Abstract
The influence of altered rates of intrarenal prostaglandin synthesis on known renin control mechanisms was studied in single, filtering and nonfiltering, denervated kidneys of chloralose anesthetized dogs. Infusion of indomethacin directly into the renal artery resulted in 50% reduction in renin and prostaglandins effluxing from the renal vein. The increased plasma renin resulting from suprarenal aortic constriction was unaffected by indomethacin despite suppressed renal vein prostaglandin efflux. Renin response to furosemide was blunted by prior renal arterial indomethacin administration even though furosemide had no influence on prostaglandin efflux. Renin secretion was suppressed by intrarenal indomethacin administration in nonfiltering kidneys. Intrarenal arachidonic acid infusion resulted in parallel increases in renin and prostaglandin in both papaverine-treated and untreated, nonfiltering, denervated kidneys. Imposition of intrarenal indomethacin during arachidonic acid infusion in nonfiltering kidneys suppressed prostaglandin efflux from papaverine-treated and untreated kidneys; renin secretion was suppressed by indomethacin in only the control kidney. Since renin was stimulated by arachidonic acid in nonfiltering, denervated, papaverine-treated kidneys the in vivo intrarenal cyclooxygenase-dependent conversion of arachidonic acid to prostaglandins apparently exerts its influence on renin secretion by a direct influence on juxtaglomerular cells and is independent of other presently recognized renin control mechanisms.