RGD Reference Report - Gender related alterations of beta-adrenoceptor mechanisms in heart failure due to arteriovenous fistula. - Rat Genome Database

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Gender related alterations of beta-adrenoceptor mechanisms in heart failure due to arteriovenous fistula.

Authors: Dent, MR  Tappia, PS  Dhalla, NS 
Citation: Dent MR, etal., J Cell Physiol. 2011 Oct 20. doi: 10.1002/jcp.23058.
RGD ID: 5509867
Pubmed: PMID:22015551   (View Abstract at PubMed)
DOI: DOI:10.1002/jcp.23058   (Journal Full-text)

This study was undertaken to determine gender related changes in different components of beta-adrenoceptor (beta-AR) system in response to arteriovenous fistula (AV-shunt), which is known to produce heart failure due to volume overload. AV-shunt was induced in male and female rats for 16 wks by the needle technique; ovariectomized (OVX) rats treated with or without estrogen were also used. Although AV-shunt for 16 wks produced cardiac hypertrophy in both sexes, male animals showed cardiac dysfunction whereas cardiac performance was maintained in females. Both beta(1)-AR and beta(2)-AR protein content and mRNA levels were decreased in male and increased in female hearts post-AV-shunt. The basal adenylyl cyclase (AC) activity was lower in the female heart; however, AC protein content and the increase in epinephrine (EPi)-stimulated AC activity were greater in the female AV-shunt group as compared to males. While AC V/VI and beta-arrestin 2 mRNA levels were decreased in males, mRNA level for GRK2 was increased in females post-AV-shunt. In contrast to intact females, AV-shunt OVX animals showed depressed cardiac function, decreased beta(1)-AR, beta(2)-AR and AC protein content, as well as reduced EPi-stimulated AC activity. Treatment of OVX rats with 17-beta estradiol attenuated the AV-shunt induced changes in beta-AR and AC protein content as well as cardiac dysfunction. These results reveal that beta-AR signal transduction system in response to AV-shunt is downregulated in males and upregulated in females. Furthermore, estrogen appears to play an important role in the upregulation of beta-AR mechanisms and the maintenance of cardiac function in AV-shunt females. J. Cell. Physiol. (c) 2011 Wiley Periodicals, Inc.



RGD Manual Disease Annotations    Click to see Annotation Detail View
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
ARRB1HumanArteriovenous Fistula  ISOArrb1 (Rattus norvegicus)mRNA and protein:altered expression:left ventricle (rat)RGD 
ARRB2HumanArteriovenous Fistula  ISOArrb2 (Rattus norvegicus)mRNA and protein:altered expression:left ventricle (rat)RGD 
Arrb1RatArteriovenous Fistula  IEP mRNA and protein:altered expression:left ventricle (rat)RGD 
Arrb1MouseArteriovenous Fistula  ISOArrb1 (Rattus norvegicus)mRNA and protein:altered expression:left ventricle (rat)RGD 
Arrb2RatArteriovenous Fistula  IEP mRNA and protein:altered expression:left ventricle (rat)RGD 
Arrb2MouseArteriovenous Fistula  ISOArrb2 (Rattus norvegicus)mRNA and protein:altered expression:left ventricle (rat)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Arrb1  (arrestin, beta 1)
Arrb2  (arrestin, beta 2)

Genes (Mus musculus)
Arrb1  (arrestin, beta 1)
Arrb2  (arrestin, beta 2)

Genes (Homo sapiens)
ARRB1  (arrestin beta 1)
ARRB2  (arrestin beta 2)


Additional Information