Hypertension, Vol 19, 326-332, Copyright © 1992 by American Heart Association
Y Iwama, T Kato, M Muramatsu, H Asano, K Shimizu, Y Toki, Y Miyazaki, K Okumura, H Hashimoto and T Ito
To examine a relation between the production of acetylcholine-induced
endothelium-derived contracting factor and an increase in blood pressure,
endothelium-dependent contraction and relaxation were evaluated by
measuring the isometric tension of aortic rings from spontaneously
hypertensive rats and Wistar-Kyoto rats at 5, 10, 20, and 30 weeks of age.
In norepinephrine-precontracted rings, acetylcholine (10(-8) to 10(-5)
M)-induced relaxations diminished at the doses of 10(- 6) to 10(-5) M in
both strains except at 5 weeks of age. Treatment with a thromboxane
A2/prostaglandin H2 antagonist (ONO-3708) prevented this reduction in
acetylcholine-induced relaxations in both strains and induced
dose-dependent relaxations, which were completely inhibited by treatment
with a nitric oxide inhibitor, NG-nitro-L-arginine methyl ester. In aorta
treated with NG-nitro-L-arginine methyl ester without precontraction,
acetylcholine induced dose-dependent contractions, which were greater in
spontaneously hypertensive rats than in Wistar- Kyoto rats. These
acetylcholine-induced contractions, which were observed only in rings with
endothelium, were completely inhibited by treatment with ONO-3708 but not
with a thromboxane A2 synthetase inhibitor (OKY-046). There was a
statistically significant correlation between the acetylcholine-induced
contractions and blood pressure. Release of 6-ketoprostaglandin F1 alpha by
acetylcholine from the aorta was greater in spontaneously hypertensive
rats. In vivo administration of another thromboxane A2/prostaglandin H2
antagonist (ONO-8809) (10 or 30 micrograms per body per day) for 3 weeks
(5-8 weeks of age) did not affect blood pressure in either rat
strain.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Correlation with blood pressure of the acetylcholine-induced endothelium-derived contracting factor in the rat aorta
Second Department of Internal Medicine, Nagoya University School of Medicine, Japan.
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