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Oxidative stress induced by tert-butyl hydroperoxide causes vasoconstriction in the aorta from hypertensive and aged rats: role of cyclooxygenase-2 isoform.
J Pharmacol Exp Ther. 2000 Apr; 293(1):75-81.JP

Abstract

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 microM-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 N(G)-nitro-L-arginine methyl ester (100 microM) and tranylcypromine (100 microM), 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 microM), a nonspecific cyclooxygenase inhibitor, and SQ 29,548 (10 microM), a prostaglandin H(2)/thromboxane A(2) 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 microM). The cyclooxygenase-2 inhibitor NS-398 (10 microM) 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-A(2), probably prostaglandin-H(2), 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.

Authors+Show Affiliations

Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid, Spain.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

10734155

Citation

Garcia-Cohen, E C., et al. "Oxidative Stress Induced By Tert-butyl Hydroperoxide Causes Vasoconstriction in the Aorta From Hypertensive and Aged Rats: Role of Cyclooxygenase-2 Isoform." The Journal of Pharmacology and Experimental Therapeutics, vol. 293, no. 1, 2000, pp. 75-81.
Garcia-Cohen EC, Marin J, Diez-Picazo LD, et al. Oxidative stress induced by tert-butyl hydroperoxide causes vasoconstriction in the aorta from hypertensive and aged rats: role of cyclooxygenase-2 isoform. J Pharmacol Exp Ther. 2000;293(1):75-81.
Garcia-Cohen, E. C., Marin, J., Diez-Picazo, L. D., Baena, A. B., Salaices, M., & Rodriguez-Martinez, M. A. (2000). Oxidative stress induced by tert-butyl hydroperoxide causes vasoconstriction in the aorta from hypertensive and aged rats: role of cyclooxygenase-2 isoform. The Journal of Pharmacology and Experimental Therapeutics, 293(1), 75-81.
Garcia-Cohen EC, et al. Oxidative Stress Induced By Tert-butyl Hydroperoxide Causes Vasoconstriction in the Aorta From Hypertensive and Aged Rats: Role of Cyclooxygenase-2 Isoform. J Pharmacol Exp Ther. 2000;293(1):75-81. PubMed PMID: 10734155.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidative stress induced by tert-butyl hydroperoxide causes vasoconstriction in the aorta from hypertensive and aged rats: role of cyclooxygenase-2 isoform. AU - Garcia-Cohen,E C, AU - Marin,J, AU - Diez-Picazo,L D, AU - Baena,A B, AU - Salaices,M, AU - Rodriguez-Martinez,M A, PY - 2000/3/29/pubmed PY - 2000/4/29/medline PY - 2000/3/29/entrez SP - 75 EP - 81 JF - The Journal of pharmacology and experimental therapeutics JO - J Pharmacol Exp Ther VL - 293 IS - 1 N2 - 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 microM-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 N(G)-nitro-L-arginine methyl ester (100 microM) and tranylcypromine (100 microM), 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 microM), a nonspecific cyclooxygenase inhibitor, and SQ 29,548 (10 microM), a prostaglandin H(2)/thromboxane A(2) 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 microM). The cyclooxygenase-2 inhibitor NS-398 (10 microM) 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-A(2), probably prostaglandin-H(2), 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. SN - 0022-3565 UR - https://www.unboundmedicine.com/medline/citation/10734155/Oxidative_stress_induced_by_tert_butyl_hydroperoxide_causes_vasoconstriction_in_the_aorta_from_hypertensive_and_aged_rats:_role_of_cyclooxygenase_2_isoform_ L2 - https://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=10734155 DB - PRIME DP - Unbound Medicine ER -