated protein 4 is involved in the urinary excretion of hydrochlorothiazide and furosemide.	Hydrochlorothiazide	82-101	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	0-41
17953475-11	2007	The primary efficacy endpoint of change in mean seated SBP at week 12 was significantly greater with olmesartan medoxomil/HCTZ than with benazepril plus amlodipine besylate (least square [LS] mean change: -32.5 vs -26.5 mm Hg, p=0.024; LS mean treatment difference -6.0 mm Hg; 95% CI -11.1, -0.8 mm Hg).	Hydrochlorothiazide	122-126	selenium binding protein 1	Homo sapiens	55-58
17953475-12	2007	The LS mean change for reduction in DBP approached statistical significance with olmesartan medoxomil/HCTZ compared with the benazepril-based regimen (p=0.056) at week 12 (end of study).	Hydrochlorothiazide	102-106	D-box binding PAR bZIP transcription factor	Homo sapiens	36-39
17953475-13	2007	BP reductions showed statistically significant differences between treatment groups favoring olmesartan medoxomil/HCTZ in both SBP and DBP at week 8.	Hydrochlorothiazide	114-118	selenium binding protein 1	Homo sapiens	127-130
17953475-13	2007	BP reductions showed statistically significant differences between treatment groups favoring olmesartan medoxomil/HCTZ in both SBP and DBP at week 8.	Hydrochlorothiazide	114-118	D-box binding PAR bZIP transcription factor	Homo sapiens	135-138
17135398-2	2007	Significant ATP-dependent uptake of hydrochlorothiazide (HCT) and furosemide was observed in membrane vesicles that expressed multidrug resistance-associated protein 4 (MRP4) and breast cancer resistance protein (BCRP).	Hydrochlorothiazide	36-55	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	126-167
17135398-2	2007	Significant ATP-dependent uptake of hydrochlorothiazide (HCT) and furosemide was observed in membrane vesicles that expressed multidrug resistance-associated protein 4 (MRP4) and breast cancer resistance protein (BCRP).	Hydrochlorothiazide	36-55	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	169-173
17135398-2	2007	Significant ATP-dependent uptake of hydrochlorothiazide (HCT) and furosemide was observed in membrane vesicles that expressed multidrug resistance-associated protein 4 (MRP4) and breast cancer resistance protein (BCRP).	Hydrochlorothiazide	36-55	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	179-211
17135398-2	2007	Significant ATP-dependent uptake of hydrochlorothiazide (HCT) and furosemide was observed in membrane vesicles that expressed multidrug resistance-associated protein 4 (MRP4) and breast cancer resistance protein (BCRP).	Hydrochlorothiazide	36-55	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	213-217
17135398-2	2007	Significant ATP-dependent uptake of hydrochlorothiazide (HCT) and furosemide was observed in membrane vesicles that expressed multidrug resistance-associated protein 4 (MRP4) and breast cancer resistance protein (BCRP).	Hydrochlorothiazide	57-60	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	126-167
17135398-2	2007	Significant ATP-dependent uptake of hydrochlorothiazide (HCT) and furosemide was observed in membrane vesicles that expressed multidrug resistance-associated protein 4 (MRP4) and breast cancer resistance protein (BCRP).	Hydrochlorothiazide	57-60	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	169-173
17135398-2	2007	Significant ATP-dependent uptake of hydrochlorothiazide (HCT) and furosemide was observed in membrane vesicles that expressed multidrug resistance-associated protein 4 (MRP4) and breast cancer resistance protein (BCRP).	Hydrochlorothiazide	57-60	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	179-211
17135398-2	2007	Significant ATP-dependent uptake of hydrochlorothiazide (HCT) and furosemide was observed in membrane vesicles that expressed multidrug resistance-associated protein 4 (MRP4) and breast cancer resistance protein (BCRP).	Hydrochlorothiazide	57-60	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	213-217
17135398-7	2007	Our results suggest that Mrp4, together with other unknown transporters, accounts for the luminal efflux of HCT and furosemide from proximal tubular epithelial cells.	Hydrochlorothiazide	108-111	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	25-29
16595585-0	2006	Hydrochlorothiazide in CLDN16 mutation.	Hydrochlorothiazide	0-19	claudin 16	Homo sapiens	23-29
17143194-0	2007	Renin inhibition with aliskiren provides additive antihypertensive efficacy when used in combination with hydrochlorothiazide.	Hydrochlorothiazide	106-125	renin	Homo sapiens	0-5
17143194-13	2007	Renin inhibition with aliskiren neutralized the compensatory rise in PRA induced by HCTZ.	Hydrochlorothiazide	84-88	renin	Homo sapiens	0-5
17703637-2	2007	The renin-angiotensin-aldosterone-system-activating effect of hydrochlorothiazide augments the efficacy of blocking the angiotensin II type 1 (AT1) receptor with losartan.	Hydrochlorothiazide	62-81	renin	Homo sapiens	4-9
17703637-2	2007	The renin-angiotensin-aldosterone-system-activating effect of hydrochlorothiazide augments the efficacy of blocking the angiotensin II type 1 (AT1) receptor with losartan.	Hydrochlorothiazide	62-81	angiotensin II receptor type 1	Homo sapiens	120-156
16825334-6	2006	Moreover, in response to hydrochlorothiazide administration, pendrin was downregulated despite a marked secondary hyperaldosteronism.	Hydrochlorothiazide	25-44	solute carrier family 26, member 4	Mus musculus	61-68
16595585-1	2006	BACKGROUND: Hydrochlorothiazide (HCT) is applied in the therapy of familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC) caused by claudin-16 (CLDN16) mutation.	Hydrochlorothiazide	12-31	claudin 16	Homo sapiens	151-161
16595585-1	2006	BACKGROUND: Hydrochlorothiazide (HCT) is applied in the therapy of familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC) caused by claudin-16 (CLDN16) mutation.	Hydrochlorothiazide	12-31	claudin 16	Homo sapiens	163-169
16595585-1	2006	BACKGROUND: Hydrochlorothiazide (HCT) is applied in the therapy of familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC) caused by claudin-16 (CLDN16) mutation.	Hydrochlorothiazide	33-36	claudin 16	Homo sapiens	151-161
16595585-1	2006	BACKGROUND: Hydrochlorothiazide (HCT) is applied in the therapy of familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC) caused by claudin-16 (CLDN16) mutation.	Hydrochlorothiazide	33-36	claudin 16	Homo sapiens	163-169
16240160-8	2005	We conclude that the combination hydrochlorothiazide/amiloride/cyclooxygenase-2 inhibitor could be successfully used to treat congenital nephrogenic diabetes insipidus.	Hydrochlorothiazide	33-52	prostaglandin-endoperoxide synthase 2	Homo sapiens	63-79
16450155-0	2006	Hydrochlorothiazide efficacy and polymorphisms in ACE, ADD1 and GNB3 in healthy, male volunteers.	Hydrochlorothiazide	0-19	adducin 1	Homo sapiens	55-59
16450155-0	2006	Hydrochlorothiazide efficacy and polymorphisms in ACE, ADD1 and GNB3 in healthy, male volunteers.	Hydrochlorothiazide	0-19	G protein subunit beta 3	Homo sapiens	64-68
16326922-8	2006	Hydralazine/hydrochlorothiazide normalized systolic blood pressure (BP) and abolished mRNA up-regulation of hypertrophic markers sk-alpha-actin and BNP and of preproAM, CLR, RAMP2, and RAMP3 but did not normalize cardiomyocyte width nor preproIMD or RAMP1 mRNA expression.	Hydrochlorothiazide	12-31	natriuretic peptide B	Rattus norvegicus	148-151
16326922-8	2006	Hydralazine/hydrochlorothiazide normalized systolic blood pressure (BP) and abolished mRNA up-regulation of hypertrophic markers sk-alpha-actin and BNP and of preproAM, CLR, RAMP2, and RAMP3 but did not normalize cardiomyocyte width nor preproIMD or RAMP1 mRNA expression.	Hydrochlorothiazide	12-31	calcitonin receptor like receptor	Rattus norvegicus	169-172
16326922-8	2006	Hydralazine/hydrochlorothiazide normalized systolic blood pressure (BP) and abolished mRNA up-regulation of hypertrophic markers sk-alpha-actin and BNP and of preproAM, CLR, RAMP2, and RAMP3 but did not normalize cardiomyocyte width nor preproIMD or RAMP1 mRNA expression.	Hydrochlorothiazide	12-31	receptor activity modifying protein 2	Rattus norvegicus	174-179
16326922-8	2006	Hydralazine/hydrochlorothiazide normalized systolic blood pressure (BP) and abolished mRNA up-regulation of hypertrophic markers sk-alpha-actin and BNP and of preproAM, CLR, RAMP2, and RAMP3 but did not normalize cardiomyocyte width nor preproIMD or RAMP1 mRNA expression.	Hydrochlorothiazide	12-31	receptor activity modifying protein 3	Rattus norvegicus	185-190
16326922-8	2006	Hydralazine/hydrochlorothiazide normalized systolic blood pressure (BP) and abolished mRNA up-regulation of hypertrophic markers sk-alpha-actin and BNP and of preproAM, CLR, RAMP2, and RAMP3 but did not normalize cardiomyocyte width nor preproIMD or RAMP1 mRNA expression.	Hydrochlorothiazide	12-31	receptor activity modifying protein 1	Rattus norvegicus	250-255
16766279-6	2006	RESULTS: Treatment with HCT-spironolactone caused an increase in PAI-I (p&lt;0.001) and t-PA ( p&lt;0.001), while no changes were observed in PAI-I/t-PA (P&gt;0.05).	Hydrochlorothiazide	24-27	serpin family E member 1	Homo sapiens	65-68
16766279-6	2006	RESULTS: Treatment with HCT-spironolactone caused an increase in PAI-I (p&lt;0.001) and t-PA ( p&lt;0.001), while no changes were observed in PAI-I/t-PA (P&gt;0.05).	Hydrochlorothiazide	24-27	plasminogen activator, tissue type	Homo sapiens	88-92
16766279-6	2006	RESULTS: Treatment with HCT-spironolactone caused an increase in PAI-I (p&lt;0.001) and t-PA ( p&lt;0.001), while no changes were observed in PAI-I/t-PA (P&gt;0.05).	Hydrochlorothiazide	24-27	serpin family E member 1	Homo sapiens	142-145
16766279-6	2006	RESULTS: Treatment with HCT-spironolactone caused an increase in PAI-I (p&lt;0.001) and t-PA ( p&lt;0.001), while no changes were observed in PAI-I/t-PA (P&gt;0.05).	Hydrochlorothiazide	24-27	inosine triphosphatase	Homo sapiens	146-152
16939632-14	2006	The data suggest that lipid lowering agents, ACE inhibitors, ARBs, antidiabetic agents, antiinflammatory and antiplatelet agents, vitamin E, and beta-adrenoreceptor antagonists lower serum or plasma levels of CRP, while vitamin C, oral estrogen and hydrochlorothiazide do not affect CRP levels.	Hydrochlorothiazide	249-268	C-reactive protein	Homo sapiens	209-212
16266470-0	2005	[Association of polymorphism in alpha-adducin gene with antihypertensive effect of Hydrochlorothiazide].	Hydrochlorothiazide	83-102	adducin 1	Homo sapiens	32-45
16172412-7	2005	Polymorphisms in genes regulating renal sodium transport, in particular WNK1, predict interindividual differences in antihypertensive responses to hydrochlorothiazide.	Hydrochlorothiazide	147-166	WNK lysine deficient protein kinase 1	Homo sapiens	72-76
16266470-1	2005	OBJECTIVE: To explore the association between G614T single nuclear polymorphism (SNP) of the alpha-adducin gene and the antihypertensive effect of hydrochlorothiazide (HCTZ) in essential hypertensive (EH) patients.	Hydrochlorothiazide	147-166	adducin 1	Homo sapiens	93-106
16266470-1	2005	OBJECTIVE: To explore the association between G614T single nuclear polymorphism (SNP) of the alpha-adducin gene and the antihypertensive effect of hydrochlorothiazide (HCTZ) in essential hypertensive (EH) patients.	Hydrochlorothiazide	168-172	adducin 1	Homo sapiens	93-106
16266470-5	2005	RESULTS: After 6 weeks of HCTZ treatment, the decreases in DBP and MAP of patients carrying 614T allele of alpha-adducin were significantly greater than that of those carrying GG homozygotes (P &lt; 0.05).	Hydrochlorothiazide	26-30	adducin 1	Homo sapiens	107-120
16266470-9	2005	CONCLUSION: The present study suggests that the alpha-adducin G614T polymorphism is associated with the antihypertensive effect of HCTZ, which is more effective in patients with TT genotype.	Hydrochlorothiazide	131-135	adducin 1	Homo sapiens	48-61
16154480-3	2005	OBJECTIVE: This was a study of the effects on sitting systolic BP (SBP)of 2 combinations of valsartan and hydrochlorothiazide (HCTZ) compared with valsartan monotherapy in patients with stage 2 or 3 systolic hypertension (SBP &gt; or =160 mm Hg and &lt; or =200 mm Hg) with or without other cardiovascular risk factors.	Hydrochlorothiazide	106-125	selenium binding protein 1	Homo sapiens	67-70
15998706-9	2005	By regression analysis, predictors of mean PAI-1 response were spironolactone versus triamterene (P=0.014), hypertension (P=0.002), and PAI-1 response to HCTZ (P=0.019), with a trend for aldosterone (P=0.061).	Hydrochlorothiazide	154-158	serpin family E member 1	Homo sapiens	43-48
15998706-9	2005	By regression analysis, predictors of mean PAI-1 response were spironolactone versus triamterene (P=0.014), hypertension (P=0.002), and PAI-1 response to HCTZ (P=0.019), with a trend for aldosterone (P=0.061).	Hydrochlorothiazide	154-158	serpin family E member 1	Homo sapiens	136-141
16080804-0	2005	[Association of polymorphisms in ACE and CYP11B2 genes with antihypertensive effects of hydrochlorothiazide].	Hydrochlorothiazide	88-107	angiotensin I converting enzyme	Homo sapiens	33-36
16080804-0	2005	[Association of polymorphisms in ACE and CYP11B2 genes with antihypertensive effects of hydrochlorothiazide].	Hydrochlorothiazide	88-107	cytochrome P450 family 11 subfamily B member 2	Homo sapiens	41-48
16080804-1	2005	OBJECTIVE: To determine whether the blood pressure (BP) response to hydrochlorothiazide (HCTZ) was associated with the angiotensin converting-enzyme (ACE) I/D and aldosterone synthase (CYP11B2)-344T/C polymorphisms.	Hydrochlorothiazide	68-87	angiotensin I converting enzyme	Homo sapiens	119-148
16080804-1	2005	OBJECTIVE: To determine whether the blood pressure (BP) response to hydrochlorothiazide (HCTZ) was associated with the angiotensin converting-enzyme (ACE) I/D and aldosterone synthase (CYP11B2)-344T/C polymorphisms.	Hydrochlorothiazide	68-87	angiotensin I converting enzyme	Homo sapiens	150-153
16080804-1	2005	OBJECTIVE: To determine whether the blood pressure (BP) response to hydrochlorothiazide (HCTZ) was associated with the angiotensin converting-enzyme (ACE) I/D and aldosterone synthase (CYP11B2)-344T/C polymorphisms.	Hydrochlorothiazide	68-87	cytochrome P450 family 11 subfamily B member 2	Homo sapiens	163-183
16080804-1	2005	OBJECTIVE: To determine whether the blood pressure (BP) response to hydrochlorothiazide (HCTZ) was associated with the angiotensin converting-enzyme (ACE) I/D and aldosterone synthase (CYP11B2)-344T/C polymorphisms.	Hydrochlorothiazide	68-87	cytochrome P450 family 11 subfamily B member 2	Homo sapiens	185-192
16080804-1	2005	OBJECTIVE: To determine whether the blood pressure (BP) response to hydrochlorothiazide (HCTZ) was associated with the angiotensin converting-enzyme (ACE) I/D and aldosterone synthase (CYP11B2)-344T/C polymorphisms.	Hydrochlorothiazide	89-93	angiotensin I converting enzyme	Homo sapiens	119-148
16080804-1	2005	OBJECTIVE: To determine whether the blood pressure (BP) response to hydrochlorothiazide (HCTZ) was associated with the angiotensin converting-enzyme (ACE) I/D and aldosterone synthase (CYP11B2)-344T/C polymorphisms.	Hydrochlorothiazide	89-93	angiotensin I converting enzyme	Homo sapiens	150-153
16080804-1	2005	OBJECTIVE: To determine whether the blood pressure (BP) response to hydrochlorothiazide (HCTZ) was associated with the angiotensin converting-enzyme (ACE) I/D and aldosterone synthase (CYP11B2)-344T/C polymorphisms.	Hydrochlorothiazide	89-93	cytochrome P450 family 11 subfamily B member 2	Homo sapiens	163-183
16080804-8	2005	CONCLUSIONS: The present study suggested that the ACE DD genotype was associated with the systolic BP response to HCTZ, and that the subjects with the combination of ACE DD and CYP11B2 CC genotypes might have a better BP response to HCTZ than the other genotypic combinations of these 2 genes.	Hydrochlorothiazide	114-118	angiotensin I converting enzyme	Homo sapiens	50-53
16080804-8	2005	CONCLUSIONS: The present study suggested that the ACE DD genotype was associated with the systolic BP response to HCTZ, and that the subjects with the combination of ACE DD and CYP11B2 CC genotypes might have a better BP response to HCTZ than the other genotypic combinations of these 2 genes.	Hydrochlorothiazide	233-237	angiotensin I converting enzyme	Homo sapiens	166-169
16080804-8	2005	CONCLUSIONS: The present study suggested that the ACE DD genotype was associated with the systolic BP response to HCTZ, and that the subjects with the combination of ACE DD and CYP11B2 CC genotypes might have a better BP response to HCTZ than the other genotypic combinations of these 2 genes.	Hydrochlorothiazide	233-237	cytochrome P450 family 11 subfamily B member 2	Homo sapiens	177-184
15864129-5	2005	RESULTS: Two polymorphisms in the sodium channel gamma-subunit promotor gene, and a polymorphism in the endothelial nitric oxide synthase gene, were significantly associated with blood pressure response to hydrochlorothiazide.	Hydrochlorothiazide	206-225	nitric oxide synthase 3	Homo sapiens	104-137
15902302-5	2005	Second, HCTZ administration still induced hypocalciuria in transient receptor potential channel subfamily V, member 5-knockout (Trpv5-knockout) mice, in which active distal Ca2+ reabsorption is abolished due to inactivation of the epithelial Ca2+ channel Trpv5.	Hydrochlorothiazide	8-12	transient receptor potential cation channel, subfamily V, member 5	Mus musculus	128-133
15902302-5	2005	Second, HCTZ administration still induced hypocalciuria in transient receptor potential channel subfamily V, member 5-knockout (Trpv5-knockout) mice, in which active distal Ca2+ reabsorption is abolished due to inactivation of the epithelial Ca2+ channel Trpv5.	Hydrochlorothiazide	8-12	transient receptor potential cation channel, subfamily V, member 5	Mus musculus	255-260
15960151-6	2005	Based on the diagnosis of the gain-of-function mutation in the CaSR, oral hydrochlorothiazide administration and supplemental hydration were started in addition to calcium supplementation.	Hydrochlorothiazide	74-93	calcium sensing receptor	Homo sapiens	63-67
15864129-9	2005	CONCLUSIONS: Two polymorphisms in the sodium channel gamma-subunit promotor gene, and a polymorphism in the endothelial nitric oxide synthase gene, were associated with significant differences in odds of DBP response to hydrochlorothiazide.	Hydrochlorothiazide	220-239	nitric oxide synthase 3	Homo sapiens	108-141
15631279-6	2004	After 6 weeks of treatment with valsartan 160 mg and HCTZ 25 mg, a significant decrease in BP was observed both at home (146 +/- 17/83 +/- 12 mmHg) and at the office (151 +/- 18/87 +/- 11 mmHg), with a difference from baseline of -4 mmHg, p &lt; 0.001 for DBP and of -6 mmHg for SBP, p &lt; 0.001.	Hydrochlorothiazide	53-57	D-box binding PAR bZIP transcription factor	Homo sapiens	256-282
15590878-1	2005	OBJECTIVE: To report a child born with renal impairment following severe anhydramnios due to maternal exposure to an angiotensin II receptor type 1 (AT1) antagonist, valsartan, and hydrochlorothiazide during the first 28 weeks of pregnancy.	Hydrochlorothiazide	181-200	angiotensin II receptor type 1	Homo sapiens	149-152
15631278-3	2004	HCTZ was doubled after the first 4 weeks in non-responders (DBP &gt; or =90 mmHg or SBP &gt; 180 mmHg).	Hydrochlorothiazide	0-4	D-box binding PAR bZIP transcription factor	Homo sapiens	60-63
15631278-3	2004	HCTZ was doubled after the first 4 weeks in non-responders (DBP &gt; or =90 mmHg or SBP &gt; 180 mmHg).	Hydrochlorothiazide	0-4	selenium binding protein 1	Homo sapiens	84-87
15504936-0	2004	Antidiuretic effect of hydrochlorothiazide in lithium-induced nephrogenic diabetes insipidus is associated with upregulation of aquaporin-2, Na-Cl co-transporter, and epithelial sodium channel.	Hydrochlorothiazide	23-42	aquaporin 2	Rattus norvegicus	128-139
15564765-8	2004	The abundance of NKCC2 and NCC is increased by furosemide and hydrochlorothiazide, respectively.	Hydrochlorothiazide	62-81	solute carrier family 12 member 1	Homo sapiens	17-22
15564765-8	2004	The abundance of NKCC2 and NCC is increased by furosemide and hydrochlorothiazide, respectively.	Hydrochlorothiazide	62-81	solute carrier family 12 member 3	Homo sapiens	27-30
15564765-10	2004	In the proximal tubule, the abundance of OAT1 is increased by chronic treatment with furosemide or hydrochlorothiazide.	Hydrochlorothiazide	99-118	solute carrier family 22 member 6	Homo sapiens	41-45
15504936-3	2004	For elucidating the molecular basis of the antidiuretic action of HCTZ in diabetes insipidus, whether administration of HCTZ may affect the expression of AQP2 and major renal Na(+) transporters in Li-induced NDI rats was investigated, using semiquantitative immunoblotting and immunohistochemistry.	Hydrochlorothiazide	120-124	aquaporin 2	Rattus norvegicus	154-158
15504936-7	2004	Semiquantitative immunoblotting using whole-kidney homogenates revealed that HCTZ treatment caused a significant partial recovery in AQP2 abundance from Li-induced downregulation.	Hydrochlorothiazide	77-81	aquaporin 2	Rattus norvegicus	133-137
15504936-11	2004	The upregulation of AQP2 and distal renal Na(+) transporters in response to HCTZ treatment may account for the antidiuretic action of HCTZ in NDI.	Hydrochlorothiazide	76-80	aquaporin 2	Rattus norvegicus	20-24
15504936-11	2004	The upregulation of AQP2 and distal renal Na(+) transporters in response to HCTZ treatment may account for the antidiuretic action of HCTZ in NDI.	Hydrochlorothiazide	134-138	aquaporin 2	Rattus norvegicus	20-24
12954402-7	2003	Plasma renin activity was elevated substantially in HCZ-treated rats, but aldosterone concentration was decreased.	Hydrochlorothiazide	52-55	renin	Rattus norvegicus	7-12
15071488-5	2004	Both combination treatments, delapril-manidipine and irbesartan-hydrochlorothiazide, produced a greater reduction in systolic BP/diastolic BP (SBP/DBP) values (-27.6/21.8 mmHg and -26.4/20.2 mmHg, respectively) than the respective monotherapies (-15.2/11.7 mmHg with delapril and -16.3/11.3 mmHg with irbesartan).	Hydrochlorothiazide	64-83	selenium binding protein 1	Homo sapiens	143-146
15071488-5	2004	Both combination treatments, delapril-manidipine and irbesartan-hydrochlorothiazide, produced a greater reduction in systolic BP/diastolic BP (SBP/DBP) values (-27.6/21.8 mmHg and -26.4/20.2 mmHg, respectively) than the respective monotherapies (-15.2/11.7 mmHg with delapril and -16.3/11.3 mmHg with irbesartan).	Hydrochlorothiazide	64-83	D-box binding PAR bZIP transcription factor	Homo sapiens	147-150
15071488-8	2004	Irbesartan monotherapy did not significantly affect the fibrinolytic balance, whereas the addition of hydrochlorothiazide worsened it, producing a significant increase in PAI-l activity (+9.5 IU/ml; P&lt;0.05).	Hydrochlorothiazide	102-121	serpin family E member 1	Homo sapiens	171-174
14553962-0	2003	Effects of endothelial nitric oxide synthase, alpha-adducin, and other candidate gene polymorphisms on blood pressure response to hydrochlorothiazide.	Hydrochlorothiazide	130-149	nitric oxide synthase 3	Homo sapiens	11-44
14553962-6	2003	After adjustment for covariates, the endothelial nitric oxide synthase Glu298--&gt;Asp polymorphism made an additional statistically significant contribution to predicting diastolic BP response to hydrochlorothiazide, accounting for another 1% of interindividual variation in response (P =.034).	Hydrochlorothiazide	197-216	nitric oxide synthase 3	Homo sapiens	37-70
12925048-0	2003	Comparative metabolic effects of hydrochlorothiazide and indapamide in hypertensive diabetic patients receiving ACE inhibitor therapy.	Hydrochlorothiazide	33-52	angiotensin I converting enzyme	Homo sapiens	112-115
12925048-9	2003	CONCLUSIONS: Hydrochlorothiazide 12.5 mg/day, when added to background ACE inhibitor therapy with fosinopril in hypertensive diabetic patients, resulted in a metabolic profile that was similar, if not superior on certain parameters, in comparison with indapamide 2.5 mg/day.	Hydrochlorothiazide	13-32	angiotensin I converting enzyme	Homo sapiens	71-74
12872052-7	2003	Fasting levels of both serum insulin and plasma glucose increased in the hydrochlorothiazide group in contrast to unaffected levels in the candesartan group.	Hydrochlorothiazide	73-92	insulin	Homo sapiens	29-36
12872052-10	2003	Both the low-density lipoprotein/high-density lipoprotein and the apolipoprotein B/apolipoprotein A-I ratios increased in the hydrochlorothiazide group.	Hydrochlorothiazide	126-145	apolipoprotein B	Homo sapiens	66-82
12872052-10	2003	Both the low-density lipoprotein/high-density lipoprotein and the apolipoprotein B/apolipoprotein A-I ratios increased in the hydrochlorothiazide group.	Hydrochlorothiazide	126-145	apolipoprotein A1	Homo sapiens	83-101
12569265-0	2003	Role of angiotensin II in L-NAME-induced systemic and renal hemodynamic effects in hydrochlorothiazide-pretreated hypertensive subjects.	Hydrochlorothiazide	83-102	angiotensinogen	Homo sapiens	8-22
12846750-10	2003	HCTZ significantly decreased mRNA expression of TRPV5 (71%+/- 6%), calbindin-D28K (53%+/- 6%), NCX1 (51%+/- 8%) and NCC (50%+/- 11%), regardless of ECV status or calciuresis.	Hydrochlorothiazide	0-4	transient receptor potential cation channel, subfamily V, member 5	Rattus norvegicus	48-53
12846750-10	2003	HCTZ significantly decreased mRNA expression of TRPV5 (71%+/- 6%), calbindin-D28K (53%+/- 6%), NCX1 (51%+/- 8%) and NCC (50%+/- 11%), regardless of ECV status or calciuresis.	Hydrochlorothiazide	0-4	solute carrier family 8 member A1	Rattus norvegicus	95-99
12897087-0	2003	Up-regulation of organic anion transporter 1 protein is induced by chronic furosemide or hydrochlorothiazide infusion in rat kidney.	Hydrochlorothiazide	89-108	solute carrier family 22 member 6	Rattus norvegicus	17-44
12897087-11	2003	OAT1 protein abundance in cortical homogenates was also increased by hydrochlorothiazide infusion (181 +/- 25 vs 100 +/- 7%, P &lt; 0.01), whereas Na-K-ATPase alpha1 subunit protein abundance was not affected (105 +/- 4 vs 100 +/- 4%, P = 0.34).	Hydrochlorothiazide	69-88	solute carrier family 22 member 6	Rattus norvegicus	0-4
24944377-3	2003	Another widely used combination of ACE inhibitor and diuretic is lisinopril plus hydrochlorothiazide (L + H).	Hydrochlorothiazide	81-100	angiotensin I converting enzyme	Homo sapiens	35-38
12897087-12	2003	CONCLUSION: Chronic furosemide or hydrochlorothiazide infusion caused increases in OAT1 protein abundance in rat kidney.	Hydrochlorothiazide	34-53	solute carrier family 22 member 6	Rattus norvegicus	83-87
12623934-1	2003	Renin-angiotensin system reactivity and the constitutive capacity of the renal tubule to reabsorb sodium play a role in the individual response to diuretic therapy; therefore we evaluated the blood pressure (BP) response to hydrochlorothiazide in 87 never-treated individuals with mild essential hypertension, according to ACE gene I/D and alpha-adducin Gly460Trp polymorphism.	Hydrochlorothiazide	224-243	renin	Homo sapiens	0-5
12623934-7	2003	Alpha-adducin and ACE I/D polymorphism may be useful to predict the interindividual degree of response to hydrochlorothiazide; the analysis of the combination of the 2 genotypes increases the accuracy of the prediction of response to the drug.	Hydrochlorothiazide	106-125	adducin 1	Homo sapiens	0-13
12623934-7	2003	Alpha-adducin and ACE I/D polymorphism may be useful to predict the interindividual degree of response to hydrochlorothiazide; the analysis of the combination of the 2 genotypes increases the accuracy of the prediction of response to the drug.	Hydrochlorothiazide	106-125	angiotensin I converting enzyme	Homo sapiens	18-21
12468570-7	2002	Hydrochlorothiazide increased plasma PAI-1 (P=0.013) but not tissue-type plasminogen activator (tPA) (P=0.431) antigen.	Hydrochlorothiazide	0-19	serpin family E member 1	Homo sapiens	37-42
12388392-7	2003	HCTZ infusion increased the abundances of thiazide-sensitive Na(+)-Cl(-) cotransporter and beta-ENaC in the cortex and beta- and gamma-ENaC in the outer medulla.	Hydrochlorothiazide	0-4	sodium channel epithelial 1 subunit beta	Rattus norvegicus	91-100
12388392-7	2003	HCTZ infusion increased the abundances of thiazide-sensitive Na(+)-Cl(-) cotransporter and beta-ENaC in the cortex and beta- and gamma-ENaC in the outer medulla.	Hydrochlorothiazide	0-4	sodium channel epithelial 1 subunit gamma	Rattus norvegicus	96-100
12207569-22	2002	In summary, 1 year of treatment with captopril plus hydrochlorothiazide increases wall elastin content and reduces WS and stiffness in old SHR.	Hydrochlorothiazide	52-71	elastin	Rattus norvegicus	87-94
12371972-5	2002	In regression models that considered the effects of baseline BP, race, gender, age, waist-to-hip ratio, and measures of the RAAS, there was significant interaction between the effects of the ACE genotype and gender on the responses of both systolic and diastolic BP to HCTZ (for systolic BP response, P = 0.03; for diastolic BP response, P = 0.001).	Hydrochlorothiazide	269-273	angiotensin I converting enzyme	Homo sapiens	191-194
12371972-7	2002	In models that included the effects of race, gender, age, and waist-to-hip ratio, there was also significant interaction between the effects of the ACE genotype and gender on pre-treatment urinary aldosterone excretion (P = 0.01) and change in urinary aldosterone excretion in response to HCTZ (P = 0.007).	Hydrochlorothiazide	289-293	angiotensin I converting enzyme	Homo sapiens	148-151
12371972-9	2002	CONCLUSION: The relationship between the ACE I/D polymorphism and antihypertensive response to a standard dose of HCTZ differs significantly between women and men.	Hydrochlorothiazide	114-118	angiotensin I converting enzyme	Homo sapiens	41-44
12371972-10	2002	Because the D-allele was associated with significant, co-dominant increases in serum ACE activity in both genders, the gender-specific effects of the I/D polymorphism on BP response to HCTZ may be mediated subsequent to the enzymatic generation of angiotensin II.	Hydrochlorothiazide	185-189	angiotensin I converting enzyme	Homo sapiens	85-88
12371972-10	2002	Because the D-allele was associated with significant, co-dominant increases in serum ACE activity in both genders, the gender-specific effects of the I/D polymorphism on BP response to HCTZ may be mediated subsequent to the enzymatic generation of angiotensin II.	Hydrochlorothiazide	185-189	angiotensinogen	Homo sapiens	248-262
12572707-3	2002	The alpha-blocker doxazosin has favourable effects on plasma lipids, insulin resistance and blood pressure, while the diuretic hydrochlorothiazide (HCTZ) principally affects blood pressure and increases insulin resistance.	Hydrochlorothiazide	127-146	insulin	Homo sapiens	203-210
12572707-3	2002	The alpha-blocker doxazosin has favourable effects on plasma lipids, insulin resistance and blood pressure, while the diuretic hydrochlorothiazide (HCTZ) principally affects blood pressure and increases insulin resistance.	Hydrochlorothiazide	148-152	insulin	Homo sapiens	203-210
11836266-5	2002	Angiotensin II increased from baseline during both HCTZ (P = 0.02) and spironolactone (P = 0.02 vs. baseline; P = 0.19 vs. HCTZ) treatments.	Hydrochlorothiazide	51-55	angiotensinogen	Homo sapiens	0-14
12107202-0	2002	Hydrochlorothiazide effectively reduces urinary calcium excretion in two Japanese patients with gain-of-function mutations of the calcium-sensing receptor gene.	Hydrochlorothiazide	0-19	calcium sensing receptor	Homo sapiens	130-154
12107202-4	2002	In this study, we report on the clinical course, molecular analysis, and effects of hydrochlorothiazide therapy in two Japanese patients with gain-of-function mutations of the CaR gene.	Hydrochlorothiazide	84-103	calcium sensing receptor	Homo sapiens	176-179
11849460-2	2002	Although differences in race, age and measures of the renin-angiotensin-aldosterone system (RAAS) have been associated with variation in blood pressure response to hydrochlorothiazide, whether these characteristics make additive contributions to predicting response has not been established.	Hydrochlorothiazide	164-183	renin	Homo sapiens	54-59
11849460-7	2002	RESULTS: Black race and female gender were both associated with significantly greater systolic (SBP) and diastolic (DBP) blood pressure responses to hydrochlorothiazide.	Hydrochlorothiazide	149-168	selenium binding protein 1	Homo sapiens	96-99
11849460-7	2002	RESULTS: Black race and female gender were both associated with significantly greater systolic (SBP) and diastolic (DBP) blood pressure responses to hydrochlorothiazide.	Hydrochlorothiazide	149-168	D-box binding PAR bZIP transcription factor	Homo sapiens	116-119
11849460-9	2002	Additional statistically significant predictors of greater systolic and diastolic responses to hydrochlorothiazide included, shorter duration of diagnosed or treated hypertension (P &lt; 0.001), higher baseline BP level (P &lt; 0.0001), lower baseline plasma renin activity (P &lt; 0.05), lower baseline urinary aldosterone excretion (P &lt; 0.002), and greater decrease in urinary sodium excretion (P &lt; or = 0.004).	Hydrochlorothiazide	95-114	renin	Homo sapiens	259-264
11821713-6	2002	RESULTS: In vivo irbesartan, amlodipine and hydrochlorothiazide/hydralazine produced similar falls in blood pressure, from 162 +/- 4 to 125 +/- 5, 132 +/- 4 and 131 +/- 6 mmHg, respectively, but irbesartan caused a greater reduction in superoxide and p22phox; superoxide levels in carotid arteries being 3.1 +/- 0.3, 1.1 +/- 0.2, 1.9 +/- 0.3 and 2.0 +/- 0.3 nmoles/mg per min, respectively.	Hydrochlorothiazide	44-63	cytochrome b-245 alpha chain	Rattus norvegicus	251-258
12147929-8	2002	On analysis of variance, blood pressure reductions by calcium channel blockers, HCTZ, and ACE inhibitor/HCTZ combinations were significantly greater than that with placebo, while those of ACE inhibitors and beta blockers as monotherapy were not.	Hydrochlorothiazide	104-108	angiotensin I converting enzyme	Homo sapiens	90-93
11836266-9	2002	There was a significant correlation between PAI-1 antigen and serum aldosterone during both baseline and HCTZ study days (r(2) = 0.57; P = 0.0003); however, treatment with spironolactone abolished this correlation (r(2) = 0.13; P = 0.33).	Hydrochlorothiazide	105-109	serpin family E member 1	Homo sapiens	44-49
11836266-5	2002	Angiotensin II increased from baseline during both HCTZ (P = 0.02) and spironolactone (P = 0.02 vs. baseline; P = 0.19 vs. HCTZ) treatments.	Hydrochlorothiazide	123-127	angiotensinogen	Homo sapiens	0-14
11836266-7	2002	HCTZ increased PAI-1 antigen (P = 0.02), but did not alter t-PA antigen.	Hydrochlorothiazide	0-4	serpin family E member 1	Homo sapiens	15-20
11929332-5	2002	Treatment for 8 weeks with candesartan cilexetil 16 mg/hydrochlorothiazide 12.5 mg or candesartan cilexetil 16 mg induced SBP/DBP reductions of 12.0/7.5 mm Hg and 7.5/5.5mm Hg, respectively (p &lt; 0.05 both comparisons).	Hydrochlorothiazide	55-74	selenium binding protein 1	Homo sapiens	122-125
11929332-6	2002	Moreover, data from a randomised, double-blind, placebo-controlled, dose-finding study in 1038 patients with mild to moderate hypertension showed that the greatest reductions in SBP/DBP were achieved by candesartan cilexetil 16 mg/hydrochlorothiazide 12.5 mg.	Hydrochlorothiazide	231-250	selenium binding protein 1	Homo sapiens	178-181
11687919-4	2001	At the end of double-blind treatment, patients receiving telmisartan 80 mg/HCTZ 12.5 mg had significant additional decrements in clinic SBP/DBP over telmisartan 80 mg of -5.7/-3.1 mm Hg (P &lt; 0.01).	Hydrochlorothiazide	75-79	selenium binding protein 1	Homo sapiens	136-139
11687919-4	2001	At the end of double-blind treatment, patients receiving telmisartan 80 mg/HCTZ 12.5 mg had significant additional decrements in clinic SBP/DBP over telmisartan 80 mg of -5.7/-3.1 mm Hg (P &lt; 0.01).	Hydrochlorothiazide	75-79	D-box binding PAR bZIP transcription factor	Homo sapiens	140-143
11433085-5	2001	METHODS: The effect of hydrochlorothiazide (HCTZ) on clinical and radiologic progression of nephrocalcinosis was evaluated in 11 children with XLH.	Hydrochlorothiazide	44-48	phosphate regulating endopeptidase homolog X-linked	Homo sapiens	143-146
11703585-10	2001	Furthermore, rofecoxib completely reversed diuresis and saluresis and prevented the increase of plasma renin activity induced by hydrochlorothiazide.	Hydrochlorothiazide	129-148	renin	Rattus norvegicus	103-108
11806817-7	2001	In order to reach the target BP (sitting SBP &lt;150 mmHg), the first line agent, nitrendipine, could be associated with enalapril and/or hydrochlorothiazide.	Hydrochlorothiazide	138-157	selenium binding protein 1	Homo sapiens	41-44
11549204-0	2001	Pharmacokinetic and dynamic interactions of the angiotensin-converting enzyme inhibitor imidapril with hydrochlorothiazide, bisoprolol and nilvadipine.	Hydrochlorothiazide	103-122	angiotensin I converting enzyme	Homo sapiens	48-77
11433085-13	2001	However, when compared with the control period, HCTZ prevented the progression of nephrocalcinosis in children with XLH.	Hydrochlorothiazide	48-52	phosphate regulating endopeptidase homolog X-linked	Homo sapiens	116-119
11408035-8	2001	Concentration-response curves for the endothelin-1-induced contraction were displaced to the right after hydrochlorothiazide+losartan treatment (toward the curves for healthy controls); however, E(max) from treated hamsters was significantly reduced when compared to E(max) from untreated cardiomyopathic animals (1.016+/-0.073 vs. 1.346+/-0.153 g, P&lt;0.05, n=6).	Hydrochlorothiazide	105-124	endothelin 1	Homo sapiens	38-50
11881111-5	2001	The telmisartan/HCTZ combination produced the greatest reductions in trough DBP (-44+/-1.5 mmHg), SBP (-60+/-1.9 mmHg) and mean BP (mBP; -53+/-1.7 mmHg) after five days of therapy (p&lt;0.05 vs. vehicle and vs. telmisartan).	Hydrochlorothiazide	16-20	D-box binding PAR bZIP transcription factor	Rattus norvegicus	76-79
11881111-5	2001	The telmisartan/HCTZ combination produced the greatest reductions in trough DBP (-44+/-1.5 mmHg), SBP (-60+/-1.9 mmHg) and mean BP (mBP; -53+/-1.7 mmHg) after five days of therapy (p&lt;0.05 vs. vehicle and vs. telmisartan).	Hydrochlorothiazide	16-20	spermine binding protein	Rattus norvegicus	98-101
11881111-5	2001	The telmisartan/HCTZ combination produced the greatest reductions in trough DBP (-44+/-1.5 mmHg), SBP (-60+/-1.9 mmHg) and mean BP (mBP; -53+/-1.7 mmHg) after five days of therapy (p&lt;0.05 vs. vehicle and vs. telmisartan).	Hydrochlorothiazide	16-20	myelin basic protein	Mus musculus	77-79
11881111-5	2001	The telmisartan/HCTZ combination produced the greatest reductions in trough DBP (-44+/-1.5 mmHg), SBP (-60+/-1.9 mmHg) and mean BP (mBP; -53+/-1.7 mmHg) after five days of therapy (p&lt;0.05 vs. vehicle and vs. telmisartan).	Hydrochlorothiazide	16-20	myelin basic protein	Mus musculus	132-135
11408035-14	2001	In conclusion, in this model of heart failure, chronic hydrochlorothiazide+losartan administration normalizes the vascular responses to endothelin-1, improves basal vascular tone, and prevents the development of cardiac and vascular hypertrophy.	Hydrochlorothiazide	55-74	endothelin 1	Homo sapiens	136-148
10991988-4	2000	p-[(14)C]Aminohippurate (PAH) uptake by rOAT1-expressing oocytes was inhibited in the presence of a thiazide (chlorothiazide, cyclothiazide, hydrochlorothiazide), a loop diuretic (bumetanide, ethacrynic acid, furosemide), or a carbonic anhydrase inhibitor (acetazolamide, ethoxzolamide, methazolamide).	Hydrochlorothiazide	141-160	solute carrier family 22 member 6	Rattus norvegicus	40-45
11135058-11	2001	Hydrochlorothiazide treatment increased plasma renin activity twofold but did not change kidney cortical renin mRNA, COX-2 mRNA, or COX-2 immunoreactivity.	Hydrochlorothiazide	0-19	renin	Rattus norvegicus	47-52
10991988-8	2000	[(14)C]PAH efflux was significantly enhanced when the rOAT1-expressing oocytes were incubated in the presence of unlabeled PAH, alpha-ketoglutarate, acetazolamide, chlorothiazide, or hydrochlorothiazide.	Hydrochlorothiazide	183-202	solute carrier family 22 member 6	Rattus norvegicus	54-59