The effect of aging on phenylephrine response in normal subjects

Abstract

In a healthy normal aged population, a preserved SVI response in the setting of a higher baseline SVR results in an increased SBP response to α1-stimulation. Contractile responses to increased afterload are not altered with aging. Age-associated differences in the response to α1-stimulation are small and are explained by altered baroreflex sensitivity and a stiffer vasculature.

Activation of α1A‐adrenoceptors desensitizes the rat aorta response to phenylephrine through a neuronal NOS pathway, a mechanism lost with ageing

“…This mechanism of desensitization in the aorta could be important as it might prevent significant increases in cardiac afterload on the left ventricle. In this way, the loss of the α 1A ‐adrenoceptor/nNOS desensitization observed in aorta from aged rats, if extrapolated to humans, would result in an increased afterload on the LV, explaining the larger increases in systolic blood pressure produced by Phe in older compared with younger normotensives patients (White et al , ; Madden et al , ). Therefore, the loss of this modulatory mechanism could have important implications in the alterations of the adrenergic tone in cardiovascular pathologies associated with age, especially if we consider that plasma noradrenaline concentrations are elevated in elderly subjects due to a combination of augmented noradrenaline spillover and reduced metabolic clearance (Moore et al , ).…”

Basal activity of voltage-gated Ca2+ channels controls the IP3-mediated contraction by α1-adrenoceptor stimulation of mouse aorta segments

“…Hence, the phenotypic switch of VSMC from a contractile to a non-contractile phenotype (and vice versa) in culture (Berra-Romani et al, 2008) or in a large number of vascular diseases (House et al, 2008) is expected to alter α 1 -adrenoceptor-mediated contractions. Indeed, α 1 -adrenoceptor signaling, VSMC and endothelial Ca 2 þ signaling and VSMC NO sensitivity alter with aging (Madden et al, 2003), autophagy (Decuypere et al, 2011), hypertension (Abou-Saleh et al, 2013Giachini et al, 2009) and atherosclerosis (Ewart et al, 2014;. Moreover, VSMCs in cross-talk with endothelial cells, determine arterial mechanics (Zulliger et al, 2004), including the basal tonus of the blood vessel, and reduced nitric oxide (NO) bioavailability induces physiological alterations including arterial stiffness, vascular wall remodeling and hypertension (Isabelle et al, 2012;Leloup et al, 2014;Soucy et al, 2006).…”