Endogenous Adrenergic Regulation of Renin Release in Normotensive Man

SUMMARY Exogenous infusion of catecholamines in man and electrical stimulation of renal nerves in anaesthetized animals have suggested the importance of adrenergic influence on renin release. We have studied the effect of endogenous adrenergic stimulation on renin release in seventeen apparently healthy, unanaesthetized normotensive men (mean arterial pressure 100 mEq sodium per 24 h. Plasma renin activity (PRA), expressed as nanograms angiotensin I per millilitre per hour, increased 4.1±0.76 ng/ml (range 0.3–9.7 ng/ml) in all subjects 5 h after ingestion of 80 mg frusemide. Amyl nitrite inhalation and cold pressor testing produced the appropriate haemodynamic alterations but failed to increase PRA significantly ( P >0.05). The alpha agonist, phenylephrine, decreased PRA from an average basal level of 1.21±0.16 ng/ml to 0.83±0.13 ng/ml, and the alpha blocker, phentolamine, increased PRA from an average initial level of 1.26±0.3 ng/ml to 3.61±0.6 ng/ml. Repeat inhalation of amyl nitrite with alpha blockade further elevated PRA to 4.36±0.97 ng/ml in contrast to the effect of amyl nitrite alone. These data suggest that endogenous stimulation of sympathetic nerves with amyl nitrite inhalation or cold pressor testing is not associated with measurable increase in PRA. Alpha adrenergic stimulation with phenylephrine causes a significant decrement in PRA, and alpha blockade with phentolamine significantly increases PRA. Amyl nitrite inhalation in the presence of alpha blockade further elevated PRA in direct contrast to the effect of amyl nitrite alone. Haemodynamic correlates, the elevation of PRA with alpha blockade, and the decrement of PRA with alpha stimulation suggest that alpha adrenergic receptor inhibition may account for the lack of PRA increase with endogenous sympathetic stimulation.