Abstract
The bioactivc phospholipids of the cardiac cell membrane (sarcolemma) and their signaling pathways are emerging as important mediators of the myocardial response to external stimuli, including catecholamines [1]. It is known that the activity of the sympathetic nervous system is increased in congestive heart failure; this results in elevated levels of plasma catecholamines, which downregulate the β-adrenoceptors in failing hearts, leading to subsensitivity of the β-agonist-mediated biochemical and mechanical responses [2]. The α1-adrenoceptors, which are associated with the positive inotropic effect of catecholamines via activation of the membranal phosphoinositide-phospholipase C (PLC) [1], were found to remain unchanged [3] or to increase [4,5] in heart failure. In view of the downregulation of the β-adrenoceptors, the α1 type reflects a greater proportion of the total adrenoceptor population in the failing ventricle [3–5]. Thus α1-adrenoceptors can be seen to play a dominant role in eliciting the positive inotropic action of catecholamines in failing heart [6].
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Panagia, V., Meij, J.T.A., Mesaeli, N., Singal, R.K., Dhalla, N.S. (1995). Depression of Sarcolemmal Phospholipase C Activity in Congestive Heart Failure. In: Dhalla, N.S., Pierce, G.N., Panagia, V., Beamish, R.E. (eds) Heart Hypertrophy and Failure. Developments in Cardiovascular Medicine, vol 169. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1237-6_17
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DOI: https://doi.org/10.1007/978-1-4613-1237-6_17
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