TY - JOUR
T1 - Regulation of types I and III NOS in ovine uterine arteries by daily and acute estrogen exposure
AU - Salhab, Walid A.
AU - Shaul, Philip W.
AU - Cox, Blair E.
AU - Rosenfeld, Charles R.
PY - 2000/6
Y1 - 2000/6
N2 - Nitric oxide contributes to estrogen-mediated uterine vasodilation; however, the nitric oxide synthases (NOS) involved and their location within uterine arteries are incompletely documented. We investigated the effects of repetitive daily and acute estradiol-17β (E2β) exposure on uterine hemodynamics and NOS abundance and localization in uterine arteries from nonpregnant ovariectomized ewes receiving daily intravenous E2β (1 μ/kg, n = 5) or no E2β (n = 7) for 5 days to determine NOS abundance, cGMP contents, and NOS immunohistochemistry. Daily E2β increased basal and E2β-mediated rises in uterine blood flow (UBF) 36 and 43% (<0.01), respectively, calcium-dependent NOS activity 150% (P < 0.02) in endothelium- intact and -denuded (~40% of total NOS) arteries, and cGMP contents 39% (P < 0.05). Endothelial NOS (eNOS) was detected in luminal endothelium, whereas neuronal NOS (nNOS) protein was only in the media. A second group of ewes received E2β (1 μg/kg iv) for 4 days and acute intravenous E2β (n = 8) or vehicle (n = 4) on day 5. UBF rose 5.5-fold (P < 0.001) 115 min after E2β, at which time only endothelium-derived calcium-dependent NOS activity increased 30 ± 13% (P < 0.05). Daily E2β enhances basal and E2β-mediated increases in UBF, which parallel increases in endothelium-derived eNOS and smooth muscle-derived nNOS. Acute E2β, however, selectively increases endothelium-derived eNOS.
AB - Nitric oxide contributes to estrogen-mediated uterine vasodilation; however, the nitric oxide synthases (NOS) involved and their location within uterine arteries are incompletely documented. We investigated the effects of repetitive daily and acute estradiol-17β (E2β) exposure on uterine hemodynamics and NOS abundance and localization in uterine arteries from nonpregnant ovariectomized ewes receiving daily intravenous E2β (1 μ/kg, n = 5) or no E2β (n = 7) for 5 days to determine NOS abundance, cGMP contents, and NOS immunohistochemistry. Daily E2β increased basal and E2β-mediated rises in uterine blood flow (UBF) 36 and 43% (<0.01), respectively, calcium-dependent NOS activity 150% (P < 0.02) in endothelium- intact and -denuded (~40% of total NOS) arteries, and cGMP contents 39% (P < 0.05). Endothelial NOS (eNOS) was detected in luminal endothelium, whereas neuronal NOS (nNOS) protein was only in the media. A second group of ewes received E2β (1 μg/kg iv) for 4 days and acute intravenous E2β (n = 8) or vehicle (n = 4) on day 5. UBF rose 5.5-fold (P < 0.001) 115 min after E2β, at which time only endothelium-derived calcium-dependent NOS activity increased 30 ± 13% (P < 0.05). Daily E2β enhances basal and E2β-mediated increases in UBF, which parallel increases in endothelium-derived eNOS and smooth muscle-derived nNOS. Acute E2β, however, selectively increases endothelium-derived eNOS.
KW - Endothelium
KW - Guanosine 3',5'- cyclic monophosphate
KW - Guanylyl cyclase
KW - Vascular smooth muscle
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U2 - 10.1152/ajpheart.2000.278.6.h2134
DO - 10.1152/ajpheart.2000.278.6.h2134
M3 - Article
C2 - 10843913
AN - SCOPUS:0033935574
SN - 0363-6135
VL - 278
SP - H2134-H2142
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 6 47-6
ER -