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Vol. 293, Issue 1, 75-81, April 2000
Departamento de Farmacología y Terapéutica, Facultad
de Medicina, Universidad Autónoma de Madrid, Spain (E.-C.G.-C.,
J.M., L.D.D.-P., A.B.B., M.S., M.A.R.-M.); and Servicio de
Farmacología Clínica, Clínica Puerta de Hierro,
Madrid. Spain. (J.M., M.A.R.-M.)
We analyzed the mechanisms involved in the effect of
tert-butyl hydroperoxide (t-BOOH) in
isolated aortic rings with and without endothelium from normotensive
Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) at 6, 18, and 24 months of age. t-BOOH (1 µM-10 mM) induced
concentration-dependent contractions that were scarcely modified by
aging and potentiated in SHR and by endothelium removal. The nitric
oxide synthase and prostacyclin synthase inhibitors
NG-nitro-L-arginine methyl ester
(100 µM) and tranylcypromine (100 µM), respectively, increased both
basal tone and the t-BOOH-induced contractions in intact
segments from WKY, with these effects not observed in SHR. Indomethacin
(10 µM), a nonspecific cyclooxygenase inhibitor, and SQ 29,548 (10 µM), a prostaglandin H2/thromboxane A2
receptor blocker, abolished the t-BOOH-induced
vasoconstriction, independent of age and hypertension. In both strains,
these contractile responses were unaltered by the thromboxane synthase
inhibitor imidazole (10 µM). The cyclooxygenase-2 inhibitor NS-398
(10 µM) abolished or markedly reduced the
t-BOOH-induced contractions in segments with or without
endothelium, respectively. In addition, expression of cyclooxygenase-2
protein was detected in aorta from WKY and SHR in either basal
condition or after stimulation with t-BOOH. These
results suggest that (1) t-BOOH-induced vasoconstriction in the aorta from WKY and SHR is essentially mediated by
cyclooxygenase-2 metabolites, different from
thromboxane-A2, probably prostaglandin-H2, and/or isoprostanes; (2) aging scarcely modifies, whereas endothelium negatively modulates, these contractions in both strains; and (3)
nitric oxide and prostacyclin exert a negative modulator role on the
t-BOOH-induced vasoconstriction in WKY, with this
modulator role lost in SHR.
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