Evidence for beta adrenoceptors in proximal tubules. Isoproterenol-sensitive adenylate cyclase in pars recta of canine nephron.

Murayama, Naoki; Ruggles, B T; Gapstur, Susan M.; Werness, J.L.; Douša, Thomas P.

doi:10.1172/jci111996

Cited by 16 publications

(3 citation statements)

References 30 publications

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“…25 Moreover, the majority of renal /3-adrenergic receptors are located in distal tubules, 132 and the physiological role of these /3-adrenergic receptors is not yet understood. Because renal a r adrenergic and a 2 -adrenergic receptors can act via generation of inositol phosphates and inhibition of adenylyl cyclase, respectively (see Reference 60 for review) and because renal /3-adrenergic receptor can inhibit a-adrenergic generation of inositol phosphates 136 and can stimulate adenylyl cyclase, 137 ' 138 it is tempting to speculate that the up-regulation of renal /3-adrenergic receptors is a physiological mechanism to counteract the increased renal o-adrenergic tone. No experimental data, however, are available to support or disprove this speculation.…”

Section: Renal Fi-adrenergic Receptorsmentioning

confidence: 99%

Peripheral adrenergic receptors in hypertension.

1990

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Increased sympathoadrenal activity appears to play an important role in the development or maintenance of elevated blood pressure in hypertensive patients and various annual models of hypertension. Alterations of adrenergic receptor number or responsiveness might contribute to this increased activity. We therefore reviewed the data on adrenergic receptor alterations in hypertension with special emphasis on several key cardiovascular tissues (i.e., heart, vascular smooth muscle, and kidney) and on lymphocytes and platelets as human tissues available for such studies. The data suggest that the number of o-adrenergic receptors in hypertension is regulated by catecholamines, dietary salt intake, and genetic factors. Increases in renal cv-adrenergic receptor number may be etiologic in genetic forms of essential hypertension. ^Adrenergic receptor alterations in states of elevated blood pressure do not appear to be specific for genetic hypertension. Desensitization of ^-adrenergic receptor function in hyper-tensive animals and patients contrasts with reports of decreased, unchanged, and increased /3-adrenergic receptor number, suggesting that signal transduction of /3-adrenergic (and possibly other) receptors that stimulate adenylyl cyclase is disturbed in hypertension. The mechanisms of such heterologous desensitization in states of elevated blood pressure remain to be elucidated. (Hypertension 1990;16:107-120)

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Section: Renal Fi-adrenergic Receptorsmentioning

confidence: 99%

Peripheral adrenergic receptors in hypertension.

1990

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“…Isoproterenol-sensitive cAMP accumu lation was demonstrated in intact proximal tu bule suspensions from rat kidneys, suggesting that functional (3-adrenoreceptors are present along the rat proximal tubule [16,17], How ever, isoproterenol-stimulated adenylate cy clase activity has been demonstrated in the microdissected proximal straight tubule from the dog. but not the rat kidney [18]. Studies using cultured human proximal tubule cells demonstrated that isoproterenol increases the formation of cAMP [19].…”

Section: Discussionmentioning

confidence: 93%

Isoproterenol Infusion Increases the Maximal Tubular Capacity of Phosphate Reabsorption

Leclaire

Berndt²,

Knox³

1992

Kidney Blood Press Res

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Isoproterenol, a β-adrenoreceptor agonist, decreases urinary phosphate (P_i) excretion; however, plasma phosphate concentration also decreases. The purpose of the present study was to determine the effect of isoproterenol infusion on phosphate reabsorption with concomitant phosphate infusions and in the presence and absence of parathyroid hormone (PTH). Clearance experiments were performed on male Sprague-Dawley rats which were acutely thyroparathyroidectomized (TPTX) and successive infusions of phosphate (1, 2, and 3 µmol/min) were used to determine the maximal tubular capacity of phosphate reabsorption (Tm_Pi) factored for the glomerular filtration rate (GFR) in four groups of rats. In the saline-infused control group the Tm_pi/GFR was 2.87 ± 0.19 µmol/ml (n=8). When isoproterenol was infused intravenously at a rate of 0.005 mg/kg/min, urinary cAMP excretion was significantly increased and the Tm_Pi/GFR was 3.53 ± 0.17 µmol/ml (n=10, p < 0.05). In the PTH-infused group (33 U/kg bolus followed by a sustaining infusion of 1 U/kg/min) Tm_pi/GFR was 1.69 ± 0.15 µmol/ml (n=9). Coadministration of isoproterenol and PTH significantly increased the Tm_Pi/GFR to 3.25 ± 0.64 µmol/ml (n=9). Basal cAMP excretion was similar in both groups. These results demonstrate that the stimulation of renal β-adrenoreceptors by isoproterenol infusion markedly increases phosphate reabsorption and reverses the decrease in the maximal tubular capacity of phosphate reabsorption induced by PTH infusion.

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“…These observations are at odds with the reported direct action of cAMP to inhibit fluid reabsorption in the proxi mai tubule [4], However, stimulation of adeny late cyclase activity via the (3 receptor subtype was not observed in rabbit [5] or necturus [6] proximal tubules. In contrast, canine proximal straight (but not convoluted) tubules did re spond to (3-receptor stimulation with increased adenylate cyclase activity [7] as did rat proxi mal tubules [8],…”

Section: Introductionmentioning

confidence: 99%

Interaction between Adrenergic Agonists and Forskolin on Adenylate Cyclase Activity in the Rabbit Proximal Tubule

Beck

Burgess²,

Balment³

1995

Kidney Blood Press Res

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Using a micro-radioimmunoassay, cAMP was measured in single, isolated S2 proximal straight tubules dissected from rabbit kidneys to investigate the effects of adrenergic agonists on adenylate cyclase activity. The baseline activity of adenylate cyclase was low and unaffected by either the α₂ agonist clonidine, the β agonist isoprenaline (in the absence or presence of 1 µM forskolin) or 1 µM forskolin. Adenylate cyclase activity was markedly stimulated by 20 µM forskolin, an effect which was inhibited by 1 µM clonidine. The inhibition by clonidine was not apparent in the presence of the α₂ antagonist yohimbine. These results confirm the inability of isoprenaline to stimulate adenylate cyclase in the rabbit proximal tubule and demonstrate the coupling of α₂ receptors, in an inhibitory fashion, to adenylate cyclase. The inhibitory action of the α₂-receptor agonist was independent of other hormone activity in the renal proximal tubule.

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Evidence for beta adrenoceptors in proximal tubules. Isoproterenol-sensitive adenylate cyclase in pars recta of canine nephron.

Cited by 16 publications

References 30 publications

Peripheral adrenergic receptors in hypertension.

Peripheral adrenergic receptors in hypertension.

Isoproterenol Infusion Increases the Maximal Tubular Capacity of Phosphate Reabsorption

Interaction between Adrenergic Agonists and Forskolin on Adenylate Cyclase Activity in the Rabbit Proximal Tubule

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