PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
7772233-11	1995	omega-Conotoxin did not alter the secretory response of frog neurointermediate lobes to 3APS, while nifedipine blocked the stimulation of alpha-MSH secretion induced by 3APS.	Nifedipine	100-110	proopiomelanocortin	Homo sapiens	138-147	
8622612-3	1996	The augmentative effect of endothelin-1 on CRF-induced ACTH secretion (P < .05) was counteracted by pretreatment with nifedipine.	Nifedipine	121-131	proopiomelanocortin	Homo sapiens	55-59	
32411097-9	2020	Nifedipine inhibited the basal and ACTH-, ATII-elicited aldosterone secretion.	Nifedipine	0-10	proopiomelanocortin	Homo sapiens	35-39	
21757861-7	2011	Efonidipine and nifedipine, but not other examined CCBs, also increased the N(6), 2"-O-dibutyryladenosine 3",5"-cyclic monophosphate (dbcAMP)-induced StAR mRNA, which reflects the action of adrenocorticotropic hormone, and efonidipine and R(-)-efonidipine enhanced the dbcAMP-induced DHEA-S production in NCI-H295R adrenocortical carcinoma cells.	Nifedipine	16-26	proopiomelanocortin	Homo sapiens	190-217	
11162903-8	2000	omega-Conotoxin and nifedipine were able to decrease the spontaneous alpha-MSH release from whole NILs while only omega-conotoxin had inhibitory effect on hormonal output from dispersed melanotrophs.	Nifedipine	20-30	proopiomelanocortin	Homo sapiens	69-78	
8384597-2	1993	Several evidences indicate that calcium-entry blockers agents (i.e. nifedipine) inhibit oCRH-dependent ACTH stimulation "in vitro".	Nifedipine	68-78	proopiomelanocortin	Homo sapiens	103-107	
8388880-5	1993	Pretreatment with nifedipine delayed the time of the peak plasma hormone responses after naloxone [ACTH, 32.1 +/- 2.1 vs. 51.4 +/- 4.5 min (P < 0.05); cortisol, 42.9 +/- 2.1 vs. 70.7 +/- 4.3 min (P < 0.02); for naloxone and nifedipine/naloxone, respectively].	Nifedipine	18-28	proopiomelanocortin	Homo sapiens	99-103	
8388880-6	1993	Additionally, nifedipine significantly reduced the proportion of the mean integrated ACTH response that had occurred by 30 min after naloxone administration (32.0 +/- 4.0% for naloxone vs. 17.6 +/- 2.4% for nifedipine/naloxone; P < 0.02) and the proportion of the mean integrated cortisol response by 45 min after naloxone administration (34.7 +/- 3.5% for naloxone vs. 25.0 +/- 2.6% for nifedipine/naloxone; P < 0.02).	Nifedipine	14-24	proopiomelanocortin	Homo sapiens	85-89	
8388880-6	1993	Additionally, nifedipine significantly reduced the proportion of the mean integrated ACTH response that had occurred by 30 min after naloxone administration (32.0 +/- 4.0% for naloxone vs. 17.6 +/- 2.4% for nifedipine/naloxone; P < 0.02) and the proportion of the mean integrated cortisol response by 45 min after naloxone administration (34.7 +/- 3.5% for naloxone vs. 25.0 +/- 2.6% for nifedipine/naloxone; P < 0.02).	Nifedipine	207-217	proopiomelanocortin	Homo sapiens	85-89	
8388880-6	1993	Additionally, nifedipine significantly reduced the proportion of the mean integrated ACTH response that had occurred by 30 min after naloxone administration (32.0 +/- 4.0% for naloxone vs. 17.6 +/- 2.4% for nifedipine/naloxone; P < 0.02) and the proportion of the mean integrated cortisol response by 45 min after naloxone administration (34.7 +/- 3.5% for naloxone vs. 25.0 +/- 2.6% for nifedipine/naloxone; P < 0.02).	Nifedipine	207-217	proopiomelanocortin	Homo sapiens	85-89	
1325203-2	1992	In five normal humans, we found that nifedipine pretreatment reduced integrated ACTH responses to the CRH-mediated stimulus of fenfluramine by 28% and cortisol responses by 34%, results comparable with those from in vitro reports.	Nifedipine	37-47	proopiomelanocortin	Homo sapiens	80-84	
1325203-4	1992	We conclude that (1) in humans, nifedipine inhibits ACTH release by fenfluramine by blocking Ca2+ influx via L-type channels in corticotrophs; (2) the magnitude of fenfluramine-stimulated CRH release is probably unaltered by nifedipine and (3) because the timing is unaltered, nifedipine does not affect the rate of CRH delivery to the corticotroph.	Nifedipine	32-42	proopiomelanocortin	Homo sapiens	52-56	
2552350-5	1989	GABA-induced stimulation of alpha-melanocyte-stimulating hormone release was inhibited by tetrodotoxin (10(-5) M), an Na+ -channel blocker, or nifedipine (10(-5) M), a voltage-dependent Ca2+ -channel blocker, suggesting that Na+ and Ca2+ ions are involved in the stimulatory phase of GABA action.	Nifedipine	143-153	proopiomelanocortin	Homo sapiens	28-64	
2545392-0	1989	Nifedipine blocks ACTH and cortisol release in man.	Nifedipine	0-10	proopiomelanocortin	Homo sapiens	18-22	
2545392-2	1989	The present study investigated the effect of prior administration of nifedipine on AVP-induced ACTH release in seven normal volunteers.	Nifedipine	69-79	proopiomelanocortin	Homo sapiens	95-99	
2545392-8	1989	The mean peak plasma ACTH and cortisol levels and the mean peak changes from basal in these levels were significantly lower in the nifedipine/AVP test than in the AVP alone test.	Nifedipine	131-141	proopiomelanocortin	Homo sapiens	21-25	
2545392-12	1989	Acute administration of oral nifedipine caused an inhibition of AVP-stimulated ACTH and cortisol release in normal humans.	Nifedipine	29-39	proopiomelanocortin	Homo sapiens	79-83	
3151249-6	1988	Nifedipine (10 mumol/l), which was able to block KCl (20 mmol/l)-evoked alpha-MSH release, induced a slight inhibition of basal alpha-MSH secretion, indicating that extracellular Ca2+ levels may regulate alpha-MSH release in part by Ca2+ influx through voltage-dependent Ca2+ channels.	Nifedipine	0-10	proopiomelanocortin	Homo sapiens	72-81	
3151249-6	1988	Nifedipine (10 mumol/l), which was able to block KCl (20 mmol/l)-evoked alpha-MSH release, induced a slight inhibition of basal alpha-MSH secretion, indicating that extracellular Ca2+ levels may regulate alpha-MSH release in part by Ca2+ influx through voltage-dependent Ca2+ channels.	Nifedipine	0-10	proopiomelanocortin	Homo sapiens	128-137	
3151249-6	1988	Nifedipine (10 mumol/l), which was able to block KCl (20 mmol/l)-evoked alpha-MSH release, induced a slight inhibition of basal alpha-MSH secretion, indicating that extracellular Ca2+ levels may regulate alpha-MSH release in part by Ca2+ influx through voltage-dependent Ca2+ channels.	Nifedipine	0-10	proopiomelanocortin	Homo sapiens	128-137	
3022252-5	1986	Nifedipine (both 10(-5) and 10(-4) M) inhibited CRF stimulated ACTH release but only to a maximum of 30%.	Nifedipine	0-10	proopiomelanocortin	Homo sapiens	63-67