Document Detail

Distinct cardioprotective effects of 17β-estradiol and dehydroepiandrosterone on pressure overload-induced hypertrophy in ovariectomized female rats.
MedLine Citation:
PMID:  21844826     Owner:  NLM     Status:  Publisher    
OBJECTIVE:: We recently reported decreased σ1 receptor expression in the heart after abdominal aortic stenosis in bilateral ovariectomized rats. Here, we use ovariectomized female rats to investigate the distinct cardioprotective effects of 17β-estradiol (E2) and dehydroepiandrosterone (DHEA) in pressure overload (PO)-induced cardiac dysfunction. METHODS:: E2 (0.1 mg/kg) and DHEA (30 mg/kg) were administered to rats subcutaneously and orally, respectively, for 14 days starting 2 weeks after aortic banding. RESULTS:: Both E2 and DHEA treatments significantly inhibited PO-induced increases both in heart weight/body weight ratio and lung weight/body weight ratios. Both E2 and DHEA also ameliorated hypertrophy-induced impairment of left ventricular end-diastolic pressure, left ventricular-developed pressure, left ventricular contraction and relaxation (±dp/dt) rates, heart rate, and mean arterial blood pressure. Notably, DHEA but not E2 administration rescued decreased PO-induced σ1 receptor reduction in the heart. Coadministration with N,N-Dipropyl-2-[4-methoxy-3-(2-phenylethoxy) phenyl]-ethylamine monohydrochloride, an σ1 receptor antagonist, inhibited DHEA-induced amelioration of heart dysfunction without altering E2-induced cardioprotection. Mechanistically, both E2 and DHEA treatments significantly restored PO-induced decreases in protein kinase B (Akt) phosphorylation and Akt-mediated endothelial nitric oxide synthase (eNOS) phosphorylation (Ser1179). N,N-Dipropyl-2-[4-methoxy-3-(2-phenylethoxy) phenyl]-ethylamine monohydrochloride treatment totally abolished DHEA-induced Akt and eNOS phosphorylation without altering E2-induced Akt-eNOS activation. CONCLUSIONS:: Taken together, these results from an ovariectomized rat model of PO-induced cardiac dysfunction show that DHEA but not E2 elicits a cardioprotective action through σ1 receptor activation. DHEA-induced Akt-eNOS activation through σ1 receptors is probably associated with its cardioprotective activity.
Hideaki Tagashira; Shenuarin Bhuiyan; Norifumi Shioda; Kohji Fukunaga
Related Documents :
12807346 - Dose-response related efficacy in orthostatic hypotension of a fixed combination of d-c...
2031636 - Cardiovascular adaptation during simulated microgravity: lower body negative pressure t...
3399516 - Effect of aerobic fitness on hemodynamic responses to upright tilting.
769906 - Therapeutic experience with fludrocortisone in diabetic postural hypotension.
22059756 - Pressure-induced conversion of α-connectin to β-connectin.
12589536 - Effects of non-invasive ventilation on middle ear function in healthy volunteers.
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-8-10
Journal Detail:
Title:  Menopause (New York, N.Y.)     Volume:  -     ISSN:  1530-0374     ISO Abbreviation:  -     Publication Date:  2011 Aug 
Date Detail:
Created Date:  2011-8-16     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9433353     Medline TA:  Menopause     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

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

Previous Document:  Prevalence of the Portuguese Population Attaining Sufficient Physical Activity.
Next Document:  Menopausal symptoms among healthy, middle-aged Omani women as assessed with the Menopause Rating Sca...