RESUMO
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 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 of T3 did not alter contractility. Likewise, in vitro 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 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, were decreased. Thus, in vitro 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, T33d-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.
RESUMO
El objeto de este estudio fue determinar si en forma similar a lo que sucede con la buspirona, la ipsapirona y el 8-hidroxi-2(di-N-propilamino) tetralin (8-OH-DPAT), los receptores adrenérgicos-Ó1 están relacionados con las respuestas producidas por el indorrenato en anillos de aorta de conejo. Excepto la ipsapirona, todos los agonistas 5-HT1A mencionados contrajeron los anillos. La contracción ocasionada por buspirona y 8-OH-DPAT se bloqueó con prazosina (antagonista Ó1-adrenérgico), mientras que el efecto del indorrenato no se inhibió con dicho antagonista, pero sí con ritanserina (antagonista 5-HT2). Por otra parte, la buspirona, la ipsapirona y el 8-OH-DPAT, pero no el indorrenato, relajaron anillos precontraídos con metoxamina (agonista Ó1-adrenérgico). Ninguno de los agonistas relajó preparaciones precontraídas con serotonina, acetilcolina o KCl. Los resultados indican que la buspirona y el 8-OH-DPAT son agonistas parciales de los receptores Ó1 ya que indujeron contracción, que se bloqueó con prazosina, y relajaron solamente anillos precontraídos con metoxamina. La ipsapirona se conportó como un antagonista adrenérgico-Ó1 ya que presentó el efecto relajante pero no el contráctil. Finalmente, no se encontró evidencia de que el indorrenato mostrara afinidad por receptores adrenérgicos-Ó1. La contracción inducida por este agonista, aparentemente es mediada por receptores 5-HT2 ya que se inhibió con ritanserina