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1 Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA
2 Division of Renal Diseases and Hypertension, University of Texas, Medical School at Houston, Houston, TX, USA
* To whom correspondence should be addressed. E-mail: smwall{at}emory.edu.
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 were explored. Rats received NaCl, NaHCO3, NH4Cl or nothing in their drinking water for 7 days. Total ammonia (JtAMM) and total CO2 (JtCO2) fluxes were measured in OMCD tubules perfused in vitro from rats in each treatment group. JtCO2 was reduced in tubules from rats drinking NH4Cl relative to those drinking NaHCO3. Since NH4Cl 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 JtCO2. However, angiotensin II given in vivo at 0.1 ng/min reduced JtCO2 by 35%. To determine if angiotensin II has a direct effect on acid secretion, JtCO2 was measured with angiotensin II applied in vitro. Angiotensin II (10-8 M) present in the bath solution reduced JtCO2 by 35%. This angiotensin II effect was not observed in the presence of the AT1 receptor blocker, candesartan. In conclusion, in rat OMCD JtCO2 is paradoxically reduced with NH4Cl ingestion. Increased circulating angiotensin II, as occurs during metabolic acidosis, reduces JtCO2.
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