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Mothers and Babies Research Center, Hunter Medical Research Institute, Newcastle, New South Wales, Australia
¹ Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia
² Neonatal Intensive Care Unit, Hunter Medical Research Institute, Newcastle, New South Wales, Australia

(Requests for offprints should be addressed to I M R Wright, Neonatal Intensive Care Unit, John Hunter Hospital, Locked Bag #1, Hunter Region Mail Center, Newcastle, New South Wales, 2310, Australia; Email: iwright{at}mail.newcastle.edu.au)

Females have a significantly greater life expectancy than males, which in part may be due to the cardio-protective effects of the female sex hormone, estrogen, on vascular function. However, the sex-specific mechanisms contributing to these differences are complex and not fully understood. Previously we have reported that corticotropin-releasing hormone (CRH) has potent dilator effects in the female skin circulation via mast cell degranulation. Furthermore the dilator response to CRH was more enhanced in females than in age-matched males, suggesting that estrogens may be involved. In this study we examined whether CRH-induced dilation and endothelial cell-dependent dilation in the skin circulation of pre-menopausal females were associated with changes in estrogen during the menstrual cycle. CRH-induced dilation (1 nM) was enhanced in the presence of high circulating concentrations of estrogen and a positive correlation was identified between CRH-induced dilation and plasma estrogen concentrations. Endothelial cell-dependent dilation was examined using acetylcholine. Acetylcholine-induced dilation (1 nM) was not correlated with circulating concentrations of estrogen. These data suggest the variation in CRH-induced dilation in the skin microvasculature during the menstrual cycle may be due to estrogenic effects on mast cell function and not due to direct changes in endothelial cell function.

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