Chronic hypertension pathophysiology
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Pathophysiology
Most of the secondary mechanisms associated with hypertension are generally fully understood, and are outlined at secondary hypertension. However, those associated with essential (primary) hypertension are far less understood. What is known is that cardiac output is raised early in the disease course, with total peripheral resistance (TPR) 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.
It is also known that 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
|month=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
|month=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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