Effect of sodium orthovanadate on the urinary bladder rings isolated from normal and hyperglycemic rats.
Effect of sodium orthovanadate on the urinary bladder rings isolated from normal and hyperglycemic rats was investigated. Vanadate concentrations of 0.1, 0.5 and 1 mM produced a concentration-dependant increase in isolated urinary bladder tension in both normal and hyperglycemic tissues. In normal urinary bladder rings, the response to increasing concentrations of vanadate were 12.8 +/- 0.6, 20.1 +/- 0.74 and 32.5 +/- 1.2 g tension /g tissue, respectively. Hyperglycemia significantly potentiated the response of bladder rings to vanadate. In hyperglycemic rats, the response of the urinary bladder to the same concentrations of vanadate were 21.3 +/- 0.78, 30 +/- 1.1 and 50.5 +/- 1.6 g tension/g tissue, respectively. The responses were reversible and further contractions could be elicited at 30 minutes intervals. The contractions of normal urinary bladder rings to vanadate were not altered by pretreatment with atropine or L-NAME. Melatonin, nifedipine as well as indomethacin significantly reduced the response of normal and hyperglycemic bladder rings to vanadate. On the other hand, ascorbic acid significantly enhanced the response of these rings to vanadate. Hydrogen peroxide (H(2)O(2))-induced increase in the urinary bladder tension was very similar and comparable to contractions induced by vanadate. Similarly, H(2)O(2)-induced contraction in the urinary bladder rings was significantly reduced after incubation of the bladder rings with melatonin, indomethacin or nifedipine and the response was not altered by ascorbic acid. The results of the present study indicate that vanadate produced marked contraction in the normal urinary bladder rings and this contraction was significantly enhanced by hyperglycemia. The present data shows also that the contractile effect of vanadate on isolated urinary bladder rings is partially dependent on extracellular calcium and generation of free radicals. The present results suggested a key role of H(2)O(2) in mediating the contraction of urinary bladder rings induced by vanadate.
Kafl
Hoda E
HE
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, Mansoura, 35516, Egypt.
Elkashef
Hassan A
HA
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D006861:Hydrogen Peroxide / Q000494:pharmacology; D006943:Hyperglycemia / Q000139:chemically induced / Q000503:physiopathology*; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D008550:Melatonin / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013311:Streptozocin; D001743:Urinary Bladder / Q000187:drug effects*; D014638:Vanadates / Q000494:pharmacology*
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; D004791:Enzyme Inhibitors; D014638:Vanadates; D013311:Streptozocin; D006861:Hydrogen Peroxide; D008550:Melatonin; D019331:NG-Nitroarginine Methyl Ester; D007213:Indomethacin