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[Prevention of pathological aging. The arterial hypertension example]
Insights
Distinguishing normal from pathological aging is now clearer. Many age-related declines are due to disease, not fundamental aging, highlighting the potential for preventative interventions.
Area of Science:
- Gerontology
- Cardiovascular Medicine
- Pathology
Context:
- Traditional views suggested universal decline in bodily functions with age.
- Recent studies challenge this by excluding subjects with pre-existing conditions.
- This re-evaluation separates age-related changes from disease-induced impairments.
Purpose:
- To differentiate between normal aging processes and age-related diseases.
- To investigate the impact of disease, specifically heart disease, on age-related functional decline.
- To explore the role of arterial hypertension and new treatments in arterial aging.
Summary:
- Excluding heart disease from studies on cardiac output and aging revealed that the decline was disease-related, not inherent to aging.
- Fundamental aging mechanisms differ between age groups, even when maintaining similar function.
- Arterial hypertension is linked to vascular dementia and pathological aging, with treatments showing promise.
Impact:
- Revising the understanding of aging, separating natural decline from disease.
- Suggests that preventative strategies, particularly for hypertension, can modify the aging profile.
- New antihypertensive drugs offer potential benefits for arterial aging and related conditions.
Abstract:
Studies conducted during the last decade have made it increasingly easier to distinguish between normal and pathological ageing. Previous studies on general populations had established a dogma: most of the major body functions, such as cardiac output, glomerular clearance, muscular strength, visual acuity and so forth, were supposed to decline with age. However, in recent studies on the effects of age on cardiac output all subjects with heart disease were excluded and as a result the negative correlation found between cardiac output and age disappeared, which shows that a phenomenon attributed to ageing was in fact caused by disease. This does not mean that there is no such thing as fundamental ageing, and indeed the mechanisms that maintain cardiac output are different in young and elderly subjects. These data are of more than theoretical interest, since it may be presumed that prevention, the instruments of which are already available in some fields, will modify the profile of ageing. The risk of arterial hypertension is not restricted to the classical cardiovascular diseases: it extends to other diseases, such as vascular dementia, which are potent factors of pathological ageing. Most of the controlled trials carried out in arterial hypertension have demonstrated that treating certain types of hypertension significantly reduces the morbidity and/or mortality of cardiovascular diseases. The specific properties of new antihypertensive drugs, such as angiotensin-converting enzyme inhibitors, open stimulating vistas on arterial ageing.
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