Physical Activity Prevents Age-Related Impairment in Nitric Oxide Availability in Elderly Athletes

Taddei, Stefano; Galetta, Fabio; Virdis, Agostino; Ghiadoni, Lorenzo; Salvetti, Guido; Franzoni, Ferdinando; Giusti, C; Salvetti, Antonio

doi:10.1161/01.cir.101.25.2896

Cited by 396 publications

(372 citation statements)

References 27 publications

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“…Several studies suggest that the main mechanism by which exercise improves impaired vasodilation is increased endothelial NO bioavailability (17,35). Our data are only in apparent contrast with these previous observations.…”

Section: Discussioncontrasting

confidence: 99%

Exercise restores β-adrenergic vasorelaxation in aged rat carotid arteries

Leosco

Iaccarino

Cipolletta

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Aging is associated with alterations in β-adrenergic receptor (β-AR) signaling and reduction in cardiovascular responses to β-AR stimulation. Because exercise can attenuate age-related impairment in myocardial β-AR signaling and function, we tested whether training could also exert favorable effects on vascular β-AR responses. We evaluated common carotid artery responsiveness in isolated vessel ring preparations from 8 aged male Wistar-Kyoto (WKY) rats trained for 6 wk in a 5 days/wk swimming protocol, 10 untrained age-matched rats, and 10 young WKY rats. Vessels were preconstricted with phenylephrine (10-6 M), and vasodilation was assessed in response to the β-AR agonist isoproterenol (10-10-3 × 10-8 M), the α2-AR agonist UK-14304 (10-9-10-6 M), the muscarinic receptor agonist ACh (10-9-10-6 M), and nitroprusside (10-8-10-5 M). β-AR density and cytoplasmic β-AR kinase (β-ARK) activity were tested on pooled carotid arteries. β-ARK expression was assessed in two endothelial cell lines from bovine aorta and aorta isolated from a 12-wk WKY rat. β-AR, α2-AR, and muscarinic responses, but not that to nitroprusside, were depressed in untrained aged vs. young animals. Exercise training restored β-AR and muscarinic responses but did not affect vasodilation induced by UK-14304 and nitroprusside. Aged carotid arteries showed reduced β-AR number and increased β-ARK activity. Training counterbalanced these phenomena and restored β-AR density and β-ARK activity to levels observed in young rat carotids. Our data indicate that age impairs β-AR vasorelaxation in rat carotid arteries through β-AR downregulation and desensitization. Exercise restores this response and reverts age-related modification in β-ARs and β-ARK. Our data support an important role for β-ARK in vascular β-AR vasorelaxation.

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Section: Discussioncontrasting

confidence: 99%

Exercise restores β-adrenergic vasorelaxation in aged rat carotid arteries

Leosco

Iaccarino

Cipolletta

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…In mouse models, 10-14 weeks of voluntary running is associated with reduced expression of NF-κB and pro-inflammatory cytokines 184,193 . Vitamin C infusion improves flow-mediated dilatation in older sedentary men and oestrogen-deficient women, reinforcing the concept that reduced oxidative stress is a key mechanism through which aerobic exercise can reduce vascular inflammation and improve endothelial function 184,187,190,194 . Aerobic exercise may also protect the vasculature from adverse effects of other cardiovascular risk factors such as elevated LDL cholesterol and impaired glycaemic control 184,195,196 .…”

mentioning

confidence: 63%

“…This suggests that oestrogen may be permissively involved in the beneficial effects of aerobic exercise on endothelial function in women 184 . Aerobic exercise also improves forearm vascular responses to acetylcholine in older men when assessed using venous occlusion plethysmography 184,189 and the observed differences can be abolished by inhibition of eNOS, suggesting that the benefits of aerobic exercise are at least in part mediated by increased NO bioavailability 184,190 .…”

mentioning

confidence: 99%

Drug Treatment of Hypertension: Focus on Vascular Health

Cameron

Lang

Touyz

2016

Drugs

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Hypertension, the most common preventable risk factor for cardiovascular disease and death, is a growing health burden. Serious cardiovascular complications result from target organ damage including cerebrovascular disease, heart failure, ischaemic heart disease and renal failure. While many systems contribute to blood pressure elevation, the vascular system is particularly important, because vascular dysfunction is a cause and consequence of hypertension. Hypertension is characterised by a vascular phenotype of endothelial dysfunction, arterial remodelling, vascular inflammation and increased stiffness. Antihypertensive drugs that influence vascular changes associated with high blood pressure have greater efficacy for reducing cardiovascular risk than drugs that reduce blood pressure but have little or no effect on the adverse vascular phenotype. Angiotensin converting enzyme Key Points• Hypertension is characterized by a vascular phenotype of endothelial dysfunction and structural remodeling.• Anti-hypertensive drugs that target the vascular changes associated with hypertension appear to be most efficacious• New anti-hypertensive drugs should promote vascular health as well as reducing blood pressure 3

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“…Therefore, the physical training can prevent endothelial dysfunction by maintaining the availability of NO consequent to the prevention of oxidative stress. This evidence suggests that the physical exercise can prevent or attenuate the decline in endothelium-dependent vasodilation 55 .…”

Section: Physical Exercise and The Vascular Endotheliummentioning

confidence: 94%

“…Studies have suggested that the mechanism by which the physical exercise reduces the progression of atherosclerosis and the risk of recurrent events is related to the improvement in muscle tonus and endothelial function [62][63][64][65][66][67][68][69][70][71] .…”

Section: Physical Exercise and The Vascular Endotheliummentioning

confidence: 99%