Abstract
This paper discusses the mechanisms of two basic effects of thyroid hormones on atrial responses to β-adrenergic agonists, i.e. increased inotropic sensitivity and decreased maximal contractile responsiveness. The increased sensitivity of atria to β; adrenergic agonists under thyroid hormones appears to be related to increases in β-adrenoceptor density and Gs/Gi. protein ratio, leading to activation of Gs-mediated pathway, but suppression of Gi.-mediated pathway of adenylate cyclase regulation. Therefore, the i/c concentrations of cAMP and corresponding inotropic responses achieve their maximums at lower doses of β-adrenergic agonist. Thyroid hormones also decrease the expression of phospholamban, but increase the expression of sarcoplasmic reticulum Ca2+-pump. As a result, the basal activity of sarcoplasmic reticulum Ca2+-pump increases, but its β-adrenergic activation through phosphorylation of phospholamban decreases. It is suggested that these changes are causal for decreased maximal inotropic and lusitropic responses of atria to β-adrenergic agonists.(Mol Cell Biochem 184: 419–426, 1998)
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Seppet, E.K. et al. (1998). Mechanisms of thyroid hormone control over sensitivity and maximal contractile responsiveness to β-adrenergic agonists in atria. In: Saks, V.A., Ventura-Clapier, R., Leverve, X., Rossi, A., Rigoulet, M. (eds) Bioenergetics of the Cell: Quantitative Aspects. Developments in Molecular and Cellular Biochemistry, vol 25. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5653-4_29
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DOI: https://doi.org/10.1007/978-1-4615-5653-4_29
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