Enhancement of constrictor response of spastic coronary arteries to acetylcholine but not to phenylephrine in patients with coronary spastic angina

Citation
K. Kugiyama et al., Enhancement of constrictor response of spastic coronary arteries to acetylcholine but not to phenylephrine in patients with coronary spastic angina, J CARDIO PH, 33(3), 1999, pp. 414-419
Citations number
21
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
ISSN journal
01602446 → ACNP
Volume
33
Issue
3
Year of publication
1999
Pages
414 - 419
Database
ISI
SICI code
0160-2446(199903)33:3<414:EOCROS>2.0.ZU;2-C
Abstract
This study examined the direct response of smooth muscle of coronary spasm sites to alpha(1)-adrenergic stimulation in patients with coronary spastic angina. Phenylephrine (1 mu M in the coronary circulation, for 5 min), a st imulator of alpha(1)-adrenoreceptors, was directly infused into coronary ar teries with spasm in 10 patients with coronary spastic angina and into norm al coronary arteries in IO control patients. The luminal diameter of epicar dial coronary arteries was determined by computer-assisted quantitative ang iography. The constrictor response to intracoronary injection of acetylchol ine (ACh; 50 mu g) was greater in spastic arteries than in control arteries (decrease from baseline, 48 +/- 29% vs. 12 +/- 2%, respectively; p < 0.001 ). ACh (50 or 100 mu g) induced coronary spasm associated with myocardial i schemia in all of patients with coronary spastic angina but not in any cont rol patients. On the other hand, phenylephrine infusion did not induce coro nary spasm in any of patients with coronary spastic angina or in control su bjects. The constrictor response to phenylephrine infusion was comparable b etween spasm and control coronary arteries (decrease from baseline, 11 +/- 2% vs. 9 +/- 2%, respectively; p = NS). The results indicate that smooth mu scle of spastic coronary arteries does not exhibit enhancement of constrict or response to direct stimulation of alpha(1)-adrenoreceptor on coronary sm ooth muscle. Then may be receptor-specific enhancement of constrictor respo nse to agonists in smooth muscle of spastic coronary arteries in patients w ith coronary spastic angina.