Chronic hypertension pathophysiology: Difference between revisions
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Revision as of 20:47, 22 November 2011
Hypertension Main page |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editor-In-Chief: Taylor Palmieri
Overview
While the mechanisms underlying secondary hypertension are well understood, the mechanisms underlying primary or essential hypertension are poorly understood.
Time Dependence of Pathophysiology
- Cardiac output is raised early in the disease course, while total peripheral resistance (TPR) is normal.
- Over time cardiac output drops to normal levels but TPR is increased. Three theories have been proposed to explain this:
- Inability of the kidneys to excrete sodium, resulting in natriuretic factors such as Atrial Natriuretic Factor being secreted to promote salt excretion with the side-effect of raising total peripheral resistance.
- An overactive renin / angiotension system leads to vasoconstriction and retention of sodium and water. The increase in blood volume leads to hypertension.
- An overactive sympathetic nervous system, leading to increased stress responses.
Genetics
Hypertension is highly heritable and polygenic (caused by more than one gene) and a few candidate genes have been postulated in the etiology of this condition.[1][2][3]
References
- ↑ Sagnella GA, Swift PA (2006). "The Renal Epithelial Sodium Channel: Genetic Heterogeneity and Implications for the Treatment of High Blood Pressure". Current Pharmaceutical Design. 12 (14): 2221–2234. PMID 16787251. Unknown parameter
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ignored (help) - ↑ Johnson JA, Turner ST (2005). "Hypertension pharmacogenomics: current status and future directions". Current Opinion in Molecular Therapy. 7 (3): 218–225. PMID 15977418. Unknown parameter
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ignored (help) - ↑ Hideo Izawa; Yoshiji Yamada; et al. (2003). "Prediction of Genetic Risk for Hypertension". Hypertension. 41 (5): 1035–1040. PMID 12654703. Unknown parameter
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ignored (help)