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. 1997 Jun 15;501(Pt 3):517–525. doi: 10.1111/j.1469-7793.1997.517bm.x

Stimulation of anion secretion by beta-adrenoceptors in the mouse endometrial epithelium.

H C Chan 1, S K Fong 1, S C So 1, Y W Chung 1, P Y Wong 1
PMCID: PMC1159453  PMID: 9218212

Abstract

1. Regulation of anion secretion by adrenoceptors in primary culture of mouse endometrial epithelium was investigated using the short circuit current (ISC) technique. 2. Adrenaline stimulated a sustained increase in the ISC in a concentration-dependent manner. The adrenaline-induced ISC could be inhibited by pretreatment with diphenylamine 2,2'-dicarboxylic acid (DPC) or replacement of external Cl- and HCO3-, but not by amiloride or replacement of Na+ in apical solution. 3. The concentration-dependent responses of the adrenaline-induced ISC to the Cl- channel blockers glibenclamide and DPC were examined and exhibited IC50 values of 380 and 960 microM, respectively. 4. The effect of various adrenoceptor agonists on the ISC was examined. The order of potency appeared to be isoprenaline > adrenaline > noradrenaline, while no response was elicited by the alpha-adrenoceptor agonist methoxamine, indicating a predominant involvement of beta-adrenoceptors. 5. The beta-adrenoceptor antagonist propranolol was found to be much more effective than the alpha-adrenoceptor antagonist phentolamine in inhibiting the ISC responses induced by all adrenoceptor agonists examined. 6. The effect of adrenaline on the ISC was mimicked by an adenylate cyclase activator, forskolin, but suppressed by the adenylate cyclase inhibitor MDL 12,330A, indicating the involvement of cAMP. 7. Our results demonstrate that anion secretion by the mouse endometrial epithelium is regulated by beta-adrenoceptors and involves a cAMP-dependent mechanism.

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Selected References

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