Indirect action of angiotensin infusion to inhibit renal tubular sodium reabsorption in dogs

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Abstract
In conscious dogs during water diuresis intravenous infusion of lower doses of angiotensin (<4 [mu]g/min.) caused depression of glomerular filtration rate and renal plasma flow and Na and water retention. The effects of angiotensin on renal hemodynamics were blunted by pento-barbital anesthesia, by administration of a hypertonic urea-saline infusion, and in dogs with ascites produced by caval occlusion. With these experimental modifications, and also whenever large doses (8-50 [mu]g/min) were employed, intravenous angiotensin induced natri-uresis and diuresis with characteristics ([image]CNa/Cin, [image] Cosm, [image] CH2O or [image] TH2O) indicative of inhibition of renal tubular Na reabsorption. However, direct renal artery infusion of angiotensin under similar conditions did not produce a similar natriuresis. Therefore the data suggest that angiotensin does not inhibit tubular Na transport directly, but rather as a consequence of its effects on the systemic and renal circulation. The final natriuresis may result from an induced change in intrarenal hemodynamics or from other extrarenal factors to which tubular Na transport processes are responsive.