Abstract
Abstract
The effects of intrarenal infusion of sodium chloride (NaCl) on prostacyclin (PGI2)-stimulated hyperreninemia were examined in groups of anesthetized dogs with either a single filtering kidney or a single denervated nonfiltering kidney, a model in which the renal tubules are damaged, and the macula densa is nonfunctional. After control observations, intrarenal infusion of prostacyclin at nonhypotensive doses resulted in significant increments of renin secretion and renal blood flow (RBF) in both preparations. Superimposition of intrarenal NaCl to the ongoing prostacyclin infusion produced a striking decrease of renin secretion in dogs with a filtering kidney. In contrast, dogs with a nonfiltering kidney failed to show a significant change in renin secretion during intrarenal NaCl administration. Renal blood flow remained unaffected by NaCl in both groups. The increment in renal venous plasma sodium concentration of 18-21 meq/liter was similar in both series. It is proposed that the renin response to intrarenal NaCl was mediated through the renal tubules, since renin secretion failed to decrease in the nonfiltering kidney preparation. Thus, the present results indicate that prostacyclin-stimulated renin secretion was modulated by a tubular mechanism, probably the macula densa.
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