Aging and vascular responsiveness.

With aging, the blood vessel wall becomes hyperreactive--presumably because of an augmented vasoconstrictor and a reduced vasodilator responsiveness. Autonomic nerves, vascular smooth muscle, and endothelial cells may contribute to these changes. It seems unlikely that augmented vasoconstriction following alpha-adrenergic activation plays a major role in the increased peripheral resistance seen in the elderly human. There are no major age-related changes in the responsiveness of vascular smooth muscle to angiotensin II, histamine, or potassium chloride. By contrast, the vasoconstrictor effects of 5-hydroxytryptamine (serotonin) are augmented, and the tachyphylaxis to the monoamine is reduced with aging. There are no indications of a major abnormality in either responses to vasodilator nerves or endothelium-dependent vasodilators. However, the beta-adrenergic responsiveness of most arteries is reduced, whereas that of the veins is not affected by age. When it is exposed to agents acting directly, arterial smooth muscle's ability to relax is not altered with senescence. Thus, the augmented responsiveness to the vasoconstrictor effects of serotonin and the reduced response to the beta-adrenergic dilator effects of catecholamines appear to be the hallmark of aging in the precapillary vessels.