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Titolo:
Clonidine evokes vasodepressor responses via alpha(2)-adrenergic receptorsin gigantocellular reticular formation
Autore:
Aicher, SA; Drake, CT;
Indirizzi:
Cornell Univ, Coll Med, Dept Neurol & Neurosci, Div Neurobiol, New York, NY Cornell Univ New York NY USA 10021 Neurosci, Div Neurobiol, New York, NY
Titolo Testata:
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
fascicolo: 2, volume: 289, anno: 1999,
pagine: 688 - 694
SICI:
0022-3565(199905)289:2<688:CEVRVA>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
ROSTRAL VENTROLATERAL MEDULLA; HYPOTENSIVE ACTION; SPINAL-CORD; RAT; NUCLEUS; NEURONS; GUANABENZ; SUBTYPES; ALPHA-2-ADRENOCEPTORS; IDENTIFICATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Aicher, SA Cornellt,niv, Coll Med, Dept Neurol & Neurosci, Div Neurobiol, 411 E 69th S Cornell Univ 411 E 69th St New York NY USA 10021 , 411 E 69th S
Citazione:
S.A. Aicher e C.T. Drake, "Clonidine evokes vasodepressor responses via alpha(2)-adrenergic receptorsin gigantocellular reticular formation", J PHARM EXP, 289(2), 1999, pp. 688-694

Abstract

The gigantocellular depressor area (GiDA) is a functionally defined subdivision of the medullary gigantocellular reticular formation where vasodepressor responses are evoked by glutamate nanoinjections. The GiDA also contains reticulospinal neurons that contain the alpha(2A)-adrenergic receptor (alpha(2A)-AR). In the present study, we sought to determine whether nanoinjections of the alpha(2)-AR agonist clonidine into the GiDA evoke cardiovascular responses and whether these responses can be attributed to the alpha(2)-AR. We found that nanoinjections of clonidine into the GiDA evoke dose-dependent decreases in arterial pressure and heart rate. These responses were equivalent in magnitude to responses produced by clonidine nanoinjections into the sympathoexcitatory region of the rostral ventrolateral medulla. Furthermore, the vasodepressor and bradycardic responses produced by clonidine injections into the GiDA were blocked in a dose-dependent fashion by the highly selective alpha(2)-AR antagonist 2-methoxyidazoxan, but not by prazosin, which is an antagonist at both the alpha(1)-AR and the 2B subtype of thealpha-AR. The antagonism by 2-methoxyidazoxan was site specific because injections of the antagonist into the rostral ventrolateral medulla failed toblock the responses evoked by clonidine injections into the GiDA. These findings support the notion that clonidine produces sympathoinhibition through multiple sites within the medullary reticular formation, which is consistent with the wide distribution of the alpha(2)-AR in reticulospinal neurons. These data also suggest that clonidine may have multiple mechanisms of action because it evokes a cardiovascular depressive response from regions containing neurons that have been determined to be both sympathoinhibitory and sympathoexcitatory.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 05:11:34