THYROTROPIN RELEASING HORMONE SENSITIZING MYOCARDIAL ADRENOCEPTROS DURING HEMORRHAGIC SHOCK IN RATS AND ITS MECHANISMS

Abstract

The present experiment is aimed to elucidate the relationship between the antishock property of thyrotropin-releasing hormone(TRH) and adrenoceptors. Based on this purpose, the effects of TRH on the positive inotropic actions of adrenergic agonists and on the myocardial adrenoceptors were observed during hemorrhagic shock in rats, meanwhile effects of TRH alone and combined with adrenergic agonists on calcium current(Ica) in single cardiac cells were also investigated. The results indicated that TRH potentiated the positive inotropic actions of isoprenaline(ISO) and dopamine(DA) on isolated left atria of rats subjected to hemorrhagic shock, but it did not potentiate the effect of phenylephrine(Phe).TRH(5mg.kg-1) up-regulated the number of myocardial β-adrenoceptors and DA receptors during hemorrhagic shock, and increased the affinity of β-receptors. TRH prolonged the open duration of calcium channel (Dca) and augmented the calcium ionic inward induced by ISO and DA. It was suggested that TRH could promote the cadiac adrenoceptors sensitivity of shocked animals, TRH up-regulation of myocardial adrenoceptors of shoched animal, prolongation of Dca, and increase of the calcium ionic inward of ISO and DA might be the mechanisms by which TRH sensitizes β and DA receptors.