TY - JOUR
T1 - Steroid hormones and uterine vascular adaptation to pregnancy
AU - Chang, Katherine
AU - Zhang, Lubo
N1 - Role of progesterone in a1-adrenergic and PKC-mediated contractions in uterine artery Ford has previously shown several findings on the effects of progesterone at the level of the uterine arterial smooth muscle during pregnancy. UBF during pregnancy is a physiological state that involves 2 important calcium-mediated events: phasic contractility and tone.
PY - 2008/4
Y1 - 2008/4
N2 - Pregnancy is a physiological state that involves a significant decrease in uterine vascular tone and an increase in uterine blood flow, which is mediated in part by steroid hormones, including estrogen, progesterone, and cortisol. Previous studies have demonstrated the involvement of these hormones in the regulation of uterine artery contractility through signaling pathways specific to the endothelium and the vascular smooth muscle. Alterations in endothelial nitric oxide synthase expression and activity, nitric oxide production, and expression of enzymes involved in PGI2 production contribute to the uterine artery endothelium-specific responses. Steroid hormones also have an effect on calcium-activated potassium channel activity, PKC signaling pathway and myogenic tone, and alterations in pharmacomechanical coupling in the uterine artery smooth muscle. This review addresses current understanding of the molecular mechanisms by which steroid hormones including estrogen, progesterone, and cortisol modulate uterine artery contractility to alter uterine blood flow during pregnancy with an emphasis on the pregnant ewe model. © 2008 by the Society for Gynecologic Investigation.
AB - Pregnancy is a physiological state that involves a significant decrease in uterine vascular tone and an increase in uterine blood flow, which is mediated in part by steroid hormones, including estrogen, progesterone, and cortisol. Previous studies have demonstrated the involvement of these hormones in the regulation of uterine artery contractility through signaling pathways specific to the endothelium and the vascular smooth muscle. Alterations in endothelial nitric oxide synthase expression and activity, nitric oxide production, and expression of enzymes involved in PGI2 production contribute to the uterine artery endothelium-specific responses. Steroid hormones also have an effect on calcium-activated potassium channel activity, PKC signaling pathway and myogenic tone, and alterations in pharmacomechanical coupling in the uterine artery smooth muscle. This review addresses current understanding of the molecular mechanisms by which steroid hormones including estrogen, progesterone, and cortisol modulate uterine artery contractility to alter uterine blood flow during pregnancy with an emphasis on the pregnant ewe model. © 2008 by the Society for Gynecologic Investigation.
KW - Pregnancy
KW - Steroid hormone
KW - Uterine artery
KW - Uterus/blood supply
KW - Humans
KW - Potassium Channels/physiology
KW - Progesterone/physiology
KW - Nitric Oxide/metabolism
KW - Signal Transduction/physiology
KW - Nitric Oxide Synthase Type III/physiology
KW - Receptors, Estrogen/metabolism
KW - Muscle, Smooth, Vascular/metabolism
KW - Pregnancy/physiology
KW - Hydrocortisone/physiology
KW - Arteries/physiology
KW - Female
KW - Estrogens/physiology
KW - Endothelium/enzymology
UR - http://www.scopus.com/inward/record.url?scp=43849085332&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=43849085332&partnerID=8YFLogxK
UR - https://www.mendeley.com/catalogue/4842b460-3a93-37b1-8605-1944a42e4987/
U2 - 10.1177/1933719108317975
DO - 10.1177/1933719108317975
M3 - Review article
C2 - 18497342
SN - 1933-7191
VL - 15
SP - 336
EP - 348
JO - Reproductive Sciences
JF - Reproductive Sciences
IS - 4
ER -