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Am J Physiol Heart Circ Physiol 284: H1142-H1151, 2003. First published December 12, 2002; doi:10.1152/ajpheart.00834.2002
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Vol. 284, Issue 4, H1142-H1151, April 2003

Effect of cortisol on norepinephrine-mediated contractions in ovine uterine arteries

Daliao Xiao, Xiaohui Huang, William J. Pearce, Lawrence D. Longo, and Lubo Zhang

Center for Perinatal Biology, Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, California 92350

Cortisol potentiated norepinephrine (NE)-mediated contractions in ovine uterine arteries (UA). We tested the hypothesis that cortisol regulated alpha 1-adrenoceptor-mediated pharmacomechanical coupling differentially in nonpregnant UA (NUA) and pregnant UA (PUA). Cortisol (10 ng/ml for 24 h) significantly increased contractile coupling efficiency of alpha 1-adrenoceptors in NUA, but increased alpha 1-adrenoceptor density in PUA. Cortisol potentiated NE-induced inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] synthesis in both NUA and PUA, but increased coupling efficiency of alpha 1-adrenoceptors to Ins(1,4,5)P3 synthesis only in NUA. Carbenoxolone alone did not affect NE-mediated Ins(1,4,5)P3 production, but significantly enhanced cortisol-mediated potentiation of NE-stimulated Ins(1,4,5)P3 synthesis in PUA. In addition, cortisol potentiated the NE-induced increase in Ca2+ concentration in PUA, but increased NE-mediated contraction for a given amount of Ca2+ concentration in NUA. Collectively, the results indicate that cortisol potentiates NE-mediated contractions differentially in NUA and PUA, i.e., by upregulating alpha 1-adrenoceptor density leading to increased Ca2+ mobilization in PUA while increasing alpha 1-adrenoceptor coupling efficiency and myofilament Ca2+ sensitivity in NUA. In addition, the results suggest that pregnancy increases type 2 11beta -hydroxysteroid dehydrogenase activity in the UA.

alpha 1-adrenoceptor; 11beta -hydroxysteroid dehydrogenase; inositol 1,4,5-trisphosphate; calcium; pregnancy


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