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- W2084313269 abstract "Regulation of sympathoadrenal activity has been a long-time target in the management of hypertension. Regulation of β-adrenoceptor (βAR) function has been the most therapeutically important of these targets. The development of effective antihypertensive treatments based on βAR antagonism paralleled the elucidation of the molecular basis of β-adrenergic effects by the family of βARs, which are members of the G-protein-coupled receptor (GPCR) superfamily. βARs serve as the extracellular face of the transmembrane signalling pathway that results in the consequent activation of heterotrimeric G-proteins and the activation of several other newly appreciated signalling molecules that include β-arrestins and GPCR kinases (GRKs). The aggregate effect of the activation of these signalling pathways mediates the response to βAR activation. Paradoxically, the hypertensive state is characterized by impaired βAR responsiveness. This defect is common to many other receptor systems linked to the stimulator G protein (Gs) and adenylyl cyclase activation. This impairment is principally mediated by receptor-G-protein uncoupling, which has been linked to increased expression and activity of GRK2." @default.
- W2084313269 created "2016-06-24" @default.
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- W2084313269 date "2014-05-01" @default.
- W2084313269 modified "2023-09-24" @default.
- W2084313269 title "β-Adrenoceptors as Molecular Targets in the Treatment of Hypertension" @default.
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- W2084313269 doi "https://doi.org/10.1016/j.cjca.2014.01.017" @default.
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