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Titolo:
Flow-induced constriction in arterioles of hyperhomocysteinemic rats is due to impaired nitric oxide and enhanced thromboxane A(2) mediation
Autore:
Bagi, Z; Ungvari, Z; Szollar, L; Koller, A;
Indirizzi:
New York Med Coll, Dept Physiol, Valhalla, NY 10595 USA New York Med CollValhalla NY USA 10595 t Physiol, Valhalla, NY 10595 USA Semmelweis Univ, Dept Pathophysiol, Budapest, Hungary Semmelweis Univ Budapest Hungary , Dept Pathophysiol, Budapest, Hungary
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 2, volume: 21, anno: 2001,
pagine: 233 - 237
SICI:
1079-5642(200102)21:2<233:FCIAOH>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASCULAR ENDOTHELIAL DYSFUNCTION; SKELETAL-MUSCLE ARTERIOLES; INDEPENDENT RISK FACTOR; PLASMA HOMOCYSTEINE; HYPERTENSIVE RATS; METHIONINE LOAD; HOMOZYGOUS HOMOCYSTINURIA; INDUCED ARTERIOSCLEROSIS; DEPENDENT DILATION; OCCLUSIVE DISEASE;
Keywords:
homocysteine; arteriole; flow-induced response; endothelium; nitric oxide; thromboxane A(2);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Koller, A New York Med Coll, Dept Physiol, Valhalla, NY 10595 USA New YorkMed Coll Valhalla NY USA 10595 Valhalla, NY 10595 USA
Citazione:
Z. Bagi et al., "Flow-induced constriction in arterioles of hyperhomocysteinemic rats is due to impaired nitric oxide and enhanced thromboxane A(2) mediation", ART THROM V, 21(2), 2001, pp. 233-237

Abstract

Hyperhomocysteinemia (HHcy) is thought to promote arteriosclerosis and peripheral arterial disease, in part by impairing the function of endothelium. Because flow-induced dilation is mediated by the endothelium, we hypothesized that HHcy alters this response by interfering with the synthesis/actionof NO and prostaglandins. Thus, changes in the diameter of isolated, pressurized (at 80 mm Hg) gracilis skeletal muscle arterioles (diameter approximate to 170 mum) from control and methionine diet-induced HHcy rats were investigated with videomicroscopy. Increases in intraluminal flow (from 0 to 25 muL/min) resulted in dilations of control arterioles (maximum, 34 +/-4 mum). In contrast, increases in flow elicited constrictions of HHcy arterioles (-36 +/-3 mum). In control arterioles, the NO synthase inhibitor N-omega-nitro-L-arginine-methyl ester significantly attenuated (approximate to 50%)dilation, whereas the additional administration of indomethacin, an inhibitor of cyclooxygenase, eliminated flow-induced dilation. In the arterioles of III-icy rats, flow-induced constriction was not affected by N-omega-nitro-L-arginine-methyl ester, whereas it was abolished by indomethacin or the prostaglandin H-2/thromboxane A(2) (TXA(2)) receptor antagonist SQ 29,548 or the TXA(2) synthase inhibitor CGS 13,080. Thus, in HHcy, increases in intraluminal flow elicit constrictions of skeletal muscle arterioles due to the impaired NO and enhanced TXA(2) mediation of the response, alterations that likely contribute to the development of peripheral arterial disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 04:01:18