Akademik Veri Yönetim Sistemi
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, cilt.43, sa.5, ss.692-697, 2004 (SCI-Expanded, Scopus)
The aim of this study was to investigate the acute direct effects of homocysteine (Hcy) on the vascular responsiveness of human internal mammary artery (IMA) and to define the possible underlying mechanisms. The contractile response to both phenylephrine (Phe) (-36%) and KCI (-18%) was significantly reduced in arteries that were incubated with Hey (10(-4) M, 30 minutes), compared with controls (P < 0.05). Removal of endothelium did not significantly alter the responses of human IMA to Phe. Hcy (10(-4) M) also caused a relaxation response in human IMA rings precontracted with Phe (10(-6) M) and this effect was not inhibited by N-omega--nitro-L-arginine methyl ester (L-NAME, 10(-4) M), by (L)-NAME (10(-4) M) + indomethacin (10(-5) M), or by intimal rubbing. In addition, contractions induced by stepwise addition to calcium (Ca2+) to high KCI solution with no Ca2+ were significantly inhibited by Hcy incubation as well as contractions induced by Phe in the absence of extracellular Ca2+ (P < 0.05). On the other hand, Hcy (10(-4) M, 30 minutes) did not significantly inhibit the relaxation responses to either acetylcholine (ACh) or sodium nitroprusside (SNP) (P > 0.05). These results demonstrated that short-term exposure to Hey significantly decreased vascular responsiveness in human IMA without affecting endothelium-dependent and -independent vasorelaxation. This effect is not NO-, prostaglandin- or endothelium-dependent. The mechanism is uncertain but seems to depend on the interactions of Hey with Ca2+ influxes and/or other undefined direct effects in this tissue.