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- W2014501103 abstract "It has been repeatedly reported that calcitonin treatment in various diseases with high levels of bone resorption is associated with an antalgic effect, the mechanism of which is far from been clarified. The involvment of prostaglandins and thromboxane in hyperalgesia prompted us to consider the possibility that calcitonin induces its antalgic effect through on interference with prostaglandin and thromboxane synthesis. Guinea pig lung which, perfused with arachidonic acid releases in the perfusate a mixture of thromboxane and prostaglandins, each measurable on a separate smooth muscle tissue (rabbit aorta and rat stomach strip), was used as a test system. Calcitonin added to the perfusion fluid was shown to inhibit the synthesis both of prostaglandins and thromboxane. The concentration of calcitonin (salmon) which decreased the activity of arachidonic acid by 50% (KB) was 0.27 and 0.40 nmoles for prostaglandins and thromboxane respectively. In the experiments carried out using Ca++ concentration in the perfusion fluid 50% higher than normal (0.28 g/l), calcitonin inhibition of prostaglandins and thromboxane was unchanged (KB = 0.23 and 0.36 nmoles respectively). The reported results by indicating that calcitonin has an influence on cyclooxygenase as indomethacin (used as reference standard) whose it is well known the activity at this level, support the interesting possibility that the antalgic effect consequent to the treatment with the hormone is due, at least in part, to a mechanism involving the prostaglandin synthetase system." @default.
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- W2014501103 date "1979-11-01" @default.
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- W2014501103 title "Calcitonin and prostaglandin system" @default.
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- W2014501103 doi "https://doi.org/10.1016/0024-3205(79)90433-8" @default.
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