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Adenosine modulation of neurotransmission in human uterine arteries
Author(s) -
EingMei Tsai,
J.N. Lee,
PoHan Chiang,
MingShyan Huang
Publication year - 1996
Publication title -
molecular human reproduction
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.143
H-Index - 122
eISSN - 1460-2407
pISSN - 1360-9947
DOI - 10.1093/molehr/2.2.105
Subject(s) - adenosine , adenosine receptor , biology , endocrinology , medicine , calcium in biology , vasodilation , endothelium , adenosine a1 receptor , uterine artery , phenylephrine , adenosine a3 receptor , calcium , intracellular , receptor , microbiology and biotechnology , agonist , biochemistry , pregnancy , gestation , genetics , blood pressure
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 2 x 10(-6) 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.

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