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Vasopressin affects renal tubular dynamics during hemorrhagic shock resuscitation

Novel roles of cardiovascular regulating hormones in severe hemorrhagic shock may be differentiated by their affect on renal function when used as pressor agents during resuscitation. We thus investigated whether vasopressin (VP), norepinephrine (NE), or phenylephrine (PE), differentially affect renal fluid handling when restoring mean arterial pressure (MAP) after acute rapid hemorrhage (34 ml/kg in 20 min) in anesthetized Yorkshire cross pigs (n=18, 31.4±0.4 kg body wt). A severe hypotensive state sustained for 1 hour was associated with a 77% drop in urine flow to 3.6±0.5 μl/kg/min. While glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) both decreased with shock, filtration fraction increased with hemorrhage coincident with elevated renin activity, indicating selective efferent arteriolar constriction by angiotensin. With resuscitation, MAP was equally restored by all pressor agents to 63±4 mm Hg, which resulted in restoration of urine flow, ERPF and GFR. VP caused a dramatic six‐fold increase in urine flow not seen with PE or NE, and thus not explained by a pure pressure‐related diuresis. Indeed, VP induced significantly higher osmotic clearance and fractional excretions of sodium, potassium, and urea that did not occur with PE or NE. Therefore VP appears to have a novel role of manipulating renal tubular dynamics in regulation of blood pressure in severe hemorrhagic shock.