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Departments of 1 Surgery and 2 Physiology, Faculty of Medicine, Université de Montréal, Montréal H3C 3J7, and Institut de Cardiologie de Montréal, Montréal, Québec, Canada H1T 1C8
Nitric oxide (NO) may normally impair endothelin
(ET) activity in epicardial coronary arteries. Lifting this inhibitory
feedback could reveal ET-dependent effects involving
ETA- and/or
ETB-receptor activation. In
conscious dogs, the blockade of
ETA receptors (intracoronary Ro-61-1790) increased external circumflex coronary artery diameter (CD) (sonomicrometry) by 0.10 ± 0.01 from 3.04 ± 0.12 mm
(P < 0.01) without altering coronary
blood flow (Doppler). Similarly, CD increased (0.09 ± 0.01 from
2.91 ± 0.14 mm; P < 0.01) when Ro-61-1790 was given after blockade of NO formation with
intracoronary N
-nitro-L-arginine
methyl ester (L-NAME). In
contrast, ETB-receptor blockade
(intracoronary Ro-46-8443) did not influence baseline CD with and
without L-NAME. In vitro,
increases in tension caused by
N-nitro-L-arginine
(L-NNA) or
PGF2
in arterial rings were reduced by ETA- but not
ETB-receptor blockade.
ETA-receptor blockade also reduced
the increase in tension caused by
L-NNA in human coronary arterial
rings. Thus ETA receptors, but not
ETB receptors, account for
ET-dependent constriction in canine epicardial coronary arteries in
vivo. ET-dependent effects were independent of the level of NO
formation in vitro and in vivo. In human epicardial coronary arterial
rings, ETA-receptor blockade also
caused significant relaxation.
endothelin; endothelium-derived factors
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