Circulation, Vol 86, 1116-1124, Copyright © 1992 by American Heart Association
C Indolfi, F Piscione, B Villari, E Russolillo, V Rendina, P Golino, M Condorelli and M Chiariello
BACKGROUND. Experimental studies on the effects of alpha 2- adrenoceptors
on regional coronary blood flow in normal and ischemic myocardium are
highly controversial. A beneficial effect on regional ischemic myocardium
has been demonstrated in different animal preparations with either alpha
2-adrenoceptor blockade or stimulation. Animal studies also demonstrated
that postsynaptic alpha 2- adrenoceptors mediate vasoconstriction in
coronary and femoral vascular beds. The aims of the study were 1) to
investigate the effects of regional alpha 2-adrenoceptor stimulation on
regional coronary blood flow in subjects with angiographically normal
coronary arteries, 2) to assess the effect of alpha 2-adrenoceptor blockade
on coronary circulation in control subjects, and 3) to examine the
influence of atherosclerosis on coronary blood flow response to alpha
2-adrenoceptor blockade. METHODS AND RESULTS. The effect of regional
administration of BHT 933 (a selective alpha 2-adrenoceptor agonist) was
studied in eight subjects with angiographically normal coronary arteries.
The coronary blood flow velocity was measured using a subselective
intracoronary 3F Doppler catheter and coronary diameter by quantitative
coronary angiography. BHT 933 induced a reduction in coronary artery
diameter from 2.5 +/- 0.6 mm to 1.8 +/- 0.4 mm (p less than 0.05) as well
as in coronary blood flow velocity (from 6.4 +/- 0.9 cm/sec to 4.6 +/- 1.9
cm/sec, p less than 0.01). In some subjects, ST segment abnormalities
occurred. In patients with angiographically normal coronary arteries (n =
6), the regional infusion of a selective alpha 2-adrenoceptor blocking
agent after beta-blockade did not change coronary diameter or coronary
blood flow velocity. In contrast, in patients with significant coronary
stenoses (n = 6), regional infusion of an alpha 2-adrenoceptor blocking
agent reduced regional coronary artery diameter (from 2.3 +/- 0.5 mm to 2.1
+/- 0.6 mm, p less than 0.01) as well as coronary blood flow velocity (from
5.8 +/- 0.8 cm/sec to 3.7 +/- 0.6 cm/sec, p less than 0.05); in addition,
alpha 2-adrenoceptor blockade significantly increased coronary sinus plasma
norepinephrine levels (from 300 +/- 144 pg/ml to 429 +/- 207 pg/ml, p less
than 0.01). CONCLUSIONS. The selective in vivo stimulation of alpha
2-adrenoceptors produces a reduction in coronary blood flow and diameter in
humans with angiographically normal coronary arteries. alpha 2-Adrenergic
blockade does not change coronary blood flow in subjects with
angiographically normal coronary arteries (suggesting no resting alpha
2-adrenergic vasoconstrictor tone), whereas in patients with coronary
artery stenosis, regional coronary blood flow decreases after alpha
2-receptor blockade. Finally, our data also suggest that alpha
2-adrenoceptors participate in the modulation of sympathetic neuronal
norepinephrine release in the human heart.
ARTICLES
Role of alpha 2-adrenoceptors in normal and atherosclerotic human coronary circulation
Department of Medicine, University Federico II, Napoli, Italy.
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