Angiotensin II and alpha-adrenergic control of the intrarenal circulation in hemorrhage.

Alpha receptor and angiotensin II blockade were used to study renal cortical vasoconstrictor mechanisms during hemorrhage to 70 mmHg in chloralose-urethane anesthetized dogs. A freeze-dissection 133Xe disappearance technique was utilized to assess renal blood flow patterns. Hemorrhage alone caused a 30% decrease in total renal blood flow (TRBF) and a 50% decrease in outer cortical blood flow. Inner cortical flow decreased approximately 30%. Outer medullary blood flow decreased 25%. Renal arterial infusion of phentolamine beginning 20 min posthemorrhage produced no alteration in the expected posthemorrhage TRBF or its distribution. Plasma renin activity increased 6-7 fold in the hemorrhage group as well as in the hemorrhage with phentolamine group. Saralasin treatment beginning 20 min posthemorrhage produced a pattern in which neither TRBF nor cortical blood flow was significantly reduced by the hemorrhage. It therefore appears that angiotensin II is a renal cortical vasoconstrictor during hemorrhage. These data demonstrate that during the first 30 minutes of hemorrhage the renal cortical vasoconstriction is mediated by angiotensin II and appears to be independent of alpha-adrenergic mechanisms.