The prostaglandin system. A role in canine baroreceptor control of renin release.

Abstract

SUMMARY We used the nonfiltering kidney model with contralateral nephrectomy to investigate the site where prostaglandins influence renin release. Adrenergic influences on renin release were excluded by renal denervation, bilateral adrenalectomy, and a continuous propranolol infusion. In this model, reduction of renal perfusion pressure by 50% increased renal venous renin activity from 3.10 ± 0.66 to 13.14 ± 3.8 ng of angiotensin I/ml per hour within 10 minutes (P < 0.05). This increase in renin activity was abolished by pretreatment with indomethacin, 8 mg/kg, but not by the sodium carbonate buffer in which indomethacin was dissolved. Infusion of arachidonic acid into the artery of the nonfiltering kidney at a rate of 10 ' g/kg per minute for 20 minutes also increased the renal venous renin activity from a baseline of 2.35 ± 0.37 to 5.45 ± 2.45 ng of angiotensin I/ml per hour by the end of the infusion. This effect of arachidonic acid was blocked by indomethacin. A fatty acid, 11,14,17-eicosatrienoic acid, which is not a substrate for cyclooxygenase, had no effect on renin release in this model. These data indicate that the prostaglandin system can affect the renal baroreceptor mechanism for renin release. Stimulation of prostaglandin synthesis by providing arachidonic acid increased renin secretion, and inhibition of cyclooxygenase abolished the ability of the renal baroreceptor to respond to a reduced perfusion pressure with renin release. Furthermore, this interaction is probably due to products of the renal cortical cyclooxygenase since transport of prostaglandins from the medulla to the cortex in tubular fluid cannot occur in the nonfiltering kidney.