The effect of angiotensin on renal carbonic anhydrase

Healy, J. K.; Douglas, J. B.

doi:10.1016/0005-2744(68)90119-8

Cited by 2 publications

(2 citation statements)

References 7 publications

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“…However, in contrast to angiotensin, acetazolamide does not increase chloride excretion (Berliner et al, 1951). Further, angiotensin does not inhibit rabbit renal carbonic anhydrase in vifro (Healy & Douglas, 1968). Clearly, angiotensin does not cause natriuresis primarily by inhibition of carbonic anhydrase in the kidney.…”

Section: Discussiwmentioning

confidence: 92%

Multiple Changes in Distal Stop-Flow Electrolyte Patterns and Reduction of Acid Excretion Induced in Rabbits by Angiotensin

Healy

Elliott

1976

Clinical Science

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1. Angiotensin has previously been shown to inhibit distal renal tubular sodium reabsorption. As a consequence of this, or independently, it might influence the distal handling of other electrolytes. We have therefore examined the effects of angiotensin on the distal reabsorption or secretion of a spectrum of electrolytes. 2. Standard bilateral stop-flow studies were done on anaesthetized, adrenalectomized rabbits, in which the effects of intravenous infusions of either 0-02-0-05 mug min-1 kg-1 or 1 mug min-1 kg-1 of angiotensin were compared with control stop-flow results. 3. The lower dose of angiotensin inhibited distal sodium, chloride, water and magnesium reabsorption, inhibited distal hydrogen secretion and stimulated distal potassium secretion. The higher dose of angiotensin produced these changes and additionally inhibited distal calcium reabsorption. Most of the observed changes were dose-related. The low dose of angiotensin did not significantly raise blood pressure but the high dose was pressor. 4. Changes in the stop-flow patterns induced by the higher dose of angiotensin were compatible with, and may help to explain, the changes it produced in urinary excretion of sodium, chloride, potassium, magnesium and calcium in clearance studies before stop-flow. Suppression of hydrogen secretion caused by both doses of angiotensin in the stop-flow studies was also reflected by reductions in acid excretion produced by these infusion rates in additional experiments performed by clearance methods in acid-loaded, conscious rabbits. 5. The results support the view that angiotensin may have an important intrarenal role, at least in rabbits.

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Section: Discussiwmentioning

confidence: 92%

Multiple Changes in Distal Stop-Flow Electrolyte Patterns and Reduction of Acid Excretion Induced in Rabbits by Angiotensin

Healy

Elliott

1976

Clinical Science

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“…The natriuresis is apparently due to an inhibition of tubular reabsorptive capacity, but angiotensin does not inhibit active sodium transport in isolated amphibian skin (McAfee & Locke, 1967) or isolated, perfused rabbit proximal tubules (Burg & Orloff, 1968). In addition, no inhibitory effect could be detected on renal carbonic anhydrase (Healey & Douglas, 1968) or Na-K activated adenosine triphosphatase activity (Bonting, Canady & Hawkins, 1964).…”

Section: Introductionmentioning

confidence: 96%

Renal tubular flow dynamics during angiotensin diuresis in the rat

Finberg

Peart

1970

British J Pharmacology

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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).

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The effect of angiotensin on renal carbonic anhydrase

Cited by 2 publications

References 7 publications

Multiple Changes in Distal Stop-Flow Electrolyte Patterns and Reduction of Acid Excretion Induced in Rabbits by Angiotensin

Multiple Changes in Distal Stop-Flow Electrolyte Patterns and Reduction of Acid Excretion Induced in Rabbits by Angiotensin

Renal tubular flow dynamics during angiotensin diuresis in the rat

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