SUMMARY The isolated dog kidney was perfused with blood containing 1 m-u. arginine vasopressin/ml. In other experiments 40 or 50 m-u./min. were infused into three intact dogs. Antidiuretic activity was measured in renal venous blood, arterial blood, and in the urine. Renal blood flow was determined directly in the perfused dog kidney and by p-aminohippuric acid clearance in the intact dog; glomerular filtration rate was measured by either inulin or creatinine clearance. About 38% of the hormone was extracted from the arterial blood in its passage through the kidney. Of the total amount of hormone infused, about 18% was eliminated by each kidney. The quantity of vasopressin extracted from the blood was greater than that excreted in the urine, indicating that the hormone is inactivated by the kidney. In intact dogs, the amount of hormone filtered by the kidney was less than that excreted, suggesting tubular secretion. It was calculated that the release of endogenous arginine vasopressin induced by the stimuli of anaesthesia and surgery was between 3 and 7 m-u./min. and that approximately 15% of the endogenous hormone was excreted. Ultrafiltration of dog plasma at three different concentrations of arginine vasopressin (30, 100 and 290 μ-u./ml.) showed that binding was reduced as the concentration was raised and that at the concentration of hormone in the experiments, less than 30% was bound. The difficulties of relating these findings at artificially high blood concentrations to those at physiological blood concentrations of vasopressin are discussed.
The effects of intracerebroventricular (ICV) infusion of atrial natriuretic factor (ANF; atriopeptin III) on renal function, plasma concentrations of antidiurectic hormone, aldosterone, and plasma renin activity (PRA) were examined in anesthetized rats and sodium-depleted conscious sheep. The results were compared with those obtained by intravenous infusion of the same dose of ANF. In both rats and sheep, urine volume was increased four- to sixfold over basal values by ICV infusion of ANF. The response was not associated with increased excretion of sodium or potassium. However, urine osmolality was decreased, and free water clearance increased. Intravenous infusion of the same dose of ANF was without effect. Neither mean arterial blood pressure nor heart rate was changed by the ICV infusion of ANF. In the sheep, renal plasma flow showed no significant changes and glomerular filtration rate was unaltered with the exception of a single experimental period out of four periods of ICV ANF infusion. Plasma concentration of ADH was decreased and PRA increased, whereas aldosterone levels remained unchanged as a function of ICV ANF. In the rat, the diuretic response to ANF was prevented by continuous intravenous infusion of a subpressor dose of ADH. These results suggest that ANF within the central nervous system inhibits secretion of ADH.
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