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Departments of 1 Physiology and 2 Pathology, New York Medical College, Valhalla, New York 10595
The role of nitric oxide (NO) in the control of
coronary blood flow (CBF) during the development of diabetes is
unknown. To study this, mongrel dogs were chronically instrumented
using sterile techniques for measurements of systemic hemodynamics and
CBF. With heart rate controlled (150 beats/min), veratrine (1-10
µg/kg) caused dose-dependent increases in CBF; e.g., 5 µg/kg of
veratrine increased CBF by 57 ± 7% from 41 ± 1.3 ml/min
(P < 0.05). The dogs
developed diabetes 4-5 wk after injection of alloxan (40-60 mg/kg iv, blood glucose levels were 384 ± 18 mg/dl). After diabetes the same doses of veratrine caused smaller increases in CBF; i.e., 5 µg/kg of veratrine increased CBF by 32 ± 2%
(P < 0.05 compared with control)
from 28 ± 4 ml/min. ACh- and adenosine-induced coronary vasodilation were reduced after diabetes as well. In anesthetized dogs
after diabetes, vagal stimulation caused smaller increases in CBF. ACh
and bradykinin caused smaller increases in
NO
2 production in coronary
microvessels from diabetic dogs. Furthermore, despite the fact that
mRNA for endothelial cell NO synthase from the aorta was increased
twofold with the use of Northern blotting, the protein for aortic
endothelial constitutive NO synthase was reduced by 66% after
diabetes, as determined by Western blotting. Our results indicate that
the NO-dependent coronary vasodilation by the Bezold-Jarisch reflex is
impaired in conscious dogs after diabetes. The mechanism responsible
for the impaired endothelium-dependent coronary vasodilation is most
likely the decreased release of NO from the endothelium.
Bezold-Jarisch reflex; adenosine; nitric oxide; coronary microvessels; nitrite production
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