ANG II reduces net acid secretion in rat outer medullary collecting duct

被引:14
作者
Wall, SM
Fischer, MP
Glapion, DM
De La Calzada, M
机构
[1] Emory Univ, Sch Med, Div Renal, Atlanta, GA 30322 USA
[2] Univ Texas, Sch Med, Div Renal Dis & Hypertens, Houston, TX 77030 USA
关键词
ammonium; acidification; angiotensin; 2; aldosterone; metabolic acidosis; metabolic alkalosis;
D O I
10.1152/ajprenal.00400.2002
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
In rat outer medullary collecting duct (OMCD), the mechanism(s) and regulation of H(+) secretion are not understood fully. The effect of changes in acid-base balance and the renin-angiotensin system on net H(+) secretion was explored. Rats received NaCl, NaHCO(3), NH(4)Cl, or nothing in their drinking water for 7 days. Total ammonia and total CO(2) (J(tCO 2)) fluxes were measured in OMCD tubules perfused in vitro from rats in each treatment group. J(tCO 2) was reduced in tubules from rats drinking NH(4)Cl relative to those drinking NaHCO(3). Because NH(4)Cl intake increases plasma renin and aldosterone, we asked if upregulation of the renin-angiotensin system reduces net H(+) secretion. Deoxycorticosterone pivalate administered in vivo did not affect J(tCO 2). However, ANG II given in vivo at 0.1 ng/min reduced J(tCO 2) by 35%. To determine if ANG II has a direct effect on acid secretion, J(tCO 2) was measured with ANG II applied in vitro. ANG II (10(-8) M) present in the bath solution reduced J(tCO 2) by 35%. This ANG II effect was not observed in the presence of the AT(1) receptor blocker candesartan. In conclusion, in rat OMCD, J(tCO 2) is paradoxically reduced with NH(4)(C)l ingestion. Increased circulating ANG II, as occurs during metabolic acidosis, reduces J(tCO 2).
引用
收藏
页码:F930 / F937
页数:8
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