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Molecular Human Reproduction Vol. 2, NUMBER 2 pp. 105-109, 1996
© European Society of Human Reproduction and Embryology 1996

research-article

Adenosine modulation of neurotransmission in human uterine arteries

E.M. Tsai1,4, J.N. Lee, P.H. Chiang2 and M.S. Huang3

1Department of Obstetrics and Gynecology, Kaohsiung Medical College Hospital 100, Shih-Chuan 1st Road, Kaohsiung, Taiwan 2Department of Urology, Kaohsiung Medical College Hospital 100, Shih-Chuan 1st Road, Kaohsiung, Taiwan 3Department of Medicine, Kaohsiung Medical College Hospital 100, Shih-Chuan 1st Road, Kaohsiung, Taiwan

To whom correspondence should be addressed at: 4To whom correspondence should be addressed

The relaxing effects of adenosine, N-[(R)-1-methyl-2 phenylethyl]-adenosine (R-PIA) and 5-N-ethylcarboxamide adenosine (NECA) were investigated in human uterine arteries precontracted by phenylephrine in vitro. Adenosine, R-PIA and NECA relaxed isolated uterine arteries with intact endothelium, the potency order was NECA > R-PIA > adenosine. When tested on vessels devoid of their endothelium, the relaxing effect of adenosine was the same. These results suggest the vasodilatation effect on human uterine arteries is endothelium-independent, and might be via the A2 receptor (by pharmacological classification). By administering adenosine to human uterine arterial cell culture, single cell intracellular calcium change was also determined by laser cytometry. Decreased intracellular calcium was observed after administration of adenosine 10–6 M and 2x10–5 M. We concluded from the results that adenosine acts on human uterine artery cell by A2 receptor, independently of the endothelium, and decreases the intracellular calcium concentration, thus causing uterine artery relaxation.

adenosine/human uterine artery/intracellular calcium concentration


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