Abstract
During pregnancy, maternal plasma cortisol concentrations approximately double. Given that cortisol plays an important role in the regulation of vascular reactivity, the present study investigated the potential role of cortisol in potentiation of uterine artery (UA) contractility and tested the hypothesis that pregnancy downregulated the cortisol-mediated potentiation. In vitro cortisol treatment (3, 10, or 30 ng/ml for 24 h) produced a dose-dependent increase in norepinephrine (NE)-induced contractions in both nonpregnant and pregnant (138-143 days gestation) sheep UA. However, this cortisol-mediated response was significantly attenuated by ∼50% in pregnant UA. The 11β-hydroxysteroid dehydrogenase (11-βHSD) inhibitor carbenoxolone did not change the effect of cortisol in nonpregnant UA but abolished its effect in pregnant UA by increasing the NE pD2 in control tissues from 6.20 ± 0.05 to 6.59 ± 0.11. The apparent dissociation constant value of NE α1-adrenoceptors was not changed by cortisol in pregnant UA but was decreased in nonpregnant UA. There was no difference in glucocorticoid receptor density between nonpregnant and pregnant UA. Cortisol significantly decreased endothelial nitric oxide (NO) synthase protein levels and NO release in both nonpregnant and pregnant UA, but the effect of cortisol was attenuated in pregnant UA by ∼50%. Carbenoxolone alone had no effects on NO release in nonpregnant UA but was decreased in pregnant UA. These results suggest that cortisol potentiates NE-mediated contractions by decreasing NO release and increasing NE-binding affinity to α1-adrenoceptors in nonpregnant UA. Pregnancy attenuates UA sensitivity to cortisol, which may be mediated by increasing type-2 11-βHSD activity in UA.
Original language | English |
---|---|
Pages (from-to) | H238-H246 |
Journal | American Journal of Physiology - Heart and Circulatory Physiology |
Volume | 283 |
Issue number | 1 52-1 |
DOIs | |
State | Published - 2002 |
ASJC Scopus Subject Areas
- Physiology
- Cardiology and Cardiovascular Medicine
- Physiology (medical)
Keywords
- 11-βHSD
- Glucocorticoid receptor
- Nitric oxide
- α-adrenoceptor
Access to Document
10.1152/ajpheart.00842.2001License: Unspecified
OpenUrl availability
Other files and links
Cite this
- APA
- Standard
- Harvard
- Vancouver
- Author
- BIBTEX
- RIS
Xiao, D., Huang, X., Bae, S., Ducsay, C. A. (2002). Cortisol-mediated potentiation of uterine artery contractility: Effect of pregnancy. American Journal of Physiology - Heart and Circulatory Physiology, 283(1 52-1), H238-H246. https://doi.org/10.1152/ajpheart.00842.2001
Cortisol-mediated potentiation of uterine artery contractility: Effect of pregnancy. / Xiao, Daliao; Huang, Xiaohui; Bae, Soochan et al.
In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 283, No. 1 52-1, 2002, p. H238-H246.
Research output: Contribution to journal › Article › peer-review
Xiao, D, Huang, X, Bae, S, Ducsay, CA 2002, 'Cortisol-mediated potentiation of uterine artery contractility: Effect of pregnancy', American Journal of Physiology - Heart and Circulatory Physiology, vol. 283, no. 1 52-1, pp. H238-H246. https://doi.org/10.1152/ajpheart.00842.2001
Xiao D, Huang X, Bae S, Ducsay CA, Zhang L. Cortisol-mediated potentiation of uterine artery contractility: Effect of pregnancy. American Journal of Physiology - Heart and Circulatory Physiology. 2002;283(1 52-1):H238-H246. doi: 10.1152/ajpheart.00842.2001
Xiao, Daliao ; Huang, Xiaohui ; Bae, Soochan et al. / Cortisol-mediated potentiation of uterine artery contractility : Effect of pregnancy. In: American Journal of Physiology - Heart and Circulatory Physiology. 2002 ; Vol. 283, No. 1 52-1. pp. H238-H246.
@article{d22a60f423aa4455983a945463562fa3,
title = "Cortisol-mediated potentiation of uterine artery contractility: Effect of pregnancy",
abstract = "During pregnancy, maternal plasma cortisol concentrations approximately double. Given that cortisol plays an important role in the regulation of vascular reactivity, the present study investigated the potential role of cortisol in potentiation of uterine artery (UA) contractility and tested the hypothesis that pregnancy downregulated the cortisol-mediated potentiation. In vitro cortisol treatment (3, 10, or 30 ng/ml for 24 h) produced a dose-dependent increase in norepinephrine (NE)-induced contractions in both nonpregnant and pregnant (138-143 days gestation) sheep UA. However, this cortisol-mediated response was significantly attenuated by ∼50% in pregnant UA. The 11β-hydroxysteroid dehydrogenase (11-βHSD) inhibitor carbenoxolone did not change the effect of cortisol in nonpregnant UA but abolished its effect in pregnant UA by increasing the NE pD2 in control tissues from 6.20 ± 0.05 to 6.59 ± 0.11. The apparent dissociation constant value of NE α1-adrenoceptors was not changed by cortisol in pregnant UA but was decreased in nonpregnant UA. There was no difference in glucocorticoid receptor density between nonpregnant and pregnant UA. Cortisol significantly decreased endothelial nitric oxide (NO) synthase protein levels and NO release in both nonpregnant and pregnant UA, but the effect of cortisol was attenuated in pregnant UA by ∼50%. Carbenoxolone alone had no effects on NO release in nonpregnant UA but was decreased in pregnant UA. These results suggest that cortisol potentiates NE-mediated contractions by decreasing NO release and increasing NE-binding affinity to α1-adrenoceptors in nonpregnant UA. Pregnancy attenuates UA sensitivity to cortisol, which may be mediated by increasing type-2 11-βHSD activity in UA.",
keywords = "11-βHSD, Glucocorticoid receptor, Nitric oxide, α-adrenoceptor",
author = "Daliao Xiao and Xiaohui Huang and Soochan Bae and Ducsay, {Charles A.} and Lubo Zhang",
year = "2002",
doi = "10.1152/ajpheart.00842.2001",
language = "English",
volume = "283",
pages = "H238--H246",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
number = "1 52-1",
}
TY - JOUR
T1 - Cortisol-mediated potentiation of uterine artery contractility
T2 - Effect of pregnancy
AU - Xiao, Daliao
AU - Huang, Xiaohui
AU - Bae, Soochan
AU - Ducsay, Charles A.
AU - Zhang, Lubo
PY - 2002
Y1 - 2002
N2 - During pregnancy, maternal plasma cortisol concentrations approximately double. Given that cortisol plays an important role in the regulation of vascular reactivity, the present study investigated the potential role of cortisol in potentiation of uterine artery (UA) contractility and tested the hypothesis that pregnancy downregulated the cortisol-mediated potentiation. In vitro cortisol treatment (3, 10, or 30 ng/ml for 24 h) produced a dose-dependent increase in norepinephrine (NE)-induced contractions in both nonpregnant and pregnant (138-143 days gestation) sheep UA. However, this cortisol-mediated response was significantly attenuated by ∼50% in pregnant UA. The 11β-hydroxysteroid dehydrogenase (11-βHSD) inhibitor carbenoxolone did not change the effect of cortisol in nonpregnant UA but abolished its effect in pregnant UA by increasing the NE pD2 in control tissues from 6.20 ± 0.05 to 6.59 ± 0.11. The apparent dissociation constant value of NE α1-adrenoceptors was not changed by cortisol in pregnant UA but was decreased in nonpregnant UA. There was no difference in glucocorticoid receptor density between nonpregnant and pregnant UA. Cortisol significantly decreased endothelial nitric oxide (NO) synthase protein levels and NO release in both nonpregnant and pregnant UA, but the effect of cortisol was attenuated in pregnant UA by ∼50%. Carbenoxolone alone had no effects on NO release in nonpregnant UA but was decreased in pregnant UA. These results suggest that cortisol potentiates NE-mediated contractions by decreasing NO release and increasing NE-binding affinity to α1-adrenoceptors in nonpregnant UA. Pregnancy attenuates UA sensitivity to cortisol, which may be mediated by increasing type-2 11-βHSD activity in UA.
AB - During pregnancy, maternal plasma cortisol concentrations approximately double. Given that cortisol plays an important role in the regulation of vascular reactivity, the present study investigated the potential role of cortisol in potentiation of uterine artery (UA) contractility and tested the hypothesis that pregnancy downregulated the cortisol-mediated potentiation. In vitro cortisol treatment (3, 10, or 30 ng/ml for 24 h) produced a dose-dependent increase in norepinephrine (NE)-induced contractions in both nonpregnant and pregnant (138-143 days gestation) sheep UA. However, this cortisol-mediated response was significantly attenuated by ∼50% in pregnant UA. The 11β-hydroxysteroid dehydrogenase (11-βHSD) inhibitor carbenoxolone did not change the effect of cortisol in nonpregnant UA but abolished its effect in pregnant UA by increasing the NE pD2 in control tissues from 6.20 ± 0.05 to 6.59 ± 0.11. The apparent dissociation constant value of NE α1-adrenoceptors was not changed by cortisol in pregnant UA but was decreased in nonpregnant UA. There was no difference in glucocorticoid receptor density between nonpregnant and pregnant UA. Cortisol significantly decreased endothelial nitric oxide (NO) synthase protein levels and NO release in both nonpregnant and pregnant UA, but the effect of cortisol was attenuated in pregnant UA by ∼50%. Carbenoxolone alone had no effects on NO release in nonpregnant UA but was decreased in pregnant UA. These results suggest that cortisol potentiates NE-mediated contractions by decreasing NO release and increasing NE-binding affinity to α1-adrenoceptors in nonpregnant UA. Pregnancy attenuates UA sensitivity to cortisol, which may be mediated by increasing type-2 11-βHSD activity in UA.
KW - 11-βHSD
KW - Glucocorticoid receptor
KW - Nitric oxide
KW - α-adrenoceptor
UR - http://www.scopus.com/inward/record.url?scp=0036299775&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036299775&partnerID=8YFLogxK
U2 - 10.1152/ajpheart.00842.2001
DO - 10.1152/ajpheart.00842.2001
M3 - Article
C2 - 12063296
SN - 0363-6135
VL - 283
SP - H238-H246
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 1 52-1
ER -