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. 2008 May;4(3):237-45.
doi: 10.2217/14796678.4.3.237.

Aging and the brain renin-angiotensin system: relevance to age-related decline in cardiac function

Debra I Diz  1 , Jasmina Varagic, Leanne Groban
Affiliations

Aging and the brain renin-angiotensin system: relevance to age-related decline in cardiac function

Debra I Diz et al. Future Cardiol. 2008 May.

Abstract

This article discusses evidence that impairments in control of autonomic outflow mediated by the brain renin-angiotensin system (RAS) contribute to the decline in baroreceptor reflex function and the development of insulin resistance that accompany hypertension and excess salt intake, especially during aging. Imbalances in the regulation of the sympathetic and parasympathetic limbs of the autonomic nervous system observed in older subjects underlie changes in heart-rate variability and play a role in the regulation of overall cardiac function. Age-related alterations in autonomic nervous system function may also explain the age-associated alterations in metabolism. Reduced heart-rate variability is linked to increased mortality in patients with cardiovascular disorders and, coupled with information that is known about local changes in the cardiac and brain RAS during aging, the evidence reveals potential mechanisms for the protective effects of systemic blockade of the RAS against age-related changes that impact the heart.

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Figures

Figure 1
Figure 1. Processing pathways and major components of the renin-angiotensin system
ACE: Angiotensin-converting enzyme: AT1R: Ang II type 1 receptor: AT2R: Ang II type 2 receptor: d-Ala: Ang-(1-7) Mas receptor antagonist [d-Ala7]-Ang-(1-7): NEP: Neprilysin: Sartans: AT1R antagonists class agents including losartan, candesartan, irbesartan, olmesartan and valsartan.
Figure 2
Figure 2. Effect of endogenous angiotensin peptides on baroreflex function
Baroreflex sensitivity (BRS) in young (∼15 weeks) and old (∼70 weeks) Hannover Sprague-Dawley rats at baseline and after blockade in the solitary tract nucleus with either the AT1-receptor antagonist CV (12 pmol/120 nl) or the Ang-(1-7) receptor antagonist d-Ala (144 fmol/120 nl). Older rats had significantly lower BRS than younger animals and the blockade with d-Ala had no effect on the BRS in the older rats. CV: Candesartan; d-Ala: d-Ala7-Ang-(1-7). Data taken from [27].
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