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Pathogenesis of Hypertension
- Suzanne Oparil, MD;
- M. Amin Zaman, MD; and
- David A. Calhoun, MD
- From University of Alabama at Birmingham, Birmingham, Alabama.
PHYSIOLOGY IN MEDICINE: A SERIES OF ARTICLES LINKING MEDICINE WITH SCIENCE
Co-sponsored by the American College of Physicians and the American Physiological Society
Physiology in Medicine: Dennis A. Ausiello, MD, Editor; Dale J. Benos, PhD, Deputy Editor; Francois Abboud, MD, Associate Editor; William J. Koopman, MD, Associate Editor
Annals of Internal Medicine: Paul Epstein, MD, Series Editor
Clinical Principles
A clearer understanding of the pathogenesis of hypertension will probably lead to more highly targeted therapies and to greater reduction in hypertension-related cardiovascular disease morbidity than can be achieved with current empirical treatment.
Physiologic Principles
More than 90% of cases of hypertension do not have a clear cause.
Hypertension clusters in families and results from a complex interaction of genetic and environmental factors.
The hypertension-related genes identified to date regulate renal salt and water handling.
Major pathophysiologic mechanisms of hypertension include activation of the sympathetic nervous system and renin–angiotensin–aldosterone system.
Endothelial dysfunction, increased vascular reactivity, and vascular remodeling may be causes, rather than consequences, of blood pressure elevation; increased vascular stiffness contributes to isolated systolic hypertension in the elderly.
Essential hypertension, or hypertension of unknown cause, accounts for more than 90% of cases of hypertension. It tends to cluster in families and represents a collection of genetically based diseases or syndromes with several resultant inherited biochemical abnormalities (1-4). The resulting phenotypes can be modulated by various environmental factors, thereby altering the severity of blood pressure elevation and the timing of hypertension onset.
Many pathophysiologic factors have been implicated in the genesis of essential hypertension: increased sympathetic nervous system activity, perhaps related to heightened exposure or response to psychosocial stress; overproduction of sodium-retaining hormones and vasoconstrictors; long-term high sodium intake; inadequate dietary intake of potassium and calcium; increased or inappropriate renin secretion with resultant increased production of angiotensin II and aldosterone; deficiencies of vasodilators, such …
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