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1 Department of Physiology, New York Medical College, Valhalla, New York 10595; and 2 Department of Cardiovascular Diseases, Pfizer Incorporated, Groton, Connecticut 06340
Recent evidence from our laboratory and others
suggests that nitric oxide (NO) is a modulator of in vivo and in vitro
oxygen consumption in the murine and canine heart. Therefore, the goal of our study was twofold: to determine whether NO modulates myocardial oxygen consumption in the nonhuman primate heart in vitro and to
evaluate whether the seemingly cardioprotective actions of amlodipine
may involve an NO-mediated mechanism. Using a Clark-type O2 electrode, we measured oxygen
consumption in cynomologous monkey heart at baseline and after
increasing doses of
S-nitroso-N-acetylpenicillamine (SNAP;
10
7-104
M), bradykinin
(107-104
M), ramiprilat
(107-104
M), and amlodipine
(107-105
M). SNAP (
38 ± 5.8%), bradykinin (19 ± 3.9%), ramiprilat (28 ± 2.3%), and amlodipine
(23 ± 4.5%) each caused significant
(P < 0.05) reductions in myocardial
oxygen consumption at their highest dose. Preincubation of tissue with
nitro-L-arginine methyl ester (104 M) blunted the effects
of bradykinin (5.4 ± 3.2%), ramiprilat (4.8 ± 5.0%), and amlodipine (5.3 ± 5.0%) but had no effect on
the tissue response to SNAP (38 ± 5.8%). Our results
indicate that NO can reduce oxygen consumption in the primate
myocardium in vitro, and they support a role for the calcium-channel
blocker amlodipine as a modulator of myocardial oxygen consumption via a kinin-NO mediated mechanism.
myocardial oxygen consumption; nitrite release; coronary microvessels; bradykinin; ramiprilat
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