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Gender differences in beta-adrenoceptor system in cardiac hypertrophy due to arteriovenous fistula.

Authors: Dent, MR  Tappia, PS  Dhalla, NS 
Citation: Dent MR, etal., J Cell Physiol. 2011 Jan;226(1):181-6.
Pubmed: (View Article at PubMed) PMID:20677219
DOI: Full-text: DOI:10.1002/jcp.22321

This study was undertaken to determine alterations in the beta-adrenoceptor (beta-AR) signaling system in male and female rats at 4 weeks after the induction of arteriovenous (AV) fistula or shunt. AV shunt produced a greater degree of cardiac hypertrophy and larger increase in cardiac output in male than in female animals. Increases in plasma levels of norepinephrine and epinephrine (EPI) due to AV shunt were also higher in male than females. While no difference in the beta(1)-AR affinity was seen in males and females, AV shunt induced increase in beta(1)-AR density in female rats was higher than that in males. Furthermore, no changes in basal adenylyl cyclase (AC) V/VI mRNA levels were seen; however, the increase in EPI-stimulated AC activities was greater in AV shunt females than in males. AV shunt decreased myocardial beta(1)-AR mRNA level in male rats and increased beta(2)-AR mRNA level in female hearts; an increase in G(i)-protein mRNA was detected only in male hearts. Although GRK2 gene expression was increased in both sexes, an increase in GRK3 mRNA was seen only in AV shunt female rats. beta-arrestin1 mRNA was elevated in females whereas beta-arrestin 2 gene expression was increased in both male and female AV shunt rats. While these data demonstrate gender associated differences in various components of the beta-AR system in cardiac hypertrophy due to AV shunt, only higher levels of plasma catecholamines may account for the greater increase in cardiac output and higher degree of cardiac hypertrophy in males.


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CRRD Object Information
CRRD ID: 5685025
Created: 2012-01-09
Species: All species
Last Modified: 2012-01-09
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.