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Am J Physiol Heart Circ Physiol (February 21, 2002). doi:10.1152/ajpheart.00772.2001
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Articles in PresS, published online ahead of print February 21, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00772.2001
Submitted on August 28, 2001
Accepted on February 4, 2002

Estrogen modulation of eNOS activity and its association with caveolin-3 and calmodulin in rat heart

Xu Wang1 and Abdel A Abdel-Rahman1*

1 Pharmacology, Brody School of Medicine at East Carolina University, Greenville, NC, USA

* To whom correspondence should be addressed. E-mail: abdelrahmana{at}mail.ecu.edu.

Previous studies showed that estrogen modulation of endothelial nitric oxide synthase (eNOS) may confer protection against heart disease. Here, we demonstrate an association between reductions in baroreflex-mediated bradycardia and in cardiac NOS activity in ovariectomized (OVX) rats compared with the controls. The latter resulted, at least in part, from a reduction in cardiac eNOS protein. eNOS-derived NO and its biological effects are determined by the levels of eNOS protein and by eNOS catalytic activity; the latter is regulated partly through the dynamic interaction with an inhibitory protein (caveolin), and a stimulatory protein (calmodulin). The association of eNOS immunoprecipitated with caveolin-3 and calmodulin was examined. Caveolin-3 and calmodulin binding with eNOS was increased and decreased, respectively, in OVX rats. 17ß-estradiol (E2) replacement restored, to within normal levels, the baroreflex-mediated bradycardic responses along with eNOS activity, eNOS expression and the association of eNOS with caveolin-3 and calmodulin. Our findings may help to elucidate the molecular mechanism underlying the favorable effects of estrogen on cardiac responses to baroreflex activation.




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