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Titolo:
Diminished beta-adrenoceptor-mediated relaxation of femoral arteries from young spontaneously hypertensive rats
Autore:
Fujimoto, S; Fujimoto, KS; Moriyama, A;
Indirizzi:
Nagoya City Univ, Sch Med, Dept Pharmacol, Mizuho Ku, Nagoya, Aichi 4678601, Japan Nagoya City Univ Nagoya Aichi Japan 4678601 Nagoya, Aichi 4678601, Japan Nagoya City Univ, Sch Med, Inst Nat Sci, Nagoya, Aichi 4678601, Japan Nagoya City Univ Nagoya Aichi Japan 4678601 Nagoya, Aichi 4678601, Japan
Titolo Testata:
AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL
fascicolo: 2-3, volume: 87, anno: 2001,
pagine: 178 - 186
SICI:
1566-0702(20010323)87:2-3<178:DBROFA>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
SENSITIVE POTASSIUM CHANNELS; RESISTANCE CORONARY VESSELS; CONGESTIVE HEART-FAILURE; NITRIC-OXIDE; SMOOTH-MUSCLE; ADRENERGIC RECEPTORS; ENDOTHELIAL FUNCTION; AORTIC RINGS; CYCLIC-AMP; QUINAPRIL TREATMENT;
Keywords:
beta-adrenoceptor; captopril; endothelium; nitro L-arginine; spontaneously hypertensive rat (SHR);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Fujimoto, S Nagoya City Univ, Sch Med, Dept Pharmacol, Mizuho Ku, Mizuho Cho, Nagoya, Aichi 4678601, Japan Nagoya City Univ Mizuho Cho Nagoya Aichi Japan 4678601 , Japan
Citazione:
S. Fujimoto et al., "Diminished beta-adrenoceptor-mediated relaxation of femoral arteries from young spontaneously hypertensive rats", AUTON NEURO, 87(2-3), 2001, pp. 178-186

Abstract

A beta -adrenoceptor agonist, norepinephrine (NE)-induced relaxation in the presence of an alpha -adrenoceptor antagonist and indomethacin was investigated in isolated femoral arteries from 5-week-oId Wistar Kyoto rats (WKY)and spontaneously hypertensive rats (SHR). NE elicited endothelium-dependent and -independent relaxation in WKY. In endothelium-intact WKY artery, the NE-induced relaxation was reduced by nitro L-arginine (L-NA) and methylene blue. The residual response to NE in the presence of L-NA was further reduced by tetraethylammonium (TEA). Glibenclamide attenuated the NE-induced, endothelium-independent relaxation in WKY. In SHR, on the other hand, the relaxation to NE was solely endothelium-independent, unaffected by a combination of L-NA and TEA and inhibited by glibenclamide. The relaxation in response to NE in SHR was less than that in WKY, regardless of the presence andabsence of endothelial cells. When WKY and SHR were treated for 10 days with captopril, the response to NE was increased not only in WKY but also in SHR. The relaxation in captopril-treated SI-IR consisted of endothelium-dependent and -independent components. The former was attenuated by L-NA and to a greater extent by TEA with L-NA. Sodium nitroprusside- and forskolin-induced, endothelium-independent relaxations in SHR were not significantly different from those in WKY. Captopril did not affect the response to these drugs. The present results indicate that the relaxation to NE is in part mediated by NO and a vasorelaxing factor distinct from NO in WKY but not in SHR. It is suggested that NE-induced, endothelium-independent relaxation in both groups is in part mediated by ATP-sensitive K+ channels. It is also suggested that in SHR, captopril increases the response to NE through increases in endothelial production of NO and the non-NO vasorelaxing factor. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 02:31:51