Abstract
Aging has sometimes been referred to as 'blunted hypertension', and hypertension as 'accelerated aging'. Systolic arterial pressure increases with aging; the increase encompasses both the clinically normal and hypertensive ranges of pressure and is due in part to arterial stiffening. Cardiac changes that occur with aging in otherwise healthy individuals can occur at a younger age in clinically hypertensive individuals and can be produced in young animals by experimental hypertension. Such cardiac adaptations in hypertension and aging include left ventricular hypertrophy and prolonged Ca2+ activation of contractile proteins, leading to a prolonged force-bearing capacity. This is mediated by a prolongation of the cytosolic Ca2+ transient, due to a reduced rate of Ca2+ sequestration by the sarcoplasmic reticulum. The action potential is also prolonged. The resultant delayed contractile relaxation, in part, leads to a slower velocity of early diastolic left ventricular filling; however, this is offset by enhanced atrial filling. Cardiac muscle of the aging and hypertensive heart are also less sensitive to beta-adrenergic stimulation. These myocardial adaptations with aging and hypertension, in part, are controlled from within the genome and permit a relatively normal heart volume and ejection fraction in the presence of chronically elevated afterload.
Original language | English (US) |
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Pages (from-to) | 29-38 |
Number of pages | 10 |
Journal | European heart journal |
Volume | 11 |
Issue number | SUPPL. G |
DOIs | |
State | Published - Jan 1 1990 |
Externally published | Yes |
Keywords
- aging
- cardiac excitation
- cardiac hypertrophy
- cell calcium
- contraction coupling
- hypertension
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine