Abstract
Elderly healthy individuals have a reduced exercise tolerance and a decreased left ventricle inotropic reserve related to increased vascular afterload, arterial-ventricular load mismatching, physical deconditioning and impaired autonomic regulation (the so called “β-adrenergic desensitization”). Adrenergic responsiveness is altered with aging and the age-related changes are limited to the β-adrenergic receptor density reduction and to the β-adrenoceptor-G-protein(s)-adenylyl cyclase system abnormalities, while the type and level of abnormalities change with species and tissues. Epidemiological studies have shown an high incidence and prevalence of heart failure in the elderly and a great body of evidence correlate the changes of β-adrenergic system with heart failure pathogenesis. In particular it is well known that: (a) levels of cathecolamines are directly correlated with mortality and functional status in heart failure, (b) β1-adrenergic receptor subtype is down-regulated in heart failure, (c) heart failure-dependent cardiac adrenergic responsiveness reduction is related to changes in G proteins activity. In this review we focus on the cardiovascular β-adrenergic changes involvement in the aging process and on similarities and differences between aging heart and heart failure.
Highlights
Epidemiological studies reveal an high incidence and prevalence of heart failure in the elderly (Roger et al, 2011)
In chronic heart failure substantial and characteristic changes occur in the cardiac structure and function and these modifications are not very different from those observed in the aging heart (Shioi and Inuzuka, 2012)
Beside βadrenergic receptor down-regulation, another crucial age-related alteration of this signaling pathway seems to be the coupling of the β-adrenergic receptor to adenylyl cyclase via the Gs protein, which leads to a reduction in the ability to increase cAMP and to activate protein kinases
Summary
Epidemiological studies reveal an high incidence and prevalence of heart failure in the elderly (Roger et al, 2011). The peculiar age-related cardiac structural changes are represented by an increase in cardiomyocyte size and in myocardial thickness (Scholtz et al, 1988; Olivetti et al, 1991), which are able to affect the contractile efficiency of the left ventricle. The age-associated reduction in maximal heart rate during high levels of exercise are in relationship with a reduced β-adrenergic responsivity despite an increase in circulating levels of catecholamines (Corbi et al, 2013a). Beside βadrenergic receptor down-regulation, another crucial age-related alteration of this signaling pathway seems to be the coupling of the β-adrenergic receptor to adenylyl cyclase via the Gs protein, which leads to a reduction in the ability to increase cAMP and to activate protein kinases. It is well known that (a) the levels of cathecolamines are directly correlated with mortality and functional status in heart failure, (b) cardiac β-receptors, in particular β1 subtype, are downregulated in heart failure and (c) heart failure-dependent cardiac adrenergic responsiveness reduction is related to adrenoreceptor kinases and Gαi increased activities
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