Effect of intrarenal angiotensin II infusion on the renal escape from mineralocorticoid.

This study examined the hypothesis that suppression of the antinatriuretic action of angiotensin II (ANG II) is an important determinant of the escape from the sodium-retaining effects of mineralocorticoid. In five uninephrectomized dogs aldosterone (ALDO) infusion (10 ng X kg-1 X min-1) produced a fall in sodium excretion (UNaV) on the first day that returned to control on the fourth day of ALDO infusion. Mean arterial pressure (MAP) increased from 89 +/- 1 to 100 +/- 1 mmHg, and glomerular filtration rate (GFR) increased from 38 +/- 3 to 45 +/- 3 ml/min during ALDO infusion. After recovery, intrarenal infusion of ANG II (1.5 ng X kg-1 X min-1) was initiated to maintain a constant level of ANG II during the subsequent aldosterone administration. The intrarenal ANG II infusion produced a sustained increase in MAP (12 +/- 4 mmHg) and a sustained decrease in GFR (11 +/- 5 ml/min) and effective renal plasma flow (42 +/- 17 ml/min). With intrarenal ANG II levels fixed, ALDO infusion again produced a marked decrease in UNaV on the first day followed by a return to control levels on the third day. Again, MAP and GFR increased significantly during ALDO infusion (from 101 +/- 2 to 119 +/- 2 mmHg and from 27 +/- 6 to 35 +/- 4 ml/min, respectively). The absolute increase in MAP was significantly greater during ALDO infusion with intrarenal ANG II infusion as compared with ALDO infusion with intrarenal vehicle infusion alone.(ABSTRACT TRUNCATED AT 250 WORDS)