Transient receptor potential vanilloid channels in hypertension, inflammation, and end organ damage: an imminent target of therapy for cardiovascular disease?
OBJECTIVE
The possible role of several neurohormonal factors in pathogenesis of hypertension has been studied extensively both in humans and in experimental animal models. However, controversial data from some previous studies are indecisive and call for reassessment and development of new targets. This mini-review presents some of the most recent findings about the role of transient receptor potential vanilloid type 1 channels in the development of hypertension and its pathology.


RESULTS
The transient receptor potential vanilloid type 1, channel activated by novel endovanilloids or altered pH, temperature, and/or local hemodynamics, may serve as a distinct molecular sensor detecting sodium and water balance and may play a role in preventing salt-induced hypertension and tissue damage. Impairment of the function of the transient receptor potential vanilloid type 1 channels may contribute to increased salt sensitivity, inflammation, and end organ damage.


CONCLUSIONS
Emerging evidence indicates that the transient receptor potential vanilloid type 1 channel plays a key role in cardiovascular health and disease by acting as a sensor and regulator of cardiovascular homeostasis and a protector against cardiovascular injury. Given the huge population who suffers from cardiovascular disease, the study of the transient receptor potential vanilloid channels may improve our understanding of pathogenesis of several common cardiovascular disorders and may lead to the development of therapy for hypertension, inflammation, and organ damage.
Wang
Donna H
DH
Department of Medicine, Michigan State University, East Lansing, Michigan 48824, USA. donna.wang@ht.msu.edu
D000959:Antihypertensive Agents / Q000494:pharmacology; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D007249:Inflammation / Q000378:metabolism; D007668:Kidney / Q000502:physiology; D017673:Sodium Chloride, Dietary / Q000378:metabolism; D050916:TRPV Cation Channels / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*
D000959:Antihypertensive Agents; D017673:Sodium Chloride, Dietary; D050916:TRPV Cation Channels