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Titolo:
Nitric oxide modulates evoked catecholamine release from canine adrenal medulla
Autore:
Barnes, RD; Ward, LE; Frank, KP; Tyce, GM; Hunter, LW; Rorie, DK;
Indirizzi:
Mayo Clin & Mayo Fdn, Dept Anesthesiol, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 siol, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn, Dept Physiol & Biophys, Rochester, MN 55905 USA MayoClin & Mayo Fdn Rochester MN USA 55905 phys, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn, Vasc Smooth Muscle Physiol Lab, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 Lab, Rochester, MN 55905 USA
Titolo Testata:
NEUROSCIENCE
fascicolo: 4, volume: 104, anno: 2001,
pagine: 1165 - 1173
SICI:
0306-4522(2001)104:4<1165:NOMECR>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
INHIBITS NOREPINEPHRINE RELEASE; BOVINE CHROMAFFIN CELLS; L-ARGININE; SYNTHASE INHIBITOR; NORADRENALINE RELEASE; TYROSINE-HYDROXYLASE; ENDOTHELIAL-CELLS; NERVE-STIMULATION; 7-NITRO INDAZOLE; CYCLIC-GMP;
Keywords:
basal catecholamine efflux; evoked catecholamine efflux; endothelial nitric oxide synthase; neuronal nitric oxide synthase; N-G-monomethyl-L-arginine; 7-nitroindazole;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Barnes, RD Mayo Clin & Mayo Fdn, Dept Anesthesiol, 200 1st St SW, Rochester, MN 55905USA Mayo Clin & Mayo Fdn 200 1st St SW Rochester MN USA 55905 05USA
Citazione:
R.D. Barnes et al., "Nitric oxide modulates evoked catecholamine release from canine adrenal medulla", NEUROSCIENC, 104(4), 2001, pp. 1165-1173

Abstract

Nitric oxide has various actions, acting in a neurotransmitter-like role and also as a paracrine messenger between vascular endothelial and smooth muscle cells. This study was done to determine whether endogenous nitric oxide has a role in modulating evoked catecholamine release from the canine adrenal medulla. Isolated adrenal glands were perfused with Krebs-Ringer solution as a control, or with Krebs-Ringer solution containing either N-G-monomethyl-L-arginine (L-NMMA: 3 x 10(-4) M) to non-selectively inhibit nitric oxide synthase or 7-nitroindazole (10(-4) M), a relatively selective inhibitor of neuronal nitric oxide synthase. Catecholamine release was evoked using the nicotinic cholinergic agonist 1,1-dimethyl-4-phenylpiperazinium iodine. From the collected perfusate epinephrine. norepinephrine, and dopamine were measured by high performance liquid chromatography. Previous studies have shown that in the presence of L-NMMA, basal releases of epinephrine. norepinephrine and dopamine are increased. 7-Nitroindazole had no effect on basal catecholamine release, suggesting that nitric oxide from an endothelialsource was responsible for the inhibition of basal catecholamine release from the adrenal medulla. Epinephrine and norepinephrine releases were augmented when either of the nitric oxide synthase inhibitors was added during submaximal nicotinic stimulation, indicating that endogenous nitric oxide inhibited release of epinephrine and norepinephrine. Both neuronal and endothelial nitric oxide synthases appeared to be responsible for this inhibition. In summary. these studies suggest that nitric oxide. from both neuronal and endothelial sources, modulates evoked catecholamine release from canine adrenal medulla, while nitric oxide from an endothelial source is most likely responsible for modulation of catecholamine release under basal conditions. (C) 2001 IBRO. Published by Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 00:17:20