Angiotensin II stimulation of hydrogen ion secretion in the rat early proximal tubule. Modes of action, mechanism, and kinetics.

Abstract

Physiologic concentrations of angiotensin II stimulate sodium transport by intestinal and renal early (SI) and late (S2) proxi- mal tubule epithelial cells. We recently found that hydrogen ion secretion, which effects sodium bicarbonate absorption, was a transport function preferentially and potently increased by angiotensin II in SI cells. SI cells are normally responsible for half of the total renal hydrogen ion secretion. The mecha- nism by which angiotensin II regulates intestinal sodium trans- port is by potentiating sympathetic nerve activity and norepi- nephrine release. Direct control of hydrogen ion secretion by angiotensin II via receptors on epithelial cells has not been previously demonstrated. We now report that stimulation of in vivo hydrogen ion secretion in the rat early proximal tubule by angiotensin II was not mediated via change in nerve activity. Rather, enhanced hydrogen ion secretion by angiotensin II correlated with increased angiotensin II receptor density on epithelial cells in the early compared to late microdissected proximal tubule. Basolateral as well as luminal angiotensin II stimulated bicarbonate absorption. Angiotensin II reduced bi- carbonate permeability and caused alteration in the apparent substrate affinity, but not maximal capacity, of the proximal hydrogen ion secretory system involving the Na+/H' anti- porter.