PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33476711-11 2021 We conclude that acute HgCl2 exposure causes renal vasoconstriction that is associated with reduced endothelial vasodilator agonist- and flow-mediated responses and inhibition of NHE3-mediated sodium reabsorption. Sodium 193-199 solute carrier family 9 member A3 Rattus norvegicus 179-183 28506883-10 2017 Our findings indicate the involvement of NKA-SRc-Kinase-Ras-Raf-ERK1/2 pathway in the downregulation of NHE3 by cardiotonic steroids in the renal proximal tubule, promoting a reduction of proximal sodium reabsorption and natriuresis. Sodium 197-203 solute carrier family 9 member A3 Rattus norvegicus 104-108 33283643-2 2021 Tenapanor is a non-binder, sodium/hydrogen exchanger isoform 3 (NHE3) inhibitor that reduces paracellular intestinal phosphate absorption. Sodium 27-33 solute carrier family 9 member A3 Rattus norvegicus 64-68 32755467-10 2020 Collectively, these results suggest that endogenous GLP-1R signaling exerts a physiologically relevant effect on BP control, which may be attributable, in part, to its tonic actions on the proximal tubule NHE3-mediated sodium reabsorption, intrarenal renin-angiotensin system, and insulin sensitivity. Sodium 219-225 solute carrier family 9 member A3 Rattus norvegicus 205-209 29537313-0 2018 Predicted effect of circadian clock modulation of NHE3 of a proximal tubule cell on sodium transport. Sodium 84-90 solute carrier family 9 member A3 Rattus norvegicus 50-54 26727380-0 2016 Inhibition of NHE3-mediated Sodium Absorption in the Gut Reduced Cardiac End-organ Damage Without Deteriorating Renal Function in Obese Spontaneously Hypertensive Rats. Sodium 28-34 solute carrier family 9 member A3 Rattus norvegicus 14-18 27510906-9 2016 Moreover, these findings support the notion that NHE3 dephosphorylation at serine 552 may represent a key event in the regulation of renal proximal tubule sodium handling by ANG II in the presence of natriuretic hormones that promote cAMP accumulation and transporter phosphorylation. Sodium 155-161 solute carrier family 9 member A3 Rattus norvegicus 49-53 26727380-2 2016 The sodium-proton-exchanger subtype 3 (NHE3) is an important mediator of intestinal sodium absorption. Sodium 4-10 solute carrier family 9 member A3 Rattus norvegicus 39-43 26727380-3 2016 The compound SAR is a new specific NHE3 inhibitor with extremely low oral absorbability leading to decreased sodium absorption in the gut and substantial systolic blood pressure reduction. Sodium 109-115 solute carrier family 9 member A3 Rattus norvegicus 35-39 26727380-10 2016 Reduction of intestinal sodium absorption by selective NHE3 inhibition in the gut lowered high blood pressure and reduced LV remodeling without deteriorating renal functional and structural parameters in SHR-ob. Sodium 24-30 solute carrier family 9 member A3 Rattus norvegicus 55-59 25656367-3 2015 Since the sympathetic nervous system and intrarenal ANG II appear to act synergistically to mediate the process of sodium reabsorption, we hypothesized that low-frequency acute electrical stimulation of the renal nerve (ESRN) activates NHE3-mediated sodium reabsorption via ANG II AT1 receptor activation in Wistar rats. Sodium 250-256 solute carrier family 9 member A3 Rattus norvegicus 236-240 26173747-2 2015 In the proximal tubule, the Na(+) /H(+) Exchanger 3 (NHE3) is responsible for normal protein reabsorption and the reabsorption of approximately 70% of the renal sodium load. Sodium 161-167 solute carrier family 9 member A3 Rattus norvegicus 28-51 26173747-2 2015 In the proximal tubule, the Na(+) /H(+) Exchanger 3 (NHE3) is responsible for normal protein reabsorption and the reabsorption of approximately 70% of the renal sodium load. Sodium 161-167 solute carrier family 9 member A3 Rattus norvegicus 53-57 25656367-8 2015 Taken together, our results demonstrate that higher NHE3-mediated proximal tubular sodium reabsorption induced by ESRN occurs via intrarenal renin angiotensin system activation and triggering of the AT1 receptor/inhibitory G-protein signaling pathway, which leads to inhibition of cAMP formation and reduction of PKA activity. Sodium 83-89 solute carrier family 9 member A3 Rattus norvegicus 52-56 21613418-10 2011 These results suggest that high sodium intake increases HCO(3)(-) absorptive capacity in the MTAL through 1) an adaptive increase in basolateral NHE1 activity that results secondarily in an increase in apical NHE3 activity; and 2) an adaptive increase in NHE3 activity, independent of NHE1 activity. Sodium 32-38 solute carrier family 9 member A3 Rattus norvegicus 209-213 23991143-8 2013 With no clear indication that the kidneys of salt-exposed offspring retained more sodium per se, we conducted a preliminary investigation of their gastrointestinal electrolyte handling and found increased expression of proximal colon solute carrier family 9 (sodium/hydrogen exchanger), member 3 (SLC9A3) together with altered faecal characteristics and electrolyte handling, relative to control offspring. Sodium 259-265 solute carrier family 9 member A3 Rattus norvegicus 297-303 23108657-2 2012 The sodium-proton-exchanger subtype 3 (NHE3) is an important mediator of sodium absorption in the gut. Sodium 4-10 solute carrier family 9 member A3 Rattus norvegicus 39-43 23108657-5 2012 In spontaneously hypertensive rats-lean, inhibition of intestinal NHE3 by SAR increased feces sodium excretion and reduced urinary sodium excretion, whereas absolute sodium balance and serum sodium concentration were not changed. Sodium 94-100 solute carrier family 9 member A3 Rattus norvegicus 66-70 23108657-5 2012 In spontaneously hypertensive rats-lean, inhibition of intestinal NHE3 by SAR increased feces sodium excretion and reduced urinary sodium excretion, whereas absolute sodium balance and serum sodium concentration were not changed. Sodium 131-137 solute carrier family 9 member A3 Rattus norvegicus 66-70 23108657-5 2012 In spontaneously hypertensive rats-lean, inhibition of intestinal NHE3 by SAR increased feces sodium excretion and reduced urinary sodium excretion, whereas absolute sodium balance and serum sodium concentration were not changed. Sodium 131-137 solute carrier family 9 member A3 Rattus norvegicus 66-70 23108657-5 2012 In spontaneously hypertensive rats-lean, inhibition of intestinal NHE3 by SAR increased feces sodium excretion and reduced urinary sodium excretion, whereas absolute sodium balance and serum sodium concentration were not changed. Sodium 131-137 solute carrier family 9 member A3 Rattus norvegicus 66-70 22031782-2 2012 We therefore hypothesized that Na(+)/H(+) exchanger isoform 3 (NHE3), the major apical transcellular pathway for sodium reabsorption in the proximal tubule, is upregulated in an experimental model of HF. Sodium 113-119 solute carrier family 9 member A3 Rattus norvegicus 31-61 22031782-2 2012 We therefore hypothesized that Na(+)/H(+) exchanger isoform 3 (NHE3), the major apical transcellular pathway for sodium reabsorption in the proximal tubule, is upregulated in an experimental model of HF. Sodium 113-119 solute carrier family 9 member A3 Rattus norvegicus 63-67 22031782-6 2012 By means of stationary in vivo microperfusion and pH-dependent sodium uptake, we demonstrated that NHE3 transport activity was significantly higher in the proximal tubule of HF compared with sham rats. Sodium 63-69 solute carrier family 9 member A3 Rattus norvegicus 99-103 22031782-10 2012 Enhanced NHE3-mediated sodium reabsorption in the proximal tubule may contribute to extracellular volume expansion and edema, the hallmark feature of HF. Sodium 23-29 solute carrier family 9 member A3 Rattus norvegicus 9-13 23108657-10 2012 Reduction of intestinal sodium absorption by selective NHE3 inhibition in the gut reduces high blood pressure and increases feces water excretion. Sodium 24-30 solute carrier family 9 member A3 Rattus norvegicus 55-59 21814178-2 2011 As the Na/H exchanger-3 (NHE3) mediates the bulk of apical sodium transport and a significant fraction of oxygen consumption in the proximal tubule, we examined mechanisms by which ischemia-reperfusion affects the expression of NHE3. Sodium 59-65 solute carrier family 9 member A3 Rattus norvegicus 7-23 21814178-2 2011 As the Na/H exchanger-3 (NHE3) mediates the bulk of apical sodium transport and a significant fraction of oxygen consumption in the proximal tubule, we examined mechanisms by which ischemia-reperfusion affects the expression of NHE3. Sodium 59-65 solute carrier family 9 member A3 Rattus norvegicus 25-29 21613418-10 2011 These results suggest that high sodium intake increases HCO(3)(-) absorptive capacity in the MTAL through 1) an adaptive increase in basolateral NHE1 activity that results secondarily in an increase in apical NHE3 activity; and 2) an adaptive increase in NHE3 activity, independent of NHE1 activity. Sodium 32-38 solute carrier family 9 member A3 Rattus norvegicus 255-259 21282559-2 2011 Ang II activates renal Na(+)/H(+) exchanger 3 (NHE3) to increase sodium reabsorption, but the mechanisms are still elusive. Sodium 65-71 solute carrier family 9 member A3 Rattus norvegicus 23-45 21389090-10 2011 The downregulation of NHE3 and NCC may contribute to the BP-attenuating effect of dietary potassium associated with increased urinary sodium excretion. Sodium 134-140 solute carrier family 9 member A3 Rattus norvegicus 22-26 21282559-2 2011 Ang II activates renal Na(+)/H(+) exchanger 3 (NHE3) to increase sodium reabsorption, but the mechanisms are still elusive. Sodium 65-71 solute carrier family 9 member A3 Rattus norvegicus 47-51 20630932-2 2010 The Na(+)/H(+) exchanger isoform 3 (NHE3) represents the major route for sodium entry across the apical membrane of renal PT cells. Sodium 73-79 solute carrier family 9 member A3 Rattus norvegicus 36-40 20630932-9 2010 The molecular mechanisms of this adaptation possibly include an increase of P-NHE3/total and a redistribution of the NHE3-DPPIV complex from the body to the base of the PT microvilli, both predicted to decrease sodium reabsorption. Sodium 211-217 solute carrier family 9 member A3 Rattus norvegicus 117-121 18322024-7 2008 The decreased NHE3 expression is likely to be responsible for the reduction of sodium, bicarbonate, and fluid reabsorption in the proximal tubule consistently perceived in experimental models of PTH disorders. Sodium 79-85 solute carrier family 9 member A3 Rattus norvegicus 14-18 18177483-13 2008 We conclude that noradrenaline-induced increases in the expression of NHE-3, NBC-1, BSC-1 and aquaporin-2 are likely to play an important role in the regulation of salt and water transport by noradrenaline in the kidney and may explain, at least in part, the altered renal sodium and water handling associated with overactivation of the sympathetic system. Sodium 273-279 solute carrier family 9 member A3 Rattus norvegicus 70-75 17684771-4 2008 The isoform of the Na(+)/H(+) exchanger mediating proximal tubule sodium absorption, NHE3, is virtually absent in the neonatal rat kidney. Sodium 66-72 solute carrier family 9 member A3 Rattus norvegicus 85-89 16189294-14 2006 The decreased abundance of NHE3, NKCC2, NCC, and Na-K-ATPase may play a compensatory role in promoting sodium excretion. Sodium 103-109 solute carrier family 9 member A3 Rattus norvegicus 27-31 16339392-8 2006 The attenuation of sodium retention by clofibrate treatment is linked to decreased expression of NHE-3 in renal cortex. Sodium 19-25 solute carrier family 9 member A3 Rattus norvegicus 97-102 16633989-8 2006 Quantitative polymerase chain reaction (PCR) and Western blot analysis reveal that in diabetic rats compared with controls, mRNA and protein abundance was higher for type 3 sodium/hydrogen exchanger (NHE3) in proximal tubule and ascending limbs of Henle"s loop, and higher for bumetanide-sensitive sodium-potassium-2 chloride cotransporter (NKCC2) in ascending limbs of Henle"s loop. Sodium 173-179 solute carrier family 9 member A3 Rattus norvegicus 200-204 11160999-4 2001 The third blood pressure QTL (QTL region 2) was close to the centromere between 1p11 and 1q12, which includes the candidate gene Slc9a3 for sodium/hydrogen exchange. Sodium 140-146 solute carrier family 9 member A3 Rattus norvegicus 129-135 15075188-13 2004 The decreased abundance of NHE3, BSC-1, TSC, and Na-K-ATPase may play a compensatory role to promote sodium excretion. Sodium 101-107 solute carrier family 9 member A3 Rattus norvegicus 27-31 12464626-2 2003 Expression of sodium-hydrogen exchanger isoform 3 (NHE3) in the intestinal and renal epithelium plays a critical role in sodium absorption and acid/base homeostasis. Sodium 14-20 solute carrier family 9 member A3 Rattus norvegicus 51-55 11868817-4 2002 NHE3 is an apical membrane NHE responsible for sodium absorption in renal proximal tubule and intestinal epithelium. Sodium 47-53 solute carrier family 9 member A3 Rattus norvegicus 0-4 12191963-10 2002 In conclusion, increased sodium reabsorption might be associated with a shift of NHE3 from an inactive pool to an active pool, thus contributing to sodium retention in a state of proteinuria. Sodium 25-31 solute carrier family 9 member A3 Rattus norvegicus 81-85 12191963-10 2002 In conclusion, increased sodium reabsorption might be associated with a shift of NHE3 from an inactive pool to an active pool, thus contributing to sodium retention in a state of proteinuria. Sodium 148-154 solute carrier family 9 member A3 Rattus norvegicus 81-85 11703600-0 2001 Coordinated down-regulation of NBC-1 and NHE-3 in sodium and bicarbonate loading. Sodium 50-56 solute carrier family 9 member A3 Rattus norvegicus 41-46 9887076-8 1999 In contrast, chronic metabolic alkalosis, regardless of whether it is associated with high sodium intake or not, leads to an appropriate adaptation of NHE-3 activity, which involves a decrease in NHE-3 protein and mRNA abundance. Sodium 91-97 solute carrier family 9 member A3 Rattus norvegicus 151-156 10569186-1 1999 The sodium-hydrogen exchanger isoform, NHE-3 is essential for the absorption of sodium and water from intestine. Sodium 4-10 solute carrier family 9 member A3 Rattus norvegicus 39-44 10444581-9 1999 In conclusion, in this rat CRF model: 1) increased fractional sodium excretion is associated with altered expression of proximal tubule Na transporter expression (NHE-3, NaPi-II, and Na-K-ATPase), consistent with glomerulotubular imbalance in the face of increased single-nephron glomerular filtration rate; and 2) compensatory increases in BSC-1 and TSC expression per nephron occur in distal segments. Sodium 62-68 solute carrier family 9 member A3 Rattus norvegicus 163-168 9950829-4 1999 In proximal colon, dietary sodium depletion enhanced both NHE2 and NHE3 isoform-specific Na+/H+ exchange activities, protein expression, and mRNA abundance. Sodium 27-33 solute carrier family 9 member A3 Rattus norvegicus 67-71 9950829-5 1999 In contrast, in distal colon both NHE2 and NHE3 isoform-specific Na+/H+ exchange activities, protein expression, and mRNA abundance were inhibited by sodium depletion. Sodium 150-156 solute carrier family 9 member A3 Rattus norvegicus 43-47 9050969-1 1997 OBJECTIVE: To examine the mechanisms affecting proximal tubule sodium reabsorption, we studied the gene expression and functional changes of the Na+/H+-exchanger 3 (NHE3) and its gene expression in spontaneously hypertensive rats (SHR). Sodium 63-69 solute carrier family 9 member A3 Rattus norvegicus 165-169 35285452-7 2022 CONCLUSION: Inhibition of SGLT2 in combination with an angiotensin II receptor blocker effectively improved BP salt sensitivity by reducing renal expression levels of sodium transporters including NHE3 and NKCC2, which eventually led to improvement of BP salt sensitivity and cardiorenal protection. Sodium 167-173 solute carrier family 9 member A3 Rattus norvegicus 197-201