ALTERED REACTIVITY OF CORONARY-ARTERIES LOCATED DISTAL TO A CHRONIC CORONARY-OCCLUSION

Citation
Ja. Rapps et al., ALTERED REACTIVITY OF CORONARY-ARTERIES LOCATED DISTAL TO A CHRONIC CORONARY-OCCLUSION, American journal of physiology. Heart and circulatory physiology, 42(4), 1997, pp. 1879-1887
Citations number
35
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Physiology
ISSN journal
0363-6135
Volume
42
Issue
4
Year of publication
1997
Pages
1879 - 1887
Database
ISI
SICI code
0363-6135(1997)42:4<1879:AROCLD>2.0.ZU;2-P
Abstract
The coronary vasculature located distal to a chronic occlusion (collat eral-dependent) has been shown to exhibit altered reactivity to vasoac tive agonists. Thus we evaluated effects of chronic coronary artery oc clusion on vasomotor responsiveness of collateral-dependent arteries i solated from a canine model of Ameroid occlusion of the left circumfle x (LCX) coronary artery. We compared in vitro responses of large (simi lar to 1.3- to 1.4-mm-ID) and small (similar to 0.6-mm-ID) LCX arterie s located distal to an occlusion with responses of similar-sized segme nts of the unoccluded left anterior descending (LAD) coronary artery. alpha-Adrenergic receptor-mediated contractile responses to norepineph rine (10(-9)-10(-4) M) and phenylephrine (10(-9)-10(-4) M) in the pres ence of propranolol were markedly enhanced in large LCX arteries compa red with LAD arteries (P < 0.001). Prazosin (1 alpha M), an alpha(1)-a drenergic receptor antagonist, abolished contractile responses of LCX and LAD arteries to norepinephrine. Inhibition of nitric oxide synthes is with N-omega-nitro-L-arginine methyl ester (100 mu M) enhanced nore pinephrine-induced contractions of LAD arteries to a greater extent th an contractions of LCX arteries. We simultaneously measured myoplasmic free Ca2+ (fura 2 fluorescence ratio) and contractile responses in LC X and LAD arteries denuded of endothelium; norepinephrine-induced incr eases in myoplasmic free Ca2+ and contractile tension were significant ly enhanced in LCX arteries compared with LAD arteries. In addition, l arge and small LCX arteries exhibited impaired relaxation in response to adenosine (10(-8)-10(-3) M) compared with LAD arteries (P < 0.05). In contrast, relaxation in response to the P-adrenergic agonist isopro terenol(10(-9)-10(-4) M) and sodium nitroprusside (10(-10)-10(-4) M) w as not significantly different in LCX and LAD arteries. Thus collatera l-dependent coronary arteries exhibit enhanced alpha-adrenergic vasoco nstriction and impaired vasorelaxation in response to adenosine. The e nhanced alpha-adrenergic contractile responsiveness involves at least two mechanisms: 1) enhanced alpha(1)-adrenergic reactivity of smooth m uscle and 2) decreased oc-adrenergic-induced synthesis of nitric oxide by the endothelium.