Chronic hypertension pathophysiology: Difference between revisions
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{{Template:Hypertension}} | {{Template:Hypertension}} | ||
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==Overview== | ==Overview== | ||
While the mechanisms underlying secondary hypertension are well understood, the mechanisms underlying primary or essential hypertension are poorly understood. | While the mechanisms underlying secondary hypertension are well understood, the mechanisms underlying primary or essential hypertension are poorly understood. | ||
==Pathophysiology== | |||
==Time Dependence of Pathophysiology== | ===Time Dependence of Pathophysiology=== | ||
*[[Cardiac output]] is raised early in the disease course, while [[total peripheral resistance]] (TPR) is normal. | *[[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: | * Over time [[cardiac output]] drops to normal levels but TPR is increased. Three theories have been proposed to explain this: | ||
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*: An overactive [[sympathetic nervous system]], leading to increased stress responses. | *: An overactive [[sympathetic nervous system]], leading to increased stress responses. | ||
==Genetics== | ===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> | 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> | ||
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[[Category:Aging-associated diseases]] | |||
[[Category:Cardiology]] | |||
[[Category:Emergency medicine]] | |||
[[Category:Cardiovascular diseases]] | |||
[[Category:Medical conditions related to obesity]] | |||
[[Category:Nephrology]] | |||
[[Category:Up-To-Date]] | |||
[[Category:Up-To-Date cardiology]] | |||
Revision as of 04:28, 28 September 2012
|
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.
Pathophysiology
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)