Bk. Julius et al., Alpha-adrenoceptor blockade prevents exercise-induced vasoconstriction of stenotic coronary arteries, J AM COL C, 33(6), 1999, pp. 1499-1505
Citations number
37
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
OBJECTIVES
The study aimed to evaluate the role of alpha-adrenergic mechanisms during
dynamic exercise in both normal and stenotic coronary arteries.
BACKGROUND
Paradoxical vasoconstriction of stenotic coronary arteries has been reporte
d during dynamic exercise and may be due to several factors such as alpha-a
drenergic drive, a decreased release of nitric oxide, platelet aggregation
with release of serotonin, or a passive collapse of the vessel wall.
METHODS
Twenty-six patients were studied at rest, during two levels of supine bicyc
le exercise and after 1.6 mg sublingual nitroglycerin The alpha-blocker phe
ntolamine was given to 16 patients before exercise, five of whom had also t
aken a beta-adrenergic-blocker the same morning. Ten patients served as con
trols. The cross-sectional areas of a normal and a stenotic coronary vessel
were determined by biplane quantitative coronary arteriography.
RESULTS
In the normal vessel segments, coronary cross-sectional area did not change
after phentolamine injection, but increased in all patient groups similarl
y during exercise. Although coronary vasoconstriction existed in stenotic v
essel segments in control patients, phentolamine-treated patients showed ex
ercise-induced vasodilation without difference in Twenty-six patients were
patients with and without chronic beta-blockade.
CONCLUSIONS
Exercise-induced vasoconstriction of stenotic coronary arteries is prevente
d by intracoronary administration of phentolamine There was no difference i
n coronary vasomotion between patients receiving phentolamine alone;md pati
ents receiving phentolamine in addition to a beta-blocker. This finding sug
gests that exercise-induced vasoconstriction is mediated not only by endoth
elial dysfunction but also by alpha-adrenergic mechanisms. (C) 1999 by the
American College of Cardiology.