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Do hypertension and aging have a similar effect on the myocardium?
Insights
Aging and hypertension both cause vascular stiffening and impaired cardiac filling. Prolonged relaxation, not just cardiac hypertrophy, is a key factor in age-related cardiac changes, similar to hypertension effects.
Area of Science:
- Cardiovascular Physiology
- Aging Research
- Hypertension Studies
Background:
- Advancing age and chronic arterial hypertension induce similar cardiovascular changes, including vascular stiffening and altered cardiac function.
- Systolic pump function remains intact at rest in both elderly normotensive and hypertensive individuals, but early diastolic filling is reduced.
Purpose of the Study:
- To investigate the mechanisms behind age-related cardiac alterations and compare them to those seen in chronic hypertension.
- To determine if myocardial hypertrophy is the sole common factor linking cellular changes in aging and hypertension.
Main Methods:
- Comparative analysis of cardiac function and cellular changes in aged rats and younger animals with experimental hypertension.
- Examination of myoplasmic calcium transients, action potentials, sarcoplasmic reticulum function, and myosin isozyme composition.
Main Results:
- Prolonged isometric relaxation, attributed to prolonged myoplasmic Ca++ transients, is observed in aged rats.
- Cellular changes like prolonged action potentials and diminished Ca++ pumping occur in aged hearts, mirroring those in hypertensive hearts.
- Left ventricular hypertrophy is less pronounced with aging than with hypertension, and alterations affect both ventricles in aging, regardless of hypertrophy.
Conclusions:
- Myocardial hypertrophy alone does not explain the shared cellular changes between aging and hypertension.
- Prolonged relaxation, influenced by cellular mechanisms, is a significant factor in age-related cardiac dysfunction, comparable to effects of hypertension.
Abstract:
Vascular stiffening and a modest increase in cardiac mass with advancing age in man resemble similar alterations accompanying chronic arterial hypertension. In both hypertensive and elderly normotensive individuals, systolic pump function at rest is not altered, while early filling rate and volume are decreased. Although this abnormality is often attributed to the cardiac hypertrophy per se, prolonged isometric relaxation, which occurs with aging in man and animals and in some types of experimental hypertension, is an equally plausible mechanism. In the aged rat, prolonged relaxation can be attributed to a prolonged myoplasmic Ca++ transient with excitation. This occurs amidst a constellation of other cellular changes, among which are a markedly prolonged transmembrane action potential, diminished sarcoplasmic reticulum Ca++ pumping rate, and altered myosin isozyme composition. Many of these changes occur in cardiac muscle of younger animals with cardiac hypertrophy due to chronic increased afterload. While the magnitude of these alterations with advanced age is as great as those with chronic hypertension in younger animals, the magnitude of left ventricular hypertrophy with aging is far less than that in experimental hypertension. Furthermore, with aging, these alterations occur not only in the myocardium of the left but also of the right heart (which does not hypertrophy). Thus, myocardial hypertrophy per se does not appear to be the common link between cellular changes due to aging and those due to hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)