Mechanism of natriuresis during intrarenal infusion of prostaglandins

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Abstract
Intrarenal infusion of the natural prostaglandin PGE2 increases [canine] renal blood flow renal interstitial hydrostatic pressure, and urinary Na excretion. A newly synthesized PG analog, 4-3-[3-[2-(1-hydroxycyclohexyl)-ethyl-4-oxo-2-thiazolildinyl]propyl benzoic acid, increases renal blood flow without increasing Na excretion. To investigate the role of renal interstitial hydrostatic pressure in this dissociation analog. Intrarenal infusion of PGE2 increased renal blood flow, renal interstitial hydrostatic pressure, and urinary Na excretion. Following a similar increase in renal blood flow with intrarenal infusion of PG analog, renal interstitial hydrostatic pressure and urinary Na excretion were not changed. To determine whether increases in urinary Na excretion due to PGE2 infusion are causally related to the increase in renal interstitial hydrostatic pressure rather than to the increase in renal blood flow, responses to PGE2 were obtained in the absence of increases in interstitial pressure. When renal interstitial hydrostatic pressure was held constant, urinary Na excretion did not change although there was a marked increase in renal blood flow. Increased renal interstitial hydrostatic pressure is necessary to produce an increase in urinary Na excretion with PG-mediated renal vasodilation.