Hypertension, Vol 15, 475-481, Copyright © 1990 by American Heart Association
T Kato, Y Iwama, K Okumura, H Hashimoto, T Ito and T Satake
The present experiment was performed to identify endothelium-derived
contracting factor produced by acetylcholine stimulation in the aorta of
spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY)
rats. The rings of the thoracic aorta were obtained from age- matched SHR
and WKY rats, and changes in isometric tension were recorded. The relaxant
responses to acetylcholine in the aortic rings from SHR were significantly
weaker than those from WKY rats. The relaxant responses to acetylcholine
were significantly enhanced by pretreatment with a cyclooxygenase inhibitor
(indomethacin) or thromboxane A2/prostaglandin H2 receptor antagonist
(ONO-3708) in aortic rings from both SHR and WKY rats. A thromboxane A2
synthetase inhibitor (OKY-046) did not affect the acetylcholine-induced
relaxation in the aortic rings from SHR or WKY rats. In the organ bath
solution, after acetylcholine stimulation, prostaglandin E2 and 6-keto-
prostaglandin F1 alpha concentrations increased but not prostaglandin F2
alpha and thromboxane B2 concentrations. Exogenous prostaglandin H2, a
stable analogue of thromboxane A2, and prostaglandin F2 alpha induced
contractions of the SHR rings at a lower concentration than prostaglandin
E2, prostaglandin D2, and prostaglandin I2. These contractile responses to
various prostaglandins were markedly inhibited by pretreatment with
ONO-3708. A prostacyclin synthetase inhibitor did not affect the relaxant
responses to acetylcholine in the SHR rings. These results show that
endothelium-derived contracting factor is produced and released by
acetylcholine stimulation not only in the aorta of SHR but also in those of
WKY rats and suggest that prostaglandin H2, a precursor of the released
prostaglandins, is a strong candidate for endothelium-derived contracting
factor produced by acetylcholine stimulation.
ARTICLES
Prostaglandin H2 may be the endothelium-derived contracting factor released by acetylcholine in the aorta of the rat
2nd Department of Internal Medicine, Nagoya University School of Medicine, Japan.
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