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Titolo:
Role of the postsynaptic alpha(2)-adrenergic receptor subtypes in catecholamine-induced vasoconstriction
Autore:
Duka, I; Gavras, I; Johns, C; Handy, DE; Gavras, H;
Indirizzi:
Boston Univ, Sch Med, Dept Med, Hypertens & Atherosclerosis Sect, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 therosclerosis Sect, Boston, MA 02118 USA
Titolo Testata:
GENERAL PHARMACOLOGY-THE VASCULAR SYSTEM
fascicolo: 2, volume: 34, anno: 2000,
pagine: 101 - 106
SICI:
0306-3623(200002)34:2<101:ROTPAR>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALPHA(2B)-ADRENERGIC RECEPTOR; MICE; HYPERTENSION; EXPRESSION; ARTERIES;
Keywords:
alpha(2)-adrenergic receptor gene knockout mice; alpha(1)-adrenergic blockade; alpha(2)-adrenergic blockade; norepinephrine;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
20
Recensione:
Indirizzi per estratti:
Indirizzo: Gavras, H Boston Univ, Sch Med, Dept Med, Hypertens & Atherosclerosis Sect, 715 Albany St, Boston, MA 02118 USA Boston Univ 715 Albany St Boston MA USA 02118 ston, MA 02118 USA
Citazione:
I. Duka et al., "Role of the postsynaptic alpha(2)-adrenergic receptor subtypes in catecholamine-induced vasoconstriction", GEN PH-VASC, 34(2), 2000, pp. 101-106

Abstract

Catecholamines induce direct vasoconstriction mediated by postsynaptic alpha-adrenergic receptors (alpha-ARs) of both the alpha(1) and alpha(2) type. To evaluate the contribution of each alpha(2)-AR subtype (alpha(2A), alpha(2B), and alpha(2C)) to this function, we used groups of genetically engineered mice deficient for the gene to each one of these subtypes and comparedtheir blood pressure (BP) responses to their wild-type counterparts. Bloodpressure responses to a bolus of norepinephrine (NE) were assessed before and after sequential blockade of alpha(1)-ARs with prazosin and alpha(2)-ARs with yohimbine. The first NE bolus elicited a brief 32 to 44 mm Hg BP rise (p < 0.001 from baseline) in all six groups. Prazosin decreased BP by 23 to 33 mm Hg in all groups, establishing a new lower baseline. Repeat NE at that point elicited lesser but still significant (p < 0.001) brief presser responses between 32% and 45% of the previous BP rise in five of the six groups. Only the alpha(2A)-AR gene knockouts differed, responding instead with a 20-mm Hg fall in BP, a significant change from baseline (p < 0.001) anddifferent from the presser response of their wild-type counterparts (p < 0.001). The addition of yohimbine produced no further BP change in the five groups, but it did produce a small 7.5-mm Hg fall (p < 0.05) in the alpha(2A)-AR knockouts. Norepinephrine bolus during concurrent alpha(1) and alpha(2)-AR blockade produced significant (p < 0.001) hypotensive responses in all subgroups, presumably attributable to unopposed stimulation of beta(2)-vascular wall ARs. We conclude that the alpha(2)-AR-mediated vasoconstrictioninduced by catecholamines is attributable to the alpha(2A)-AR subtype because mice deficient in any one of the other subtypes retained the capacity for normal vasoconstrictive responses. However, the alpha(1)-ARs account forthe major part (as much as 68%) of catecholamine-induced vasoconstriction. (C) 2000 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 19:24:15