Angiotensin II: Intratubular and Renal Capillary Pressure Regulation in the Rat Kidney

Experiments were designed to test the hypothesis that angiotensin II, in its action on receptor sites in vascular smooth muscle and the proximal tubule, acts homeostatically to stabilize hydrostatic pressure in the proximal tubule, and as a consequence, maintains a constant flow of fluid to the distal tubule. Infusion, at 20 n1 min ‐1 , of Ileu 5 ‐angiotensin II [(Ileu 5 )‐A II] (20 ng m1 ‐1 ) into peritubular capillaries adjacent to a proximal tubule was found to be accompanied by an increase in hydrostatic pressure in both the infused capillaries and the proximal tubule and by a decrease in the rate of proximal fluid reabsorption (RPFR). RPFR was derived from timed quantitative collections of tubular fluid from the last superficial proximal segments. Tubular pressure before infusion and pressures in noninfused capillaries were not related to plasma renin activity (PRA). 1‐Sarcosine, 8‐alanine‐angiotensin II [(Sar 1 , Ala 8 )‐A II] is known to be a competitive antagonist to the action of angiotensin II on vascular smooth muscle and on adrenocortical zona glomerulosa cells. Infusion, at 20 n1 min ‐1 , of (Sar 1 , Ala 8 )‐A II (333 ng m1 ‐1 ) into peritubular capillaries caused a decrease in hydrostatic pressure in the peritubular capillaries and adjacent proximal tubules. The most striking fall in pressure (‐4 cmH 2 O) occurred in rats with high levels of PRA. No pressure change resulted from infusion with a mixture of (Ileu 5 )‐A II and (Sar 1 , Ala 8 )‐A II. (Sar 1 , Ala 8 )‐A II in this mixture blocked the inhibitory effect of (Ileu 5 )‐A II on RPFR, but infusion of the angiotensin antagonist alone did not influence RPFR. It is concluded that angiotensin II is a physiological regulator of hydrostatic pressure in both the proximal tubule and the peritubular capillaries.