Abstract
We recently showed that augmented vascular activation of STIM1/Orai1 pathway in male hypertensive rats contributes to the sex‐related impairment in intracellular Ca2+handling. We hypothesized that sex hormones contribute to the vascular protection in female hypertensive rats, via a decrease in STIM1/Orai1 activation. Endothelium‐denuded aortic rings from ovariectomized (OVX, for 15 weeks) or intact (SHAM) female stroke prone spontaneously hypertensive (SHRSP) and Wistar‐Kyoto (WKY) rats, were used to functionally evaluate Ca2+ influx‐induced contractions [upon depletion and reloading of intracellular Ca2+ (Ca2+loading period)]. Sarcoplasmic reticulum Ca+2 ATPase was inhibited with thapsigargin (10μM). During the Ca2+loading period, force development was augmented in aortas from SHRSP OVX vs. other groups and increased contraction was normalized with gadolinium (100μM, CRAC channel inhibitor), as well as blockade of STIM1 and Orai1 with neutralizing antibodies. Intracellular Ca2+ store release was increased in aortas from SHRSP vs. WKY, but no differences were observed between SHAM and OVX. Orai1 and STIM1 expression were increased in aortas from SHRSP OVX vs. the other groups. We conclude that sex hormones negatively modulate the expression and activity of STIM1/Orai1, contributing to the sex‐related differences in intracellular Ca2+ handling.Financial support: American Heart Association (AHA 09GRNT2250383)
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