Comparative study of acute in vitro and short-term in vivo triiodothyronine treatments on the contractile activity of isolated rat thoracic aortas

摘要

We aimed to characterize the participation of rapid non-genomic and delayed non-genomic/genomic or genomic mechanisms in vasoactive effects to triiodothyronine (T3), emphasizing functional analysis of the involvement of these mechanisms in the genesis of nitric oxide (NO) of endothelial or muscular origin. Influences of and T3 treatments on contractile and relaxant responsiveness of isolated rat aortas were studied. T3-treatment was 500 μg•kg •d , subcutaneous injection, for 1 (T3 ) and 3 (T3 ) days. In experiments with endothelium-intact aortic rings contracted with phenylephrine, increasing concentrations of T3 did not alter contractility. Likewise, T3 did not modify relaxant responses induced by acetylcholine or sodium nitroprusside (SNP) nor contractile responses elicited by phenylephrine or angiotensin II in endothelium-intact aortas. Concentration-response curves (CRCs) to acetylcholine and SNP in endothelium-intact aortic rings from T3 and T3 rats were unmodified. T3 , but not T3 , treatment diminished CRCs to phenylephrine in endothelium-intact aortic rings. CRCs to phenylephrine remained significantly depressed in both endothelium-denuded and endothelium-intact, nitric oxide synthase inhibitor-treated, aortas of T3 rats. In endothelium-denuded aortas of T3 rats, CRCs to angiotensin II, and high K contractures, were decreased. Thus, T3 neither modified phenylephrine-induced active tonus nor CRCs to relaxant and contractile agonists in endothelium-intact aortas, discarding rapid non-genomic actions of this hormone in smooth muscle and endothelial cells. Otherwise, T3 -treatment inhibited aortic smooth muscle capacity to contract, but not to relax, in an endothelium- and NO-independent manner. This effect may be mediated by delayed non-genomic/genomic or genomic mechanisms.