Effects of Sodium Chloride on Prostacyclin-Stimulated Renin Release in Dogs with Filtering and Nonfiltering Kidneys

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Abstract
The effects of intrarenal infusion of 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 PGI2 at nonhypotensive doses resulted in significant increments of renin secretion and renal blood flow in both preparations. Superimposition of intrarenal NaCl to the ongoing PGI2 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 Na concentration of 18-21 meq/l was similar in both series. The renin response to intrarenal NaCl apparently was mediated through the renal tubules, since renin secretion failed to decrease in the nonfiltering kidney preparation. PGI2-stimulated renin secretion apparently was modulated by a tubular mechanism, probably the macula densa.

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