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NEUROREGULATION AND MOTILITY

Prostaglandins mediate tonic contraction of the guinea pig and human gallbladder

Division of Gastroenterology and Department of Medicine of the Rhode Island Hospital and Brown University School of Medicine, Providence, Rhode Island

Submitted 24 February 2006 ; accepted in final form 12 May 2006

The gallbladder (GB) maintains tonic contraction modulated by neurohormonal 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 small interference RNA (siRNA). The results show that PGE₂, thromboxane A₂ (TxA₂), and PGF₂ cause a dose-dependent contraction of muscle strips and cells. However, only TxA₂ and PGE₂ (E prostanoid 1 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 nonselective 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; and 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.

gallbladder; muscle tension; prostaglandin E₂; thromboxane A₂; COX-1; COX-2; siRNA

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