INT156175
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Cell culture and in vivo studies demonstrate that an FSS- or a 4alphaPDD-induced activation of Trpv4 leads to an active proliferation of vascular cells and finally triggers collateral growth. | |||||||||||||||
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To detect the roles of various vasodilating factors released by vascular endothelium in the hypotensive effect induced by TRPV4 activation, the corresponding inhibitors/blockers, including indomethacin (a cyclooxygenase inhibitor, 10 mg/kg, i.v.), Nomega-nitro-L-arginine (L-NA, a nitric oxide synthase inhibitor, 20 mg/kg, i.v.), apamin [a blocker of small conductance Ca2+-activated K+ (MaxiK) channels, 50 microg/kg, i.v.] combined with charybdotoxin (a blocker of intermediate and large conductance MaxiK channels, 50 microg/kg, i.v.), were used at various time before 4alpha-PDD injection. | |||||||||||||||
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CONCLUSION: Our data show that the hypotensive effect induced by TRPV4 activation attributes to, at least in part, activation of MaxiK channels and CGRP receptors upon CGRP release from sensory nerves.
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Activation of TRPV4 results in fast retraction of growth cones in F11 cell | |||||||||||||||
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Stabilization of microtubules by Taxol reduces Ca2+-influx through TRPV4 activation | |||||||||||||||
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Thus PKC, and possibly PKA, phosphorylate TRPV4 at Ser824 leading to the enhancement of TRPV4 channel function. | |||||||||||||||
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General Comments
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