Intrarenal beta-receptor and renal baroreceptor interaction in the control of the renin response to transient reduction of the renal perfusion pressure in man.

We have examined the mechanisms mediating the release of renin elicited in man by reduction of renal perfusion pressure. Fifteen patients with essential hypertension and six normotensive subjects were investigated during diagnostic renal arteriography. Renal neural receptors were inhibited by propranolol (10 mg i.v.) and activated by a standard cold pressor test. Vascular receptors were stimulated by unilateral reduction of renal perfusion pressure by 50%, using a balloon-tipped catheter. The stimulus caused release of renin. In hypertensives, arterial plasma renin increased by 44, 69 and 73% of control at 5, 15 and 30 min, respectively. Adrenergic activation by cold raised the arterial and the renal venous renin by approximately 50% of control and caused a fourfold rise when it was combined with the arterial obstruction. Following propranolol the renin response to reduction of the renal perfusion pressure was delayed and reduced, and cold stimulation, both alone and in combination with arterial obstruction, failed to stimulate renin release. Findings were qualitatively and quantitatively similar in the normotensive group. This study supports the hypothesis that the renin response to reduction of renal perfusion pressure in man results from an interaction of adrenergic and vascular receptors. It cannot be stated whether the former are synergistic or supplementary to the latter, even though adrenergic activation by cold stimulation provides evidence that a synergism between the two may exist.