The effect of calcium and prostaglandin inhibitors on the intestinal fluid response to heat-stable enterotoxin of Escherichia coli.
The role of calcium and prostaglandins in the intestinal fluid response to Escherichia coli heat-stable enterotoxin ( ST) was investigated in infant mice. Drugs that inhibit calcium uptake-cromolyn sodium, diltiazem, and nifedipine-caused a significant (P less than 0.02, P less than 0.02, and P less than 0.01, respectively) decrease in the fluid response when administered with ST. The effect of cromolyn sodium and nifedipine was dose-dependent; both agents were effective when administered 30 min before toxin challenge. Inhibitors of prostaglandin synthesis-quinacrine hydrochloride and zomepirac sodium-caused a significant (P less than 0.05 and P less than 0.02, respectively) reduction in the fluid response when administered with or 30 min before ST. The fluid response to cyclic 8-bromoguanosine 3',5'-monophosphate or to nitroprusside, which directly activated guanylate cyclase, was not altered by inhibitors of calcium uptake or prostaglandin synthesis. These observations indicate that calcium and prostaglandins are involved in the initial events that result in an intestinal fluid response to E. coli ST.[1]References
- The effect of calcium and prostaglandin inhibitors on the intestinal fluid response to heat-stable enterotoxin of Escherichia coli. Thomas, D.D., Knoop, F.C. J. Infect. Dis. (1982) [Pubmed]
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