[논문]Flow-Induced Constriction in Arterioles of Hyperhomocysteinemic Rats Is Due to Impaired Nitric Oxide and Enhanced Thromboxane A 2 Mediation

Bagi, Zsolt; Ungvari, Zoltan; Szollá; r, Lajos; Koller, Akos

doi:10.1161/01.atv.21.2.233

[해외논문] Flow-Induced Constriction in Arterioles of Hyperhomocysteinemic Rats Is Due to Impaired Nitric Oxide and Enhanced Thromboxane A 2 Mediation 원문보기

Arteriosclerosis, thrombosis, and vascular biology, v.21 no.2, 2001년, pp.233 - 237

Bagi, Zsolt (From the Department of Pathophysiology, Semmelweis University, Budapest, Hungary (Z.B., Z.U., L.S., A.K.)) , Ungvari, Zoltan (and Department of Physiology, New York Medical College, Valhalla, NY (A.K.).) , Szollár, Lajos (From the Department of Pathophysiology, Semmelweis University, Budapest, Hungary (Z.B., Z.U., L.S., A.K.)) , Koller, Akos (and Department of Physiology, New York Medical College, Valhalla, NY (A.K.).)

Abstract ▼ AI-Helper

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/action of NO and prostaglandins. Thus, changes in the diameter of isolated, pressurized (at 80 mm Hg) gracilis skeletal muscle arterioles (diameter ≈170 μm) from control and methionine diet-induced HHcy rats were investigated with videomicroscopy. Increases in intraluminal flow (from 0 to 25 μL/min) resulted in dilations of control arterioles (maximum, 34±4 μm). In contrast, increases in flow elicited constrictions of HHcy arterioles (−36±3 μm). In control arterioles, the NO synthase inhibitor Nω -nitro- l -arginine-methyl ester significantly attenuated (≈50%) dilation, whereas the additional administration of indomethacin, an inhibitor of cyclooxygenase, eliminated flow-induced dilation. In the arterioles of HHcy rats, flow-induced constriction was not affected by Nω -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.

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