Chronic hypertension pathophysiology: Difference between revisions
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(New page: {{Template:Hypertension}} {{CMG}} '''Associate Editor in Chief''': Firas Ghanem, M.D. and Atif Mohammad, M.D. {{EH}} ==Pathophysiology== Most of the secondary mechanisms associated wit...) |
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'''Associate Editor in Chief''': Firas Ghanem, M.D. and Atif Mohammad, M.D. | '''Associate Editor in Chief''': Firas Ghanem, M.D. and Atif Mohammad, M.D. | ||
==Overview== | |||
While the mechanisms underlying secondary hypertension are well understood, the mechanisms underlying primary or essential hypertension are poorly understood. | |||
==Pathophysiology== | ==Time Dependence of Pathophysiology== | ||
*[[Cardiac output]] is raised early in the disease course, while [[total peripheral resistance]] (TPR) is normal. | |||
* 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. | * Over time [[cardiac output]] drops to normal levels but TPR is increased. Three theories have been proposed to explain this: | ||
* An overactive [[renin / angiotension system]] leads to [[vasoconstriction]] and retention of sodium and water. The increase in blood volume leads to hypertension. | *: 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 [[sympathetic nervous system]], leading to increased stress responses. | *: 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.<ref name="polymorphism">{{cite journal |author= Sagnella GA, Swift PA |journal=Current Pharmaceutical Design |title=The Renal Epithelial Sodium Channel: Genetic Heterogeneity and Implications for the Treatment of High Blood Pressure |year = 2006 |month = June |volume = 12 |issue = 14 |pages = 2221-2234 |id = PMID 16787251}}</ref><ref name="polymorphism2">{{cite journal |author= Johnson JA, Turner ST |journal=Current Opinion in Molecular Therapy |title=Hypertension pharmacogenomics: current status and future directions. |year = 2005 |month = June |volume = 7 |issue = 3 |pages = 218-225 |id = PMID 15977418}}</ref><ref name="polymorphism3">{{cite journal|author= Hideo Izawa; Yoshiji Yamada et al |journal=Hypertension |title=Prediction of Genetic Risk for Hypertension |year = 2003 |month = May |volume = 41 |issue = 5 |pages = 1035-1040 |id = PMID 12654703 | url=http://hyper.ahajournals.org/cgi/content/short/01.HYP.0000065618.56368.24v1}}</ref> | |||
==References== | ==References== | ||
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[[Category:Cardiology]] | [[Category:Cardiology]] | ||
[[Category: Up-To-Date]] | |||
[[Category: Up-To-Date Cardiology]] | |||
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Revision as of 22:06, 1 November 2011
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Hypertension Main page |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor in Chief: Firas Ghanem, M.D. and Atif Mohammad, M.D.
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
|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
|month=ignored (help)