Phasic activity of urinary bladder smooth muscle in the streptozotocin-induced diabetic rat: Effect of potassium channel modulators
Vahabi, B. , Lawson, K. , McKay, N. and Sellers , D. (2011) Phasic activity of urinary bladder smooth muscle in the streptozotocin-induced diabetic rat: Effect of potassium channel modulators. European Journal of Pharmacology, 660 (2-3). pp. 431-437. ISSN 0014-2999
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Publisher's URL: http://dx.doi.org/10.1016/j.ejphar.2011.03.053
Increased phasic activity in the bladder smooth muscle of animal models and patients with detrusor overactivity has been suggested to underlie the pathophysiology of overactive bladder. Potassium (K(+)) channels are key regulators of bladder smooth muscle tone and thus may play a role in this altered phasic activity. In this study the effects of K(+) channel modulators on the phasic activity of bladder strips from the streptozotocin-induced diabetic rat model of bladder dysfunction were investigated. Bladder strips from rats 1week following streptozotocin administration and age-matched controls were mounted in tissue baths at 37°C and the effects of K(+) channel modulators on resting basal tension or phasic activity induced by a low concentration of carbachol (0.5μM) were investigated. Activation of BK(Ca) channels by NS1619 had a minor inhibitory effect on carbachol-induced phasic activity of bladder strips from control and diabetic rats, and significantly inhibited amplitude only at 30μM. Activation of K(ATP) channels by cromakalim inhibited the frequency of carbachol-induced phasic activity of bladder strips, although strips from diabetic rats showed a trend towards being less sensitive to cromakalim. The BK(Ca) channel blocker iberiotoxin was able to induce phasic activity in resting tissues, with diabetic bladder strips demonstrating significantly enhanced phasic activity compared to controls. In contrast, inhibition of SK(Ca) and K(ATP) channels did not induce phasic activity in resting tissues. In conclusion, responses of diabetic rat bladder to BK(Ca) and K(ATP) channel modulators are altered, suggesting altered function and/or expression of channels which may contribute to bladder dysfunction in this model.
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