Renal vascular changes during hemorrhagic shock and the pharmacologic modification by angiotensin and catecholamine antagonists

Renal angiograms were taken at various stages of hemorrhagic shock. Hemorrhage resulted in a 40% reduction in the diameter of the main renal artery and a 70% decrease in the intrarenal branches during the decompensation stage. The substantial contribution of the renin angiotensin system to renal vasoconstriction in shock was demonstrated by infusion of an inhibitor of angiotensin biosynthesis during decompensation which decreased arterial blood pressure and peripheral resistance and simultaneously caused a 2 to 3 fold increase in renal arterial diameter. The response to the inhibitor was transient and reversible. Phenoxybenzamine (α adrenergic blocker) administration during decompensation reduced blood pressure, accelerated the rate or reuptake of blood, and produced a profound and sustained renal vasodilation. The combined treatment with the angiotensin synthesis antagonist and the α adrenergic antagonist fully restored renal cortical vascular diameter to levels equal to or greater than the controls.