RESUMO
On the basis of the experimental model of angiotensin (Ang) II-induced vasoconstriction by means of the pharmacological agents with various mechanisms of vasoactive action (including verapamil, lidocaine, papaverine, atropine, phentolamine) dependence of Ang II-mediated vascular effect on the state of L-type voltage-dependent calcium channels, voltage-gated sodium channels, phosphodiesterase 3, acetylcholine muscarinic receptors, α-adrenergic receptors were investigated. As a result of the detailed studying of mechanisms of Ang II-mediated vascular effect, it was confirmed that Ang II-induced contraction of isolated rat portal vein depends on the influx of extracellular Ca 2+ through L-type voltage-dependent calcium channels, is less dependent on the phosphodiesterase 3 activity, but it's not dependent on the functional properties of voltage-gated sodium channels, acetylcholine muscarinic receptors and α-adrenergic receptors.
Assuntos
Angiotensina II/farmacologia , Veia Porta/fisiopatologia , Vasoconstrição , Angiotensina II/fisiologia , Animais , Canais de Cálcio Tipo L/fisiologia , Nucleotídeo Cíclico Fosfodiesterase do Tipo 3/fisiologia , Feminino , Técnicas In Vitro , Masculino , Veia Porta/metabolismo , Ratos , Receptores Adrenérgicos alfa/fisiologia , Receptores Muscarínicos/fisiologia , Vasoconstrição/efeitos dos fármacos , Canais de Sódio Disparados por Voltagem/fisiologiaRESUMO
We developed and tested an experimental model to study in vitro the type 1 angiotensin antagonistic activity of compounds on the isolated portal vein of rats. The reliability of this method was confirmed in tests with saralasin (nonselective antagonist of angiotensin receptors) and losartan (selective antagonist of type 1 angiotensin receptors) in concentrations of 10(-9)-10(-5) mol/liter. The half-maximal inhibitory concentrations (IC50) of these substances were calculated.
