EVIDENCE FOR THE PARTICIPATION OF β1‐ADRENOCEPTORS IN ISOPRENALINE‐INDUCED RENIN RELEASE FROM RAT KIDNEY SLICES in vitro

E, Desaulles; Miesch, F; Schwartz, Jean

doi:10.1111/j.1476-5381.1978.tb07793.x

Cited by 17 publications

(6 citation statements)

References 12 publications

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“…The present investigation provides evidence that nerve-mediated renin release in the cat occurs via activation of 3-adrenoceptors which are more like those of the heart than those of the peripheral vascu-lature. This supports studies in other species such as man (Esler & Nestel, 1973;Aberg 1974;Gavras et al, 1979), rat (Desaulles, et al, 1978;Oates et al, 1978) and dog (Himori et al, 1980;Kopp et al, 1980) all of which suggested that adrenergicallymediated renin release relied on Pl-adrenoceptors.…”

Section: Discussionsupporting

confidence: 81%

“…It is entirely possible that during the preparation of the renal cortical cells (Johns et al, 1975) the pretreatment could have in some way modified receptors on the surface membranes of the cells. Such a suggestion is supported by the fact that relatively high doses of catecholamines were used as compared to other in vitro studies which employed kidney slices (Desaulles et al, 1978;Weinberger, Aoi & Henry, 1975) in which the use of collagenase-like enzymes had been avoided. Weber et aL (1974) using the conscious rabbit, indicated that P2-adrenoceptors were involved in mediating renin release.…”

Section: Discussionmentioning

confidence: 99%

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An INVESTIGATION INTO THE TYPE OF Β‐ADRENOCEPTOR MEDIATING SYMPATHETICALLY ACTIVATED RENIN RELEASE IN THE CAT

Johns

1981

British J Pharmacology

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1 Stimulation of the renal nerves in the cat was previously shown to cause renin release which could be blocked by propranolol. An attempt was made in this study to determine the type -ofadrenoceptor mediating this response. 2 In anaesthetized, unilaterally nephrectomized cats, a comparison was made of the ability of two selective 3-adrenoceptor antagonists to block the tachycardia and hypotension caused by isoprenaline (mediated respectively by 3l-and P2-adrenoceptors) and the release of renin caused by renal nerve stimulation. 3 Isoprenaline (mean dose of 0.224 ± 0.022 nmol/kg), increased heart rate by approximately 43 beats/min and decreased mean blood pressure by 47 mmHg. Stimulation of the distal cut ends of the renal nerves, at a rate sufficient to reduce renal blood flow by 30%, resulted in an approximately 150% increase in plasma renin activity.4 Administration of the selective ,1-adrenoceptor antagonist, atenolol (0.38 to 11.28 pmol/kg), caused a dose-related inhibition of nerve stimulated renin release and of isoprenaline-induced tachycardia, with no diminution of the vasodepressor response to isoprenaline; in contrast, the selective 32-adrenoceptor antagonist, erythro-DL-(7-methylindan-4-yloxy)-3-isopropylaminobutan-2-ol (ICI 118, 551, 0.03 to 2.86 imol/kg), caused a dose-related inhibition of the isoprenaline-induced vasodepression without altering the increase in plasma renin activity caused by renal nerve stimulation. Only at the highest dose of ICI 118, 551 was there a reduction of isoprenaline-induced tachycardia, by about 40%. 5 The selective inhibition of neurally activated renin release by atenolol but not by ICI,118,551 is consistent with the suggestion that the 13-adrenoceptors mediating renin release resemble those in the heart more closely than those in peripheral blood vessels.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

An INVESTIGATION INTO THE TYPE OF Β‐ADRENOCEPTOR MEDIATING SYMPATHETICALLY ACTIVATED RENIN RELEASE IN THE CAT

Johns

1981

British J Pharmacology

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“…In our experiments after pindolol, propranolol or practolol pre treatment, P R A and R R A remained un changed (table IV); however, A R F devel oped in all cases despite low PRA and R R A . We did not find any differences in the adren ergic activity and PRA-and RRA-decreasing effect of the different beta blockers in A R F , emphasizing the primary role of intrarenal beta, receptors in mediation of renin release [12,19,28], Our results indicate that the increased activity of R A S may be the result, rather than the cause, of cortical ischemia in A R F , but the increased R R A may be an aggravat ing factor in the pathomechanism of mercu ry-induced A R F ; and that the increase in renin release is mediated through beta recep tors, bot of beta, and beta, types.…”

Section: Discussionmentioning

confidence: 83%

Effect of Beta-Receptor Antagonists on HgCl2-Induced Acute Renal Failure in Rats

K¹,

Siklós²

1982

Kidney Blood Press Res

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During the first 48 h of HgCl₂-induced acute renal failure (ARF), a single intraperitoneal injection of 100–100 µg/kg of the beta-adrenergic blockers pindolol, pro-pranolol and practolol caused a significant rise in urinary sodium excretion and a decrease in plasma renin activity (PRA), renal cortical renin activity (RRA) and urinary catecholamine excretion. A single intraperitoneal injection of 3 mg/kg HgCl₂ resulted in ARF characterized by progressive azotemia, a transient increase in PRA, a progressive rise in RRA and urinary catecholamine excretion. After pretreatment with these beta blockers, PRA, RRA and urinary catecholamine excretion remained unchanged and azotemia was markedly reduced; urine flow rates did not fall, and were significantly higher than control flows till after 48 h. These results indicate that pretreatment with beta blockers decreases the severity of ARF, though they cannot prevent is; that increased activity of the sympathetic nervous system is involved in ARF and that increase in RRA may be an aggravating factor in the pathomechanism of the nephrotoxic model in ARF.

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“…In each tube a single slice was incubated at 370C in 2 ml of gassed (95% 02: 5% C02) medium. (Desaulles, Miesch & Schwartz, 1978).…”

Section: Methodsmentioning

confidence: 99%

“…the actions of drugs) were reversible. The amounts of renin released during periods II and III are expressed as percentages of renin released during reference period I (Desaulles, Miesch & Schwartz, 1978).…”

Section: Incubation Of Kidney Slicesmentioning

confidence: 99%

A Comparative Study of the Action of Frusemide and Methyclothiazide on Renin Release by Rat Kidney Slices and the Interaction With Indomethacin

Schwartz

1979

British Journal of Pharmacology

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The effects of frusemide (a diuretic acting on the loop of Henle) and methyclothiazide (a thiazide diuretic) on renin release were studied on rat kidney slices. Frusemide at concentrations of 1.5 and 7.5 mmol/1 produced significant increases in renin release but had no effect at 0.15 mmol/1. Methyclothiazide in a similar concentration range did not increase renin release; instead, at the highest concentration used, methyclothiazide (3.5 mmol/1) inhibited renin release. Indomethacin (25 μmol/1) did not inhibit the increase of renin induced by frusemide. Our limited study in vitro is consistent with the findings of other workers who have shown in vivo, in the absence of systemic electrolyte depletion, that only loop diuretics' increase renin secretion. Under our experimental conditions, it is suggested that frusemide exerts a direct action either upon the epithelioid cells or upon the macula densa since the renal prostaglandin system does not intervene.

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EVIDENCE FOR THE PARTICIPATION OF β₁‐ADRENOCEPTORS IN ISOPRENALINE‐INDUCED RENIN RELEASE FROM RAT KIDNEY SLICES in vitro

Cited by 17 publications

References 12 publications

An INVESTIGATION INTO THE TYPE OF Β‐ADRENOCEPTOR MEDIATING SYMPATHETICALLY ACTIVATED RENIN RELEASE IN THE CAT

An INVESTIGATION INTO THE TYPE OF Β‐ADRENOCEPTOR MEDIATING SYMPATHETICALLY ACTIVATED RENIN RELEASE IN THE CAT

Effect of Beta-Receptor Antagonists on HgCl<sub>2</sub>-Induced Acute Renal Failure in Rats

A Comparative Study of the Action of Frusemide and Methyclothiazide on Renin Release by Rat Kidney Slices and the Interaction With Indomethacin

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