Influence of hypertonic saline on canine renal blood flow and renin release

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Abstract
An intrarenal artery infusion of NaCl to increase plasma osmolality by 60 mosM in the canine kidney induced an initial transient increase in renal blood flow (RBF) followed by a sustained reduction in RBF from 179 .+-. 11 to 82 .+-. 10 ml/min (P < 0.01). Ten minutes after the start of the infusion, the glomerular filtration rate was reduced proportionately to the RBF (from 26 .+-. 3 to 11 .+-. 2 ml/min, P < 0.01), so that the filtration fraction remained unchanged. Renal renin secretion rate was almost completely inhibited, while urinary Na excretion increased by 84-fold. A similar infusion of hypertonic NaCl into the superior mesenteric artery or an intrarenal infusion of hypertonic glucose or urea only induced vasodilation. The renal vasoconstrictor response to hypertonic NaCl was abolished by prior therapy with deoxycorticosterone acetate and a high Na diet, an acute i.v. load of NaCl or by high doses of furosemide. Prior therapy with SQ 20881, saralasin, phentolamine or indomethacin had no effect on the vasoconstriction. The vasoconstrictor response to infusion of hypertonic NaCl appears to be unique to the renal vasculature and independent of the renin-angiotensin system. NaCl in renal tubules can initiate a feedback to alter renal vascular resistance.

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