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 anddelayed non-genomic/genomic or genomic mechanisms in vasoactive effects totriiodothyronine (T3), emphasizing functional analysis of the involvement of thesemechanisms in the genesis of nitric oxide (NO) of endothelial or muscular origin.Influences of in vitro and in vivo T3 treatments on contractile and relaxant responsiveness of isolated rat aortas were studied. In vivo T3-treatment was 500 μg·kg–1·d–1,subcutaneous injection, for 1 (T31d) and 3 (T33d) days. In experiments with endothelium-intact aortic rings contracted with phenylephrine, increasing concentrations ofT3 did not alter contractility. Likewise, in vitro T3 did not modify relaxant responsesinduced by acetylcholine or sodium nitroprusside (SNP) nor contractile responseselicited by phenylephrine or angiotensin II in endothelium-intact aortas. Concentration-response curves (CRCs) to acetylcholine and SNP in endothelium-intact aorticrings from T31d and T33d rats were unmodified. T33d, but not T31d, 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 T33d rats. In endotheliumdenuded aortas of T33d rats, CRCs to angiotensin II, and high K+ contractures, weredecreased. Thus, in vitro T3 neither modified phenylephrine-induced active tonusnor CRCs to relaxant and contractile agonists in endothelium-intact aortas, discarding rapid non-genomic actions of this hormone in smooth muscle and endothelialcells. Otherwise, T33d-treatment inhibited aortic smooth muscle capacity to contract,but not to relax, in an endothelium- and NO-independent manner. This effect may bemediated by delayed non-genomic/genomic or genomic mechanisms.