Sympathetic nervous system as a target for aging and obesity-related cardiovascular diseases

Abstract

Chronic sympathetic nervous system overactivity is a hallmark of aging and obesity and contributes to the development of cardiovascular diseases including hypertension and heart failure. The cause of this chronic sympathoexcitation in aging and obesity is multifactorial and centrally mediated. In this mini-review, we have provided an overview of the key and emerging central mechanisms contributing to the pathogenesis of sympathoexcitation in obesity and healthy aging, specifically focusing on hypertension. A clear understanding of these mechanisms will pave way for targeting the sympathetic nervous system for the treatment of cardiovascular diseases in obesity and aging.

Left ventricular hypertrophy and linked cardiovascular risk factors among Congolese licensed civilian aircrew

“…[12] Insulin resistance and subsequent hyperinsulinemia have been reported to activate the sympathetic nervous and the renin angiotensin systems resulting in endothelial dysfunction. [34,35] With reference to Laplace's law, high BP and obesity could trigger cardiac remodeling through hemodynamic and these humoral mechanisms and the thickening of cardiac wall may occur through collagen deposits. [36] Mehta et al in the Dallas Heart Study found LVH to be an independent risk factor for subclinical atherosclerosis diagnosed by cardiac MRI, coronary artery calcium, and C-reactive protein measurements.…”

The enigmatic role of growth hormone in age-related diseases, cognition, and longevity

“…On the other hand, IGF-1 promotes neuronal cell survival and repair, neurogenesis, synaptogenesis, cerebrovascular integrity (Ashpole et al 2015;Logan et al 2018;Sonntag et al 2013;Labandeira-Garcia et al 2017), and autophagic function in cortical neurons (Renna et al 2013), all of which could favorably impact possible underlying contributors to age-related cognitive decline, as well as neurological disease. It has to be recognized that age-dependent IGF-1 decline or IGF-1 deficiency may also impact aging through modulation of autonomic nervous system (Balasubramanian et al 2019). Interestingly, low IGF-1 levels have been associated with subsequent risk for vascular dementias (Quinlan et al 2017), while IGF-1 deficiency in young animals has been shown to impair cerebrovascular function and exacerbate hypertension-induced cerebrovascular microhemorrhages (Sonntag et al 2013;Tarantini et al 2017;Toth et al 2015).…”

The Danger of Being Too Sympathetic: Norepinephrine in Alzheimer's Disease and Graying of Hair

“…Tonic central nervous system sympathetic nerve firing helps maintain resting vasomotor tone. 1 The SNS is involved in regulation of renal functions, metabolism, and blood pressure through altering the arterial baroreflex. 2 Chronic SNS activity can cause pathological conditions such as hypertension, 3 renal failure, 4 endothelial dysfunction, 5 diastolic dysfunction, 6 increases in ventricular and aortic wall thickness, 7 and metabolic abnormalities.…”

“…8 Moreover, there is a tendency for only specific target organs to be affected by changes in SNS activation to have a ''sympathetic signature'' depending on its source: heart failure leads to increased kidney SNS activity, but not in the gut. 1 Aging as well as obesity has been known to alter the SNS, especially through increased activation observed in cardiovascular diseases such as hypertension and heart failure. It has been speculated that cell senescence may be a key factor linked to activation of the SNS, although specifics remain to be elucidated.…”

“…It has been speculated that cell senescence may be a key factor linked to activation of the SNS, although specifics remain to be elucidated. 1 Moreover, disruption of circadian peripheral clock with age has its basis in SNS dysfunction, which in turn may be due to decline of sympathetic-adrenal-medullary and hypothalamic-pituitary-adrenal axes. 9 The former potentially connects SNS dysfunction to the hypothalamus, 10 which has been hypothesized by some to exert control over the rate of aging in mammals.…”