Summary1. Tubular size and lissamine green transit times were measured in rat kidneys undergoing a diuretic response to angiotensin II (0-5 jug/kg per min), and compared with the changes observed during diuresis induced by osmotic diuretics, noradrenaline and chlorothiazide. 2. Angiotensin always caused a marked prolongation in proximal and distal tubular transit times; individual distal convolutions were coloured for prolonged periods, and lissamine green appeared in high concentration in distal tubules. 3. Marked changes were observed in superficial tubular calibre during a stable diuretic response to angiotensin. Where distal tubular diameter was normal for the rate of urine flow, proximal tubular volume was generally reduced. In a number of experiments, however, distal tubules were markedly dilated, and in these cases proximal tubular volume was also often increased. Angiotensin may therefore be capable of causing a degree of internal hydronephrosis in the rat kidney. 4. Prolongation of dye transit times, and the appearance of a concentrated lissamine green bolus in distal tubules, was suggestive of a decreased superficial nephron flow rate, indicating that the diuretic effect of angiotensin may take place only through deeper nephrons.
IntroductionAngiotensin II has been implicated in the control of sodium balance, since it is a potent stimulus to the release of aldosterone, and exerts its own anti-natriuretic effect on the kidney. Since peripheral blood renin (Brown, Davies, Lever & Robertson, 1964) and angiotensin II (Boyd, Landon & Peart, 1969) concentrations are elevated following dietary salt restriction, such a function would seem appropriate, although recent evidence indicates that animals actively immunized to angiotensin II respond normally to salt restriction and overload (Peart, 1969). Although angiotensin, infused intravenously in normal subjects in pressor and sub-pressor doses, reduces sodium and fluid excretion (De Bono, Lee, Mottram, Pickering, Brown, Keen, Peart & Sanderson, 1963), a diuretic and natriuretic response occurs in hypertensives (Nijensohn, 1957;Brown & Peart, 1962). The physiological significance of this reversal of the renal response is unknown; the diuretic effect is not maintained on continued infusion of angiotensin (Brown, 1963) and so is unlikely to play a role in causing the hyponatraemia of severe hypertension (Brown, Davies, Lever & Robertson, 1966).