Document Detail


Alike but not the same: anatomic heterogeneity of estrogen receptor-mediated vasodilation.
MedLine Citation:
PMID:  23615160     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In view of recent findings on the anatomic heterogeneity of rapid vasodilation via estrogen receptor (ER)-dependent mechanisms, it is obvious that with regard to human physiology and disease much of it is still unknown, and research in this area is urgently needed. This is also important because chronic drug therapy with estrogens in women systemically affects the circulation and may affect certain arterial beds but not others. It is conceivable that the presence of any vascular disease (as was the case for coronary and carotid atherosclerosis in many of the patients in the large randomized controlled trials HERS and WHI) is likely to affect vascular responses to estrogens as well, and that any beneficial effects may be attenuated or even completely lost. Further work is required to decipher the mechanisms of vasodilation brought about by estrogens in humans and experimental animals, whether anatomic heterogeneity exists with regard to vascular beds and individual estrogen receptors, and how vascular disease (atherosclerosis in particular) affects responsiveness. Also, pharmacologcial tools for newly identified ERs are now available. The hypothesis that disease may modify or even abrogate estrogen-dependent or ER-selective vasodilation should also be tested. Finally, given that certain clinically approved drugs such as SERM or SERDs (thought only to block or downregulate nuclear ERs) actually cause vasodilation through GPER and have been shown in recent clinical studies to provide cardiovascular protection in postmenopausal women, we may have to rethink our current understanding, concepts, and strategies of how to interfere with the increased risk of vascular disease in women with estrogen deficiency or after menopause.
Authors:
Matthias Barton; Matthias R Meyer; Eric R Prossnitz
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Journal of cardiovascular pharmacology     Volume:  62     ISSN:  1533-4023     ISO Abbreviation:  J. Cardiovasc. Pharmacol.     Publication Date:  2013 Jul 
Date Detail:
Created Date:  2013-07-11     Completed Date:  2013-12-11     Revised Date:  2014-07-02    
Medline Journal Info:
Nlm Unique ID:  7902492     Medline TA:  J Cardiovasc Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  22-5     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Cardiovascular Diseases / prevention & control
Estrogens / deficiency,  pharmacology
Female
Humans
Male
Receptors, Estrogen / physiology*
Selective Estrogen Receptor Modulators / pharmacology
Vasodilation / physiology*
Grant Support
ID/Acronym/Agency:
CA163890/CA/NCI NIH HHS; R01 CA127731/CA/NCI NIH HHS; R01 CA127731/CA/NCI NIH HHS; R01 CA163890/CA/NCI NIH HHS; UL1 TR000041/TR/NCATS NIH HHS
Chemical
Reg. No./Substance:
0/Estrogens; 0/Receptors, Estrogen; 0/Selective Estrogen Receptor Modulators
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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