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Aging is accompanied by significant cardiovascular modifications, both structural and functional. A slight degree of left ventricular hypertrophy develops, while the resting heart rate and early filling rate are somewhat decreased. In contrast, end-diastolic and end-systolic dimensions, stroke volume, and ejection fraction are largely unchanged. The effort tachycardic and inotropic responses are clearly attenuated, whereas the concomitant increase in end-diastolic diameter is enhanced. Large arterial conduits become less distensible and somewhat hypertrophic. Total blood volume is reduced, whereas total peripheral resistance is moderately increased. Neurohumoral systems relevant to cardiovascular regulation are nonuniformly affected by aging: the sympathetic nervous system is overactive and the circulating levels of vasopressin and atrial natriuretic factor are enhanced, while the activity of the renin-angiotensin system is blunted. Elderly individuals have altered cardiovascular homeostasis, with a typical propensity to postural and postprandial hypotension. “Spontaneous” blood pressure variability is increased, whereas heart rate variability is diminished. Vagally mediated chronotropic responses, including those dependent on baroreflex modulation, are attenuated, although end-organ (cardiac) parasympathetic responsiveness is exaggerated. Arterial baroreceptor control of blood pressure is largely preserved in advanced age, whereas cardiopulmonary-mediated reflex responses are definitely impaired.