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Departments of 1 Physiology and 2 Anesthesiology, Mie University School of Medicine, 514-8507 Mie, Japan
We determined the role of an endothelium-derived
contracting factor in the impaired relaxation response to ACh of
conduit pulmonary arteries (PAs) isolated from rats with hypoxic
pulmonary hypertension (PH). A
PGH2/thromboxane
A2
(TxA2)-receptor antagonist (ONO-3708) partially restored the impairment of ACh-induced relaxation, whereas TxA2 synthase inhibitors
(OKY-046 and CV-4151) did not affect the impaired relaxation in
phenylephrine-precontracted hypertensive PAs. Endothelium-denuded
hypertensive PA rings showed no difference in the response to ACh
between preparations with and without ONO-3708. In both
endothelium-denuded control and hypertensive PAs, exogenous
PGH2 induced contractions, and the magnitude of the contractions was greater in the control than in
hypoxic PH preparations. An endothelin A-receptor antagonist (BQ-485),
an endothelin B-receptor antagonist (BQ-788), and a superoxide anion
scavenger (superoxide dismutase) did not restore the impaired response
to ACh in hypertensive PAs. These findings suggest that
PGH2 produced from the conduit PAs
of rats with chronic hypoxic PH may be the endothelium-derived
contracting factor responsible for the impairment of ACh-mediated vasorelaxation.
chronic hypoxia; prostaglandin H2; thromboxane A2; nitric oxide
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