THE EFFECT OF PHENOXYBENZAMINE AND SARALASIN ON THE ALTERED RENAL BLOOD FLOW DISTRIBUTION IN BABOONS WITH OBSTRUCTIVE JAUNDICE

1. Using the ¹³³xenon (¹³³Xe) washout technique, renal cortical perfusion was measured in fourteen baboons before and 1 and 2 weeks after ligation of the common bile duct. 2. In the 1‐week group (seven animals), ligation of the common bile duct caused no significant changes in cortical perfusion in comparison with preligation values. 3. Intrarenal infusion of the angiotensin II blocking agent, saralasin, at a rate of 0.1 mmol/min caused no change in cortical perfusion in the 1‐week group. However, an infusion of 0.3 mmol/min of the α‐adrenoreceptor blocking agent, phenoxybenzamine, caused significant increases in outer cortical flow over control (P < 0.05) and 1‐week values (P < 0.05). 4. In the 2‐week group (seven animals), ligation of the common bile duct caused a non‐significant decrease in outer cortical flow and a significant decrease in the percentage distribution of radioactivity distributed to the outer cortex (P < 0.001). 5. A 0.1 mmol/min intrarenal infusion of saralasin had no effect on outer cortical flow in the 2 week group, but significantly raised the percentage distribution of flow to the outer cortex (P < 0.001) over the 2‐week value. An intrarenal infusion of 0.3 mmol/min phenoxybenzamine in the 2‐week group significantly increased outer cortical flow levels over the 2‐week (P < 0.001) and control (P < 0.05) values. The percentage distribution to the outer cortex was also significantly raised (P < 0.001) over the 2‐week values. 6. There was a significant correlation between the changes in outer cortical blood flow induced by phenoxybenzamine at 1 and 2 weeks and the percentage increases in total serum bilirubin (r= 0.802, P < 0.001) and cholesterol (r= 0.668, P < 0.01) plasma levels over baseline values. 7. These results demonstrate that in baboons with experimentally‐induced obstructive jaundice there is increased activity of the renal a‐adrenoreceptors, and when renal cortical vasoconstruction is present, the renin‐angiotensin system may also be activated and contributes to the cortical vasoconstriction.