Stretch receptor control of renin release in perfused rat kidney: effect of high perfusate potassium.

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Abstract
These studies were conducted in the isolated perfused rat kidney to determine the effect of high perfusate K on the renin release induced by low perfusion pressure, renal vasoconstriction and isoprenaline, and to determine whether the magnitude of the K-induced inhibition equalled that observed with renal vasodilation and high perfusion pressure. Raising perfusate K concentration from 4.2 to 56 mM suppressed basal renin release and the 56 mM-K inhibited the renin release induced by low perfusion pressure (50 mmHg) or phenylephrine (0.83 .mu.M). Isoprenaline (0.79 .mu.M) induced a marked increase in renin release; but high perfusate K, propranolol (0.28 mM), papaverine (0.39 mM) or high perfusion pressure (150 mmHg) inhibited this effect. Apparently high perfusate K has a powerful inhibitory effect on the renin release induced by renal hypotension, vasoconstriction, and isoprenaline infusion, and that this effect may be mimicked by high perfusion pressure or renal vasodilation. A mechanism is proposed whereby these signals may inhibit renin release by depolarizing the juxtaglomerular granular cells.

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