Hypertension, Vol 15, 699-703, Copyright © 1990 by American Heart Association
W Auch-Schwelk, ZS Katusic and PM Vanhoutte
Endothelium-dependent contractions to acetylcholine and endothelium-
independent contractions to oxygen-derived free radicals in the aorta of
the spontaneously hypertensive rat (SHR) are mediated by an unidentified
product of the cyclooxygenase pathway of arachidonic acid metabolism. To
determine the role of thromboxane A2 (TXA2) or prostaglandin H2 (PGH2) in
these contractions, rings of the thoracic aorta of SHR were suspended in
organ chambers for measurement of isometric force. Acetylcholine caused
endothelium-dependent contractions in quiescent rings from SHR aortas.
Oxygen-derived free radicals generated with xanthine plus xanthine oxidase
caused contractions in rings without endothelium. Dazoxiben (thromboxane
synthetase inhibitor) did not affect contractions evoked by acetylcholine.
AH 23,848, SQ 29,548, or R 68,070 (TXA2/PGH2 receptor antagonists)
inhibited contractions to U 46,619 (a TXA2/PGH2 receptor agonist),
acetylcholine, and oxygen-derived free radicals. Acetylcholine stimulated
the release of prostacyclin from Wistar-Kyoto (WKY) rat and SHR aortas but
not the release of other prostaglandins (PGE2, PGF2 alpha, TXA2).
Oxygen-derived free radicals did not stimulate the release of
prostaglandins from either SHR or WKY rat aortas. These results demonstrate
that stimulation of TXA2/PGH2 receptors probably by PGH2 might be involved
in endothelium-dependent contractions. Oxygen-derived free radicals, which
might be an endothelium-derived contracting factor or factors, ultimately
cause contraction by stimulation of TXA2/PGH2 receptors.
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Thromboxane A2 receptor antagonists inhibit endothelium-dependent contractions
Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota.
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