Regulation of sodium excretion by renal interstitial hydrostatic pressure.
Renal interstitial hydrostatic pressure (RIHP) appears to play a crucial role in linking the renal circulation to the rate of tubular reabsorption of sodium and water. Various physiological and pharmacological maneuvers that increase RIHP are associated with increases in sodium excretion. Renal vasodilators that increase RIHP also increase sodium excretion, whereas the vasodilators that do not alter RIHP do not affect sodium excretion. Preventing increases in RIHP during intrarenal infusion of vasodilators markedly attenuates the normal increase in sodium and water excretion. Techniques that directly increase RIHP by renal interstitial volume expansion increase urinary excretion of sodium and water. RIHP may be an important mediator of renal perfusion pressure (RPP) natriuresis. Experimental evidence suggests that the proximal tubule of deep nephrons may be an important nephron site that is sensitive to changes in RPP.
D000042:Absorption; D000818:Animals; D001794:Blood Pressure; D005110:Extracellular Space / Q000502:physiology*; D006801:Humans; D006874:Hydrostatic Pressure; D007668:Kidney / Q000098:blood supply / Q000502:physiology*; D007687:Kidney Tubules, Proximal / Q000502:physiology; D009318:Natriuresis; D011312:Pressure; D014664:Vasodilation