Abstract
Endothelial‐derived hyperpolarizing factor (EDHF) plays an important role in the regulation of vascular microcirculatory tone. This study aimed to explore the role of estrogen in the control of EDHF‐mediated responses in reproductive and non‐reproductive vasculature, and to study the contribution of endothelial cell (EC) Ca2+ signaling to this process. Mature female rats (n = 63) underwent ovariectomy, with one‐half receiving 17β‐estradiol replacement and the other half serving as estrogen‐deficient controls. Uterine or mesenteric resistance arteries were cannulated, pressurized, and loaded with fura‐2 for measurements of EC [Ca2+]i. NO and prostacyclin production were inhibited with 200 µM LNNA and 10 µM indomethacin, respectively. ACh effectively dilated arteries pre‐constricted with phenylephrine, but failed to induce dilatation of vessels pre‐constricted with depolarizing K+ solution. Estrogen replacement increased arterial sensitivity (EC50) to ACh five‐ and two‐fold in uterine and mesenteric arteries, respectively. Estrogen replacement was also associated with both increased basal and ACh‐stimulated elevations of EC [Ca2+]i in uterine, but not mesenteric vessels. These data demonstrate that estrogen promotes EDHF‐related mechanism(s) more effectively in reproductive vs. non‐reproductive vessels, in part through enhanced EC Ca2+ signaling.Supported by NIH HL067250 and HL073895
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
