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Am J Physiol Gastrointest Liver Physiol 293: G1244-G1251, 2007. First published September 27, 2007; doi:10.1152/ajpgi.00206.2007
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NEUROREGULATION AND MOTILITY

Reactive oxygen species are messengers in maintenance of human and guinea pig gallbladder tonic contraction

Ping Cong, Zuo-Liang Xiao, Piero Biancani, and Jose Behar

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

Submitted 7 May 2007 ; accepted in final form 19 September 2007

The tonic contraction of human and guinea pig gallbladder (GB) is dependent on basal levels of PGE2 and thromboxane A2 (TxA2). The pathway involved in the genesis of these prostaglandins has not been elucidated. We aimed to examine the source of reactive oxygen species (ROS) and whether they contribute to the genesis of GB tonic contraction by generating basal prostaglandin levels. Tonic contraction was studied in human and guinea pig GB muscle strips treated with ROS scavengers (Tiron and catalase), apocynin (an inhibitor of NADPH oxidase), and NOX-1 small interference RNA (siRNA). The subunits of NADPH oxidase and their functional roles were determined with specific antibodies in GB muscle cells. ROS scavengers reduced the GB tonic contraction and H2O2 and PGE2 levels. Apocynin also inhibited the tonic contraction. Antibodies against subunits of NADPH oxidase present in GB muscle cells lowered H2O2 and PGE2 levels. NOX-1 siRNA transfection reduced the tonic contraction, NOX-1 expression, and levels of H2O2 and PGE2. Tiron and apocynin inhibited the expected increase in tension and H2O2 levels induced by stretching of muscle strips. H2O2 increased the levels of PGE2 and TxA2 by increasing platelet-activating factor-like lipids that phosphorylate p38 and cPLA2 sequentially. H2O2 generated by NADPH oxidase participates in a signal transduction pathway that maintains the GB tonic contraction by activating PAF, p38, and cPLA2 to generate prostaglandins.

muscle; NADPH oxidase; prostaglandins


Address for reprint requests and other correspondence: J. Behar, Division of Gastroenterology, APC 406, Rhode Island Hospital/Brown Univ. Medical School, 593 Eddy St., Providence, RI 02903 (e-mail: Jose_Behar{at}brown.edu)




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Am J Physiol Gastrointest Liver Physiol, July 1, 2008; 295(1): G209 - G209.
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