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Status of Post Adrenergic Receptor Mechanisms in Cardiac Hypertrophy and Heart Failure

  • Chapter
Heart Hypertrophy and Failure

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 169))

Abstract

It is now well known that heart function is regulated by the sympathetic nervous system, in which norepinephrine released from the nerve endings activates J3-adrenergic receptors in the myocardium and increases the development of contractile force [1,2]. The activation of the contractile apparatus by catecholamines occurs through the formation of cyclic AMP and a subsequent increase in the intracellular concentration of Ca2+. At the biochemical level, this signal transduction pathway, in which β-adrenoceptors are coupled to adenylyl cyclase through guanine nucleotide binding proteins (G-proteins), is considered to influence cardiac contraction and relaxation processes by phosphorylation of various membrane and contractile proteins. A schematic representation of events involved in the β-adrenergic receptor mechanisms, leading to increased heart function, is shown in Figure 1.

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Sethi, R., Dhalla, K.S., Panagia, V., Dhalla, N.S. (1995). Status of Post Adrenergic Receptor Mechanisms in Cardiac Hypertrophy and 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_31

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