The effect of streptozotocin‐induced diabetes on cholinergic motor transmission in the rat urinary bladder

Abstract

1The effect of streptozotocin (STZ)-induced diabetes on cholinergic motor transmission in the rat urinary bladder was investigated by recording contractile activity of detrusor strips in vitro. 2 The Ca2+-channel antagonist, nifedipine, was found to be more effective in blocking the noncholinergic motor transmission than P2-purinoceptor desensitization by ocxJ-methylene ATP. 3 The neurogenic contractile responses to electrical field stimulation in the presence of nifedipine (cholinergic) were larger in the diabetic detrusor than in the non-diabetic controls. The potentiation of the cholinergic transmission was more evident at higher frequencies. 4 Concentration-response curves for acetylcholine were identical in detrusors from diabetic and nondiabetic animals, thus excluding a postsynaptic supersensitivity to acetylcholine being responsible for the potentiation of cholinergic motor transmission. 5 It is concluded that the potentiation of cholinergic motor transmission is due to enhanced release of acetylcholine in diabetic detrusor. Possible reasons for this enhancement are discussed in relation to diabetes.

Diabetes mellitus- and cooling-induced bladder contraction: an in vitro study

“…Nevertheless, results of previous animal studies on cholinergic transmission in diabetic bladders have been controversial. While some investigators reported increased contractile responses (Latifpour et al, 1989;Hegde et al, 1997;Geirsson et al, 1999;Yanilmez et al, 2006) others reported decreased contractile responses (Longhurst and Bellis, 1986;Ichiyanagi et al, 2002), and some other investigators mentioned no change in contractile response (Lincoln et al, 1984;Luheshi and Zar, 1991;Nakamura et al, 1992) of the bladder smooth muscle to muscarinic agonists. The differences in these various reports may be related to differences in methodology, sex differences, ages of the experimental animals and variations in the durations of diabetes.…”

“…It has been shown that in diabetic animals, contractile responses of the urinary bladder to muscarinic agonists are inconsistent. Some investigators have reported increased responses (Tong et al, 2002;Nsabimana and Ojewole, 2008), while others have reported decreased responses (Licoln et al, 1984;Longhurst et al, 1986), or no change in contractile responses (Luheshi and Zar, 1991;Atalık et al, 2000) of diabetic urinary bladder smooth muscle strip to muscarinic agonists.…”

The M2-Muscarinic Receptor Inhibits the Development of Streptozotocin-Induced Neuropathy in Mouse Urinary Bladder

“…In a study on the mouse urinary bladder, Liu and Lin-Shiau (1996) show decreased contraction to EFS after STZ treatment. The cholinergic component of the EFS contraction in bladder from the STZtreated Wistar rat increases (Luheshi and Zar, 1991;Benkó et al, 2003), whereas that measured in the Sprague-Dawley rat decreases (Liu and Daneshgari, 2005). After STZ treatment, the purinergic component of EFS contraction was reported to be unchanged in the Sprague-Dawley rat (Liu and Daneshgari, 2005) and slightly increased in the Wistar rat (Benkó et al, 2003).…”

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“…2,3,4,5 On other hand, others report either decreased or little change in EFS-induced contractile response. 6,7,8 In the same vein, experiments measuring contractile responses of the bladder to exogenous muscarinic agonists have also produced contradictory results.…”