Interactions among renal nerves, prostaglandins, and renal arterial pressure in the regulation of renin release
Osborn, J.L.; Kopp, U.C.; Thames, M.D.; DiBona, G.F.
American Journal of Physiology 247(5 Pt 2): F706-F713
1984
ISSN/ISBN: 0002-9513 PMID: 6388358 Document Number: 227276
To examine the interactions among the renal nerves, prostangladins and renal arterial pressure in the regulation of renin secretion, experiments using low-frequency renal nerve stimulation (LFRNS; supramaximal voltage, 0.5 ms, 0.5 Hz) were performed in anesthesized dogs. LFRNS, which did not affect renal hemodynamics or urinary sodium excretion, increased renin secretion rate before (79 .+-. 16 ng/min) but significantly less after renal arterial administration of indomethacin or meclofenamate (26 .+-. 7 ng/min). In a separate group of dogs, LFRNS increased both renin secretion rate (266 .+-. 139 ng/min) and renal prostaglandin E2 secretion rate (2080 .+-. 635 ng/min). LFRNS does not alter input stimuli to the renal vascular baroreceptor or tubular macula densa receptor mechanisms for renin secretion and represents a direct neural stimulus for renin secretion; this also increases renal prostaglandin E2 secretion rate, which contributes to the increase in renin secretion rate. The renin secretion rate response of innervated and denervated kidneys to reduction in renal arterial pressure to 50 mm Hg was examined before and after indomethacin/meclofenamate administration. The observation that indomethacin/meclofenamate decreased but did not abolish the renin secretion rate response to aortic constriction in innervated kidneys suggests the presence of a prostaglandin-independent mechanism that is mediated by an interaction between the renal nerves and the tubular macula densa receptor, as indomethacin/meclofenamate essentially abolished the renin secretion rate response to aortic constriction in denervated kidneys.