Inhibition of catecholamine release by alpha-adrenergic activation: Interaction with Na, K-ATPase

Gutman, Yehuda; Boonyaviroj, Punya

doi:10.1007/bf01257018

Cited by 18 publications

(8 citation statements)

References 13 publications

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“…The present paper confirms and extends our previous finding on activation of adrenal medullary Na,K-ATPase by ax-adrenoceptor agonists (Gutman & Boonyaviroj, 1977a). Enhancement of brain Na,K-ATPase activity by adrenoceptor agonists has been described by several authors (Yoshimura, 1973;Godfraind, Koch & Verbeke, 1974;Lee & Phillis, 1977).…”

Section: Discussionsupporting

confidence: 93%

“…This finding indicated the possibility that the action of a-agonists involved activation of the sodium pump (Na,K-ATPase) (Gutman & Boonyaviroj, 1977a;Gutman, 1978). This possibility was corroborated by the finding that activation of the sodium 0007-1188/80/130135-08 $01.00 pump by different means suppressed CA secretion from the adrenal medulla (Gutman & Boonyaviroj, 1977b).…”

Section: Introductionsupporting

confidence: 72%

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The MECHANISM OF Α‐ADRENERGIC INHIBITION OF CATECHOLAMINE RELEASE

Cohen

Eckstein

Gutman

1980

British J Pharmacology

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1 The effect of a-adrenoceptor agonists on membrane adenosine triphosphatase (ATPase) activity was studied in membranes from the bovine adrenal medulla and the rat submaxillary gland.2 a-Adrenoceptor agonists (10-7 to 10-s M) enhanced significantly Na,K-ATPase activity but not Mg-ATPase activity in adrenal medulla. This effect was not observed in membranes from phaeochromocytoma. Phenylephrine (10-5 M), naphazoline (10-M) and clonidine (10-M) caused a significant increase of the activity of Na,K-ATPase (but not of Mg-ATPase) in the submaxillary gland. The enhancement became more prominent after ligature of the submaxillary duct but disappeared completely after superior cervical ganglionectomy. Thus, the effect of the oa-adrenoceptor agonists was due to an action on adrenergic nerve terminals in the submaxillary gland. 3 Phenylephrine and naphazoline did not affect 45Ca uptake but enhanced the rate of 4"Ca efflux from adrenal medullary slices in vitro. 4 Phenylephrine enhanced the rate of 4"Ca efflux from slices of submaxillary gland (with previous ligation of the duct); this was blocked by phentolamine and sympathetic denervation. Therefore phenylephrine was acting on the adrenergic nerve terminals.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionsupporting

confidence: 72%

The MECHANISM OF Α‐ADRENERGIC INHIBITION OF CATECHOLAMINE RELEASE

Cohen

Eckstein

Gutman

1980

British J Pharmacology

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“…In experimental studies, pseudoephedrine and ephedrine are potent stimulants of the Na + -K + -ATPase activity [18]. Intentional ingestion of large amounts of pseudoephedrine and the abuse of ephedrine used in some cough mixture can cause severe hypokalaemia [19].…”

Section: Decongestantsmentioning

confidence: 99%

Drug-Induced Hypokalaemia

Salem¹,

Hmouda²,

Bouraoui³

2009

CDS

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Hypokalaemia (defined as a plasma potassium concentration<3.5 mEq/L) is a common electrolyte abnormality in clinical practice. Drugs are a common cause of either asymptomatic or symptomatic hypokalaemia. Drug-induced hypokalaemia is an important problem particularly in the elderly and in patients with cardiovascular, renal or hepatic disease. Hypokalaemia can complicate the use of the drug in the therapeutic concentration range, and can also be precipitated with overdose or conditions leading to drug intoxication. Because the etiologies of hypokalaemia are numerous, the diagnosis of drug-induced hypokalaemia may be overlooked. Physicians should always pay close attention to this common side effect. Evaluation and management of a hypokalaemic patient should include a careful review of medications history to determine if a drug capable of causing or aggravating this electrolyte abnormality is present.

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“…Indeed, a recent study performed using rat chromaffin cells has demonstrated an autocrine negative modulation of -type Ca 2+ channels via adrenergic receptors, representing a possible mechanism regulating Ca 2+ -dependent exocytosis through voltage-gated channels (Hernandez-Guijo et al 1999). Moreover, other studies have demonstrated an inhibitory adrenergic regulation of Na + influx, thereby affecting the extent of cell depolarization and catecholamine release (Gutman & Boonyaviroj 1977, Wada et al 1985. Because -type channels (Ca 2+ voltage-gated channels) contribute over 50% of the total Ca 2+ current, these mechanisms may form the basis of the adrenergic autocrine/paracrine control of catecholamine secretion.…”

Section: Adrenergic Regulation Of Non-cholinergic Secretagoguesmentioning

confidence: 99%

“…For example, it has been reported frequently that -adrenoceptor agonists and antagonists exert powerful influences on stimulus-evoked release of noradrenaline from nerve terminals (Starke et al 1974b, Langer et al 1977, Nilsson 1983. Although controversial, similar interactions have been described in mammalian chromaffin cells leading investigators to suggest an autocrine/paracrine regulation of catecholamine release via activation of chromaffin cell adrenergic receptors (Gutman & Boonyaviroj 1977, Boonyaviroj et al 1979, Cohen et al 1980, Greenberg & Zinder 1982, Wada et al 1982, Powis & Baker 1985, Sharma et al 1986, Orts et al 1987.…”

Section: Introductionmentioning

confidence: 99%

Adrenergic regulation of catecholamine secretion from trout (Oncorhynchus mykiss) chromaffin cells

Montpetit

Perry

2002

Journal of Endocrinology

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The interaction between extracellular catecholamines and catecholamine secretion from chromaffin cells was assessed in rainbow trout (Oncorhynchus mykiss) using an in situ saline-perfused posterior cardinal vein preparation. This was accomplished by comparing the effects of adrenergic receptor agonists and antagonists on stimulus-evoked secretion. An acute bolus injection or extended perfusion with saline containing high levels of either noradrenaline or adrenaline did not affect the baseline secretion of catecholamines. However, catecholamine secretion in response to a bolus injection of the general cholinergic receptor agonist carbachol or electrical stimulation of the nerves innervating the chromaffin cells was abolished or reduced respectively, in preparations perfused with saline containing either catecholamine.To characterize the catecholaminergic inhibition of catecholamine release, secretion in response to carbachol and electrical stimulation was compared in preparations perfused with the adrenergic receptor agonists dobutamine ( 1 ), salbutamol ( 2 ), phenylephrine ( 1 ) or clonidine ( 2 ). Prior treatment with dobutamine or phenylephrine was without effect on baseline catecholamine secretion or stimulus-evoked secretion. In contrast, pre-treatment with salbutamol significantly inhibited catecholamine secretion in response to carbachol or electrical stimulation. Pretreatment with clonidine did not affect carbachol-evoked secretion but did reduce catecholamine secretion during electrical stimulation. The significance of this adrenergic mechanism of regulating stimulus-evoked catecholamine secretion was further established using the adrenergic receptor antagonists nadolol ( ) or phentolamine ( ). Catecholamine secretion in response to cholinergic stimulation was significantly enhanced in preparations perfused with saline containing nadolol. Furthermore, pretreatment with phentolamine significantly enhanced adrenaline secretion in response to neuronal stimulation.These results suggest that the mechanisms of adrenergic inhibition of catecholamine secretion from trout chromaffin cells include activation of chromaffin cell membrane 2 -receptors and presynaptic 2 -adrenergic receptors.

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Inhibition of catecholamine release by alpha-adrenergic activation: Interaction with Na, K-ATPase

Cited by 18 publications

References 13 publications

The MECHANISM OF Α‐ADRENERGIC INHIBITION OF CATECHOLAMINE RELEASE

The MECHANISM OF Α‐ADRENERGIC INHIBITION OF CATECHOLAMINE RELEASE

Drug-Induced Hypokalaemia

Adrenergic regulation of catecholamine secretion from trout (Oncorhynchus mykiss) chromaffin cells

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