Mechanisms of adenosine-induced renal vasodilatation in hypertensive patients

Abstract

BACKGROUND: Adenosine is an endogenous nucleoside with potent vasodilatory capacities, released under ischaemic conditions in particular. Its mechanisms of action, however, remain elusive. OBJECTIVE: To evaluate the role of adenosine, using a non-selective purinergic receptor antagonist, and the possible involvement of nitric oxide in this mechanism. In addition, the production of renin and catecholamines was studied during infusion of adenosine, caffeine, or both. METHODS: Thirty-three hypertensive patients who underwent diagnostic renal angiography received intrarenal infusions of adenosine either alone or in combination with caffeine or the nitric oxide synthase inhibitor, N-monomethyl-L-arginine (L-NMMA). The effects on renal blood flow (RBF) were assessed by the xenon-133 washout technique and both arterial and renal venous blood samples were taken for measurement of renin and catecholamine concentrations. Intra-arterial blood pressure and heart rate were monitored continuously. RESULTS: Adenosine induced a dose-dependent vasodilatation. Caffeine alone did not change RBF, but shifted the dose-response curve of adenosine to the right during concomitant infusion of caffeine. RBF during combined infusion of L-NMMA and adenosine was not different from that during adenosine alone, but the decrease in renal vascular resistance was less pronounced during this combination. Renin secretion did not change during the infusion of either adenosine alone or adenosine in combination with caffeine. Catecholamine concentrations also did not change during any of the experiments. CONCLUSIONS: Adenosine induces vasodilatation in the human hypertensive kidney and this effect is mediated by the adenosine receptor. Nitric oxide plays, at most, a minor part in the adenosine-induced vasodilatation. Furthermore, renin secretion is not affected by adenosine and caffeine.