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Age-related changes in vascular responses: a review
1Departamento de Farmacología y Terapéutica, Instituto Universitario de Investigación Gerontológica y Metabólica, Facultad de Medicina, Madrid, Spain.
Insights
Aging significantly alters cardiovascular function, increasing risks for diseases like hypertension and heart failure. Vascular changes reduce blood flow and impair endothelial cell function, impacting overall health and cognitive abilities in older adults.
Area of Science:
- Cardiovascular Physiology
- Gerontology
- Vascular Biology
Background:
- Normal aging involves progressive cardiovascular system changes, elevating risks for hypertension, coronary artery disease, and heart failure.
- Vascular alterations include arterial structural and functional modifications, increased stiffness, and lipid/collagen accumulation, particularly with atherosclerosis.
- Reduced cerebral perfusion in the elderly can lead to cognitive decline, exacerbated by hypertension.
Purpose of the Study:
- To elucidate the multifaceted cardiovascular and vascular changes associated with normal aging.
- To investigate the impact of aging on endothelial cell function and vascular tone regulation.
- To analyze alterations in vascular reactivity to various agonists and the role of calcium regulation.
Main Methods:
- Review and synthesis of existing literature on age-related cardiovascular and vascular changes.
- Analysis of functional alterations in arteries, including endothelial-dependent and independent relaxations.
- Examination of changes in vascular smooth muscle contractility and receptor sensitivity.
Main Results:
- Aging reduces endothelium-dependent relaxations and beta-adrenoceptor agonist-induced vasodilation.
- Contractile responses to some agents are reduced (noradrenaline, endothelin), while others are unaffected (histamine, potassium).
- Increased plasma noradrenaline levels and altered vascular calcium regulation are observed in senescence.
Conclusions:
- Aging profoundly impacts cardiovascular health, increasing susceptibility to pathological conditions and functional decline.
- Vascular endothelial dysfunction and altered smooth muscle responsiveness contribute significantly to age-related cardiovascular changes.
- Understanding these vascular alterations is crucial for managing age-related cardiovascular diseases and improving geriatric health outcomes.
Abstract:
Normal aging is associated with different changes in the cardiovascular system that lead to an increase in pathological processes, such as hypertension, coronary artery disease, heart failure, and postural hypotension with enhancement of both morbidity and mortality. The vascular alterations consist of changes in the function and structure of the arteries, and increasing vascular stiffness, mainly when atherosclerosis is present, whose incidence is increased with age. The arteries accumulate lipids, collagen, and minerals. Cerebral perfusion may be reduced in the elderly, mainly regional cerebral blood flow, which leads to a deterioration of mental and physical functions. The degree of deterioration is increased when aging is associated with hypertension. Aging alters endothelial cells, which play an important role in vascular tone regulation. Such a process tends to reduce endothelium-dependent relaxations, and clearly reduces the vasodilation elicited by beta-adrenoceptor agonists. The contractions induced by different agents, such as 5-hydroxytryptamine, histamine, high potassium and angiotensin are barely affected with aging, whereas those elicited by noradrenaline or endothelin are usually reduced. However, plasma noradrenaline levels are increased with age, mainly due to a reduction in the sensitivity of presynaptic alpha 2-adrenoceptors and also of noradrenaline uptake. Sodium pump activity, that controls cellular ionic homeostasis, may be altered depending on animal species. Finally, vascular Ca2+ regulation appears to be altered and the extracellular Ca2+ dependence of contractile responses elicited by agonists is increased, which justifies the enhanced sensitivity to Ca2+ antagonists in senescence.