© 1995 American Heart Association, Inc.
Articles |
Endothelium-Dependent Contractions Are Associated With Both Augmented Expressionof Prostaglandin H Synthase-1 and Hypersensitivity to Prostaglandin H2in the SHR Aorta
From the Center for Experimental Therapeutics, Baylor College of Medicine, Houston, Tex.
Correspondence to Chantal M. Boulanger, PhD, Baylor College of Medicine, Center for Experimental Therapeutics, One Baylor Plaza, Room 826E, Houston, TX 77030.
Abstract Prostaglandin H2 (PGH2
[endoperoxide]) is an immediate product of prostaglandin H (PGH)
synthase activity (cyclooxygenase) and a likely candidate to mediate
endothelium-dependent contractions evoked by
acetylcholine in the aorta of the spontaneously hypertensive rat (SHR).
Experiments were designed to investigate whether or not
endothelium-dependent contractions were associated with
an increased expression of PGH synthase, an augmented
acetylcholine-induced release of PGH2, and/or a
hypersensitivity of the smooth muscle to endoperoxides in SHR aorta
compared with normotensive Wistar-Kyoto (WKY) aorta. In SHR aorta,
endothelium-dependent contractions to acetylcholine
were abolished by tenidap (10-8 mol/L), a preferential PGH
synthase-1 inhibitor, but slightly impaired by NS-398
(10-6 mol/L), a preferential PGH synthase-2 inhibitor. PGH
synthase-1 expression, which was evaluated by both reverse
transcriptase–polymerase chain reaction and Western blotting, was
about twofold greater in preparations with endothelium from SHR than
from WKY rats. There was no difference in PGH synthase-1 expression
between preparations with and those without endothelium in both
strains. In SHR but not WKY aortas, acetylcholine (10-5
mol/L, 5 minutes) caused a significant
endothelium-dependent release of
PGH2, as measured by gas chromatography/mass
spectrometry. PGH2 evoked more potent contractions in rings
without endothelium from SHR than from WKY rats, whereas the
thromboxane analogue U46619 and prostaglandin F2
caused
a comparable response in both preparations. These results show that
endothelium-dependent contractions to acetylcholine in
SHR aorta are associated with a greater expression of PGH synthase-1, a
significant release of PGH2, and a hypersensitivity
of the smooth muscle to the endoperoxide.
Key Words: thromboxane • tenidap • NS-398 • acetylcholine • cyclooxygenase
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