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The influence of hyperthyroidism on vasoconstrictor and vasodilator responses in isolated coronary and renal resistance arteries.

作者信息

Zwaveling J, Pfaffendorf M, van Zwieten P A

机构信息

Department of Pharmacotherapy, Academic Medical Center, University of Amsterdam, The Netherlands.

出版信息

Pharmacology. 1997 Sep;55(3):117-25. doi: 10.1159/000139519.

DOI:10.1159/000139519
PMID:9346400
Abstract

The influence of hyperthyroidism on the functional vascular responsiveness of isolated coronary and renal resistance vessels was investigated. Hyperthyroidism was established by feeding rats for 1 and 4 weeks with 5 mg/kg L-thyroxine (T4)-containing rat chow. Preparations of either coronary or renal resistance vessels were mounted in an isometric wire myograph. Subsequently, concentration-effect curves were determined for the effects of 5-hydroxytryptamine (5-HT), 9,11-dideoxy-11alpha,9alpha-epoxymethanoprostaglandin F2alpha (U46619) and isoproterenol in coronary vessels, and for those of methoxamine, U46619 and isoproterenol in renal vessel preparations. Our results indicate that hyperthyroidism does not induce major changes in the sensitivity of both coronary and renal resistance vessels towards 5-HT, U46619 and methoxamine. A clearly sensitizing influence of acute hyperthyroidism (1 week of T4 treatment) was found for isoproterenol-induced relaxant responses, whereas hyperthyroidism for 4 weeks did not influence the responses mediated by isoproterenol in coronary resistance arteries. Furthermore, the isoproterenol-induced relaxation in renal arteries was not influenced by the chronic hyperthyroid state of the animal. The present results indicate that in acute hyperthyroidism beta-adrenoceptor-mediated vasodilation is increased. However, in chronic hyperthyroidism changes in responsiveness to vasoconstrictor or vasodilator agents of coronary and renal resistance arteries appear not to play a major role. The influence of hyperthyroidism on the functional response of resistance arteries appears to be both tissue and time dependent.

摘要

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