Regional Hemodynamic and Endocrine Effects of Aldosterone and Cortisol in Conscious Sheep

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Abstract
Abstract We studied the cardiovascular responses to 5 days’ infusion of aldosterone (10 μg/h) and cortisol (5 mg/h) to determine the possible contribution of mineralocorticoid and glucocorticoid actions to the regional hemodynamic changes caused by corticotropin. These infusion rates produce plasma levels similar to those seen during corticotropin stimulation. In five conscious sheep aldosterone progressively increased mean arterial pressure ( P <.001) to a maximum of 11 mm Hg on day 5, whereas cortisol increased pressure by 5 mm Hg ( P <.01) within 24 hours. Cardiac outputs on the control day and on day 5 of infusion were 4.4±0.3 and 4.9±0.3 L/min, respectively, for aldosterone and 4.3±0.4 and 5.0±0.4 L/min for cortisol. Neither steroid significantly altered total peripheral conductance, but they had different, nonuniform regional hemodynamic effects. Mesenteric conductance fell progressively with aldosterone from 7.14±0.35 (mL/min)/mm Hg to a minimum of 6.17±0.38 ( P <.01) on day 5 of infusion. Mesenteric conductance was transiently reduced with cortisol, but this was not significant over the 5 days. Renal conductance was unchanged with aldosterone, but cortisol caused a rapid, sustained increase in renal conductance from 2.9±0.3 to 4.0±0.4 (mL/min)/mm Hg ( P <.001) within 24 hours, similar to the increase caused by corticotropin. As with corticotropin there were only minor changes in the coronary and iliac vascular beds. In summary, these two endogenous steroids had contrasting, nonuniform regional hemodynamic effects, aldosterone causing mesenteric vasoconstriction, and cortisol causing renal vasodilatation. These findings suggest that corticotropin-induced renal vasodilatation is caused by the cortisol released by corticotropin and the mesenteric vasoconstriction partly depends on the mineralocorticoid actions of the adrenocortical steroids released by corticotropin.