The effect of val-äangiotensin-II-amide on tubular sodium and water reabsorption in the rat kidney was studied by micropuncture techniques. An angiotensin infusion of 0.2–0.5 µg/min/kg caused a significant increase ( + 16 mEq/l) in the sodium concentration of tubular fluid collected from the distal tubule, as compared to collections made from the same site of the tubule during saline infusion alone. TF/P-inulin ratio remained unchanged. Glomerular filtration rate, sodium and water excretion were unaltered. During an angiotensin infusion of 1.0-1.5 µg/min/kg a similar elevation of the distal tubular sodium concentration was observed, but TF/P-inulin ratio decreased significantly. Urinary water and sodium excretion increased. An elevation of the intratubular concentration of angiotensin to 2.5 µg/ml had no effect upon tubular reabsorptive capacity, as measured by the ‘split oil-droplet method’ in the proximal or in the distal tubule. Direct application of angiotensin from the capillary side of the tubule by peritubular perfusion did not alter ‘reabsorptive half-time’ in the proximal tubule, but caused a significant prolongation of ‘reabsorptive half-time’ in the distal tubule from 35.6–67.7 sec. These results demonstrate that angiotensin, offered from the capillary side of the tubule, directly inhibits sodium reabsorption in the distal tubule.

A B S T R A C T The function of the short loops of Henle was investigated by micropuncture technique in normal rats, in rats with spontaneous hypertension, and in the untouched kidney of rats with experimental renal hypertension. All animals received a standard infusion of 1.2 ml of isotonic saline per hr.With increasing arterial blood pressure (range from 90 to 220 mm Hg), a continuous decrease in transit time of Lissamine green through Henle's loop from 32 to 10 sec was observed. Fractional water reabsorption along the loop declined progressively from 26 to 10%, and fractional sodium reabsorption decreased from 40 to 36% of the filtered load. The fluid volume in Henle's loop calculated from transit time and mean flow rate also decreased with increasing blood pressure. There was no change in superficial single nephron filtration rate but there was a slight increase in total glomerular filtration rate (GFR). Sodium and water reabsorption in the proximal tubule remained unchanged.Urine flow rate, sodium excretion, osmolar clearance, and negative free water clearance increased with increasing blood pressure. The osmolal urine to plasma (U/P) ratio declined but did not fall below a value of 1.5. It is concluded that the increase in sodium and water excretion with chronic elevation of arterial blood pressure is caused by a decrease of sodium and water reabsorption along the loop of Henle, presumably as a consequence of increased medullary blood pressure. The following three groups of animals were used: (a) normal rats, (b) rats with a moderate spontaneous hypertension, and (c) rats with experimental hypertension 4-5 wk after clamping one renal artery with a Goldblatt clamp. In the last group, only the untouched kidney, which is exposed to the high blood pressure, was investigated. All animals received an isotonic saline infusion of 1.2 ml/hr. Micropuncture experiments were done on superficial nephrons. Accordingly, only the function of short loops of Henle was studied. METHODSThe experiments were performed on Albino rats of about the same weight (190-210 g). The animals were divided into three groups differing from each other by the level of arterial blood pressure. For the first group male rats-of the FW4, strain (Paderborn) were chosen, having a mean arterial blood pressure between 90 and 110 mm Hg. The second group consisted of female rats of the Wistar strain with a blood pressure from 110 to 160 mm Hg. In the third group female Wistar rats with experimental renal hypertension of 4-5 wk duration (for the method see reference 12, 13) were used, their blood pressure ranging from 160 to 220 mm Hg. In this last group only the untouched kidney exposed to the high arterial blood pressure was investigated. All animals were kept on the same standard rat diet (Altromin, sodium content: 1200 mg/kg) and had free access to water. The animals were anaesthetized by intraperitoneal injection of Inactin Hamburg,(70)(71)(72)(73)(74)(75)(76)(77)(78)(79)(80) mg/kg body weight) and prepared for micropuncture as previously describe...

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Five dogs were rendered hydropenic by withholding water for 20 hours and mildly alkalotic by the infusion of sodium bicarbonate intravenously in small amounts. Under these conditions alkaline urine was formed at approximately 1.0 cc/min. In 15 control periods the pCO2 of the urine exceeded that of the plasma, the ratio averaged 2.08 ± 0.44 (S.D.) with a range of 1.45–2.79. Following the intravenous administration of 100 mg of carbonic anhydrase as a priming dose and the infusion of the enzyme at a rate of 1 mg/min., the ratio in 25 experimental periods decreased to an average of 0.988 ± 0.14 (S.D.) with a range of 0.78–1.30. We conclude that the high carbon dioxide tensions commonly observed in alkaline urines result from delayed dehydration of carbonic acid to carbon dioxide in the renal tubule.