The effect of atrial natriuretic peptide (ANP) on renal kallikrein release was investigated in barbiturate anesthetized rats. ANP injections in a pharmacological dose (1 microgram i.v.) increased kallikrein excretion for about 15 min. The effect of ANP on kallikrein excretion was abolished when amiloride (2.5 mg i.v.) was administered prior to the injection of the peptide. Intravenous infusion of ANP (1 or 5 micrograms/h) or of isotonic saline (2 or 4 ml/h) did not alter urinary kallikrein output. When the ANP infusion was discontinued, the excretory rate of the enzyme tended to decrease. This decrease was prevented by the administration of 0.1 mg/h desoxycorticosterone-glucoside. A transient increase in kallikrein excretion, coincident with the appearance of diuresis, was observed during ANP infusion in the mineralocorticoid-treated animals. The rate of kallikrein release into the incubation medium by rat kidney slices was not affected by the presence of ANP (10(-9)M). These results can be interpreted as effects following an increased distal sodium delivery rather than a direct effect of ANP on connecting tubule cells (CNT cells).
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