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1 Medicine, Rhode Island Hospital, Providence, Rhode Island, United States
* To whom correspondence should be addressed. E-mail: jose_behar{at}brown.edu.
The gallbladder (GB) maintains tonic contraction modulated by neuro-hormonal inputs but generated by myogenic mechanisms. The aim of these studies was to examine the role of prostaglandins in the genesis of GB myogenic tension. Muscle strips and cells were treated with prostaglandin agonists, antagonists, cyclooxygenase (COX) inhibitors and siRNA. The results show that PGE2, TxA2, and PGF2alpha cause a dose dependent contraction of muscle strips and cells. However, onlyTxA2 and PGE2 (EP1 receptor type) antagonists induced a dose dependent decrease in tonic tension. A COX-1 inhibitor decreased partially the tonic contraction and TxB2 (TxA2 stable metabolite) levels; a COX-2 inhibitor lowered the tonic contraction partially and reduced PGE2 levels. Both inhibitors and the non-selective COX inhibitor indomethacin abolished the tonic contraction. Transfection of human GB muscle strips with COX-1 siRNA partially lowered the tonic contraction and reduced COX-1 protein expression and TxB2 levels; COX-2 siRNA also partially reduced the tonic contraction, the protein expression of COX-2 and PGE2. Stretching muscle strips by 1, 2, 3 and 4 g increased the active tension, TxB2 and PGE2 levels; a COX-1 inhibitor prevented the increase in tension and TxB2; a COX-2 inhibitor inhibited the expected rise in tonic contraction and PGE2. Indomethacin blocked the rise in tension and TxB2 and PGE2 levels. We conclude that PGE2 generated by COX-2 and TxA2 generated by COX-1 contributes to the maintenance of GB tonic contraction and that variations in tonic contraction are associated with concomitant changes in PGE2 and TxA2 levels.
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