Patai Hiranphun, Chamnong Supatraviwat, and Siriphun Hiranyachattada

pp. 485 - 496

Abstract

The present study aimed to investigate the action of angiotensin II (AII) on renal perfusion pressure
and renal vascular resistance using noncompetitive AT₁-receptor antagonist (candesartan or CV 11974).
Experiments were performed in isolated kidney of adult male Wistar rats. Kreb's Henseleit solution was
perfused into the renal artery at the rate of 3.5 ml/min. This flow rate was designed in order to maintain
renal perfusion pressure between 80-120 mm Hg. Dose-response relationship between perfusion flow rate
and AII concentration were studied. Renal perfusion pressure in response to 1, 10 and 100 nM AII were
increased from basal perfusion pressure of 94±8 mm Hg to 127±6, 157±12 and 190±16 mm Hg, respectively.
Administration of perfusate containing 11.4 µM candesartan for 30 min had no effect on the basal perfusion
pressure. However, this significantly reduced renal perfusion pressure in the presence of AII (1, 10 and 100
nM) by 39%, 47% and 61%, (n=7, P<0.05) respectively. At the basal perfusion pressure, calculated renal vascular resistance was 27±2 mm Hg · min · ml^-1. However, the vascular resistance were found to be 41±1,
45±2 and 47±2 mm Hg · min · ml^-1 when 1, 10 and 100 nM AII were added. Moreover, this dose of candesartan
also showed a significant decrease in renal vascular resistance at the corresponding doses of AII by 38%,
48% and 43%, (n=7, P<0.05) respectively. The higher dose of candesartan (22.7 µM) completely inhibited
the action of 1, 10 and 100 nM AII on renal vasoconstriction. These results may indicate that the action of
AII on renal vascular resistance is via AT₁-receptor, at least in rat isolated perfusion kidney.