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The contractile mechanisms of sodium metavanadate in isolated vascular smooth muscle
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|Title:||The contractile mechanisms of sodium metavanadate in isolated vascular smooth muscle|
Vanadates -- Physiological effect
Metals in the body
|Abstract:||The mechanism of the contractile effect of vanadate on vascular smooth muscle was investigated in the rat aorta. Sodium metavanadate (NaV03) (10-5 M - 3 x 10-3 M) induced contractile responses in a concentration-dependent manner. Removal of endothelium did not affect the response to NaV03. NaV03 has the most efficacy agent to cause contraction as compared to vanadyl sulphate and vanadium trichloride. The response to NaV03 was inhibited by nifedipine, a voltage depedent Ca2+-channel inhibitor, 2-nitro-4-carboxyphenylN, N-diphenylcarbramate (NCDC), a phospholipase C inhibitor, H-7, a protein kinase C inhibitor, indomethacin, a cyclooxygenase inhibitor, and AA861, a 5Iipoxygenase inhibitor, but not by ouabain, a Na+, K+-ATPase inhibitor, prazosin, a a1 receptor inhibitor, methysergide, a serotonin receptor inhibitor, tripelennamine, a histamine receptor inhibitor, glyburide, a KATP-channel inhibitor, -apamin, a Kca-channel inhibitor, or Mg2+-removal, a condition to inhibit Ca2+ATPase activity. The response to arachidonic acid was also inhibited by indomethacin, AA861 , nifedipine and NCDC. H-7 inhibited the response to NaV03 but not to arachidonic acid. However, in the presence of indomethacin and AA861 , H-7 did cause inhibition of the residual response to NaV03. In Ca2+-free medium with EGTA (0.02 mM), NaV03 (3 x 10-4 M) induced a phasic contraction of rat aortas. This residual response to NaV03 was partly inhibited by NCDC and indomethacin, but not by nifedipine. The subsequent addition of Ca2+ (1.2 mM) in the presence of NaV03 caused sustained contraction. In addition, the response to Ca2 + in the presence of NaV03 was completely inhibited by both NCDC and nifedipine, but only partially inhibited by indomethacin. In rat aortas, NaV03 increased the levels of inositol monophosphate (InsP) and prostaglandin F2a. Indomethacin, AA861, and NCDC inhibited the InsP increase. In addition, NCDC and indomethacin, but not AA861 , inhibited the PGF2a increase. These results suggest that the response to NaV03 may be due to the increased phosphoinositide metabolites and partly due to a subsequent increase in the metabolism of arachidonic acid.|
|Description:||Thesis (Ph. D.)--University of Hawaii at Manoa, 1995.|
Includes bibliographical references (leaves 60-67).
xii, 67 leaves, bound ill. 29 cm
|Rights:||All UHM dissertations and theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission from the copyright owner.|
|Appears in Collections:||Ph.D. - Biomedical Sciences (Pharmacology)|
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