Influence of plasma renin content, intrarenal angiotensin II, captopril, and calcium channel blockers on the vasoconstriction and renin release promoted by adenosine in the kidney.

Our study was undertaken to assess whether the effect of intrarenal infusion of adenosine on renal blood flow and renin release in dogs is modified by the degree of stimulation of the intrarenal renin-angiotensin system. This system was modified by sodium deprivation, extracellular volume expansion, beta-adrenergic blockade and stimulation, angiotensin II infusion, and inhibition of converting enzyme by captopril. In addition, the effect of blocking slow calcium channels with verapamil on the vasoconstrictor effect of adenosine was also studied. Results demonstrate that the vasoconstrictor effect of adenosine was not modified by the status of stimulation or inhibition of the renin-angiotensin system or by the status of expansion of the extracellular volume. In all cases adenosine inhibited the renal secretion of renin. Verapamil abolished the vascular actions of adenosine, but it had no effect on the inhibition of renin release. We conclude that plasma renin or angiotensin II levels are not a necessary determinant of the renal vasoconstriction induced by adenosine. This effect seems to be mediated by the entry of calcium into the cell.