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Intracellular cGMP may promote Ca2+-dependent and Ca2+-independent release of catecholamines from sympathetic nerve terminals.

Intracellular cGMP may promote Ca2+-dependent and Ca2+-independent release of catecholamines from sympathetic nerve terminals. Research Abstract Details 

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  • Intracellular cGMP may promote Ca2+-dependent and Ca2+-independent release of catecholamines from sympathetic nerve terminals. Abstract Text:

    erin j whalenErin J Whalen,timothy b saurerTimothy B Saurer,alan kim johnsonAlan Kim Johnson,stephen j lewisStephen J Lewis,

    OBJECTIVE: This study examined the hypothesis that intracellular cGMP stimulates the release of catecholamines from sympathetic nerve terminals (SNTs) in conscious rats. METHODS: Conscious rats were prepared to determine the effects of intravenously-administered agents on heart rate (HR) and mean arterial blood pressure (MAP). RESULTS: Bolus intravenous injections of the membrane-permeable cGMP analogue, 8-(4-chlorophenylthio)-cGMP (8-CPT-cGMP), elicited immediate and pronounced increases in HR before any changes in MAP were observed. In contrast, injections of cGMP did not elicit changes in HR or MAP. The 8-CPT-cGMP-induced tachycardia was markedly diminished by (1) the beta(1,2)-adrenoceptor antagonist, propranolol, (2) the ganglion blocking agent, chlorisondamine, and (3) bretylium, which blocks Ca2+-dependent mobilization of vesicular stores of catecholamines from SNTs. 8-CPT-cGMP also elicited minor falls in MAP in propranolol-treated rats but elicited pronounced falls in MAP in rats treated with chlorisondamine, bretylium, or combined administration of bretylium and the muscarinic receptor antagonist, methyl-atropine. CONCLUSIONS: These findings suggest that (1) intracellular cGMP elicits the release of Ca2+-sensitive and Ca2+-insensitive stores of catecholamines from SNTs in conscious rats, and (2) cGMP-mediated release of catecholamines from SNTs antagonizes cGMP-mediated relaxation of vascular smooth muscle in resistance arteries. Taken together, these findings support the concept that increases in intracellular cGMP levels by atrial natriuretic peptide and endothelium- and cardiac-derived nitric oxide regulate sympathetic control of the heart and the microvasculature of conscious rats via cGMP-dependent release of catecholamines.

    Intracellular cGMP may promote Ca2+-dependent and Ca2+-independent release of catecholamines from sympathetic nerve terminals. Publishing Authors By Initials

    ej whalenEJ Whalen,tb saurerTB Saurer,ak johnsonAK Johnson,sj lewisSJ Lewis,

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    Intracellular cGMP may promote Ca2+-dependent and Ca2+-independent release of catecholamines from sympathetic nerve terminals. Journal Published:

    PUBLICATION TYPE: Research Support, U.S. Gov't,

    Journal: Vascular pharmacology

    VOLUME: 45

    Page Numbers: 102-11

    Journal Abbreviation:

    ISSN: 1537-1891

    DAY: 11

    MONTH: 05

    YEAR: 2006

    Intracellular cGMP may promote Ca2+-dependent and Ca2+-independent release of catecholamines from sympathetic nerve terminals. Information

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    LANGUAGE: eng

    NlmUniqueID: 101130615

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    Grant and Affiliation Information for Intracellular cGMP may promote Ca2+-dependent and Ca2+-independent release of catecholamines from sympathetic nerve terminals.

    AFFILIATION: Department of Psychology, University of Iowa, Iowa City, IA 52242, USA. ewhalen@receptor-biol.duke.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: Vascul Pharmacol

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