Renal Pharmacology, with Special Emphasis on Aldosterone and Angiotensin

Gross, F.; Möhring, Jan

doi:10.1146/annurev.pa.13.040173.000421

Cited by 16 publications

(1 citation statement)

References 183 publications

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“…Since for the production of renal vasoconstriction only lower concentrations of renin substrate than measured in plasma of the intact rat were necessary (Hackenthal, personal communication), our results suggest that in the intact animal, where renin substrate continuously passes through the kidney, A11 is formed intrarenally in amounts sufficient to participate in the regulation of renal haemodynamics. Further studies with purified rat plasma renin substrate are necessary to obtain information as to whether A11 formed within the kidney acts predominantly on the afferent (Thurau, 1964) or on the efferent arterioles (Schnermann et al, 1970;Gross & Mohring, 1973). Investigations of this kind could also provide information on the effect of A11 on sodium reabsorbtion through changes in hydrostatic and colloidosmotic pressures in the peritubular capillaries (KrahC, Hofbauer & Gross, 1971;Waugh, 1972).…”

Section: Intrarenal Formation Of Aiimentioning

confidence: 99%

Regulation of Renin Release and Intrarenal Formation of Angiotensin. Studies in the Isolated Perfused Rat Kidney

Hofbauer

Zschiedrich

Gross

1976

Clin Exp Pharmacol Physiol

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1. Isolated rat kidneys were perfused at a constant pressure of 90 mmHg in a single-pass system with either a cell-free medium or a suspension of washed bovine red blood cells, free of the components of the renin-angiotensin system. In red blood cell perfused kidneys renal haemodynamics and sodium reabsorption corresponded closer to values observed in the intact rat than in cell-free perfused kidneys. 2. In red blood cell-perfused kidneys in the absence of plasma renin substrate autoregulation of renal blood flow was almost complete at pressures above 90 mmHg, provided that perfusion pressure was changed rapidly. 3. Renin release varied inversely with perfusion pressure within a pressure range from 50 to 150 mmHg; the greatest changes of renin release occurred, when perfusion pressure was reduced from 90 to 70 mmHg; maximal stimulation of renin release was observed at 50 mmHg. After reduction of perfusion pressure, renin release immediately started to rise and reached a new level within 5 min. Local reduction of perfusion pressure in small arteries and arterioles by the injection of microspheres induced a short-lasting decrease in renal plasma flow and a transient stimulation of renin release. 4. High concentrations of furosemide stimulated renin release by a direct intrarenal mechanism. 5. Isoproterenol stimulated renin release in low concentrations without a concomitant vasodilation, whereas high concentrations induced an increase in both renal plasma flow and renin release. The effects of isoproterenol were completely blocked by propranolol. 6. Sodium nitroprusside induced similar increases in renal plasma flow, as did high concentrations of isoproterenol, but only a small and slow increase in renin release was observed. 7. Angiotensin II (AII) suppressed renin release in concentrations corresponding to plasma levels measured in the intact rat independently of its vasoconstrictor effects, whereas vasopressin in antidiuretic concentrations did not affect renin release. 8. AII, AI, synthetic tetradecapeptide renin substrate (TDP), crude and purified rat plasma renin substrate induced a dose-dependent reduction in renal plasma flow. SQ 20 881, a competitive inhibitor of converting enzyme, and low doses of 1-Sar-8-Ala-AII (saralasin), a competitive antagonist of AII, did not change renal plasma flow, whereas high concentrations of saralasin had a vasoconstrictor effect on their own. 9. Saralasin inhibited the vasoconstrictor effects of AII and TDP to a similar degree. SQ 20 881 inhibited the vasoconstrictor effects of AI and purified renin substrate, but did not influence the actions of TDP and the crude renin substrate preparation. 10. From these data it is concluded, that AI is converted into AII within the kidney at a rate of 1-2%. The vasoconstriction induced by the crude renin substrate probably does not involve the AII receptors. TDP may act by itself on the AII receptors or via the direct intrarenal formation of AII...

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Section: Intrarenal Formation Of Aiimentioning

confidence: 99%

Regulation of Renin Release and Intrarenal Formation of Angiotensin. Studies in the Isolated Perfused Rat Kidney

Hofbauer

Zschiedrich

Gross

1976

Clin Exp Pharmacol Physiol

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Antidiuretic effect of [Sar¹, Val⁵, Ala⁸] angiotensin II in Lophius americanus

et al. 1985

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We have reported previously that angiotensin I1 increases urine flow and Na and K excretion rates in the aglomerular goosefish Lophius americanus. The present experiments were undertaken to determine if antagonism of endogenous angiotensin has the opposite renal effects. Arterial blood pressure, urine flow, and plasma and urine electrolytes were measured during two consecutive clearance periods in two groups of goosefish. The control group (n = 7) received saline intravenously during both periods; the experimental group (n = 8) received saline during the first period and a competitive antagonist of angiotensin I1 (saralasin, or [Sarl, Val5, Alas] angiotension 11) dissolved in saline during the second period. The control group exhibited no significant change over time in any of the measured variables: arterial blood pressure; plasma "a], [K], [Mg], [Ca]; osmolality; urine flow; and excretion rates of Na, K, Ca, and Mg. Arterial blood pressure and plasma electrolytes and osmolality were stable over time in the experimental group also. However, during Saralasin infusion there were significant decreases in urine flow and in excretion rates of K, Mg, and Ca. Taken together with our previous results, these observations suggest that endogenous levels of angiotensin in goosefish are sufficient to have direct renal effects. The mechanisms of action of angiotensin are not clear, but involve neither changes in systemic blood pressure nor filtration but might involve inhibitory effects of angiotensin on tubular reabsorptive processes.

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Lack of renal effects of DOCA, ACTH, spironolactone, and angiotensin II in Squalus acanthias

1985

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Angiotensin II was infused intravenously in spiny dogfish sharks (Squalus acanthias). There were no significant effects on arterial blood pressure, glomerular filtration rate, urine flow, or Na excretion either in comparison with pre- and postinfusion values or in comparison with values measured in a control group of fish given elasmobranch saline intravenously. In other dogfish, glomerular filtration rate, urine flow, and Na and K excretory rates were measured for 3 days following implantation of desoxycorticosterone (DOCA), adrenocorticotropin (ACTH), or spironolactone; a control group was given no drug. There were no significant differences between these four groups of fish with respect to any of the measured parameters. These results suggest that the dogfish kidney is not a target organ for several substances known to affect renal function, either directly or indirectly, in other animals.

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Renal Pharmacology, with Special Emphasis on Aldosterone and Angiotensin

Cited by 16 publications

References 183 publications

Regulation of Renin Release and Intrarenal Formation of Angiotensin. Studies in the Isolated Perfused Rat Kidney

Regulation of Renin Release and Intrarenal Formation of Angiotensin. Studies in the Isolated Perfused Rat Kidney

Antidiuretic effect of [Sar¹, Val⁵, Ala⁸] angiotensin II in Lophius americanus

Lack of renal effects of DOCA, ACTH, spironolactone, and angiotensin II in Squalus acanthias

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Renal Pharmacology, with Special Emphasis on Aldosterone and Angiotensin

Cited by 16 publications

References 183 publications

Regulation of Renin Release and Intrarenal Formation of Angiotensin. Studies in the Isolated Perfused Rat Kidney

Regulation of Renin Release and Intrarenal Formation of Angiotensin. Studies in the Isolated Perfused Rat Kidney

Antidiuretic effect of [Sar1, Val5, Ala8] angiotensin II in Lophius americanus

Lack of renal effects of DOCA, ACTH, spironolactone, and angiotensin II in Squalus acanthias

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Antidiuretic effect of [Sar¹, Val⁵, Ala⁸] angiotensin II in Lophius americanus