Effects of alpha- and beta-adrenoceptor blockade on purine secretion induced by sympathetic nerve stimulation in the rat kidney

To characterize the effects of renal sympathetic nerve activation (RSNA) on renal purine secretion, 13 perfused rat kidneys were stimulated with peria rterial electrodes at 7 Hz for 3 min, and purine secretion was determined b y measuring with highperformance liquid chromatography purines in the renal venous perfusate 1 min before and during the last minute of RSNA. RSNA sig nificantly increased renal perfusion pressure and significantly increased t he secretion of adenosine and adenosine metabolites (inosine, hypoxanthine, and xanthine) by 2- to 5-fold. To investigate the participation of alpha- and beta-adrenoceptors in this response, four groups of perfused kidneys (n = 5/group) were pretreated with either vehicle, prazosin (alpha(1)-adrenoc eptor antagonist; 0.03 mu M), phentolamine (alpha(1/2)-adrenoceptor antagon ist; 3 mu M), or propranolol (beta(1/2)-adrenoceptor antagonist; 0.1 mu M), and purine secretion was measured before and during RSNA at 1, 3, 5, 7, an d 9 Hz. Prazosin, phentolamine, and propranolol abolished the RSNA-induced increase in the secretion of adenosine, inosine, hypoxanthine, and xanthine . In contrast, prazosin and phentolamine nearly abolished, whereas proprano lol only slightly reduced, renal vascular responses to RSNA. Our results in dicate that RSNA increases renal purine secretion via a mechanism that requ ires both alpha- and beta-adrenoceptors. It is well known that in the kidne y adenosine activates renal afferent nerves, enhances renovascular response s to norepinephrine and angiotensin II, and increases sodium reabsorption; therefore, RSNA-induced adenosine production may contribute to the hyperten sive effects of RSNA, Moreover, the antihypertensive effects of beta-adreno ceptor antagonists may in part be due to inhibition of RSNA-induced renal a denosine production.