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.