MECHANISMS OF UROLOGIC COMPLICATIONS IN STREPTOZOTOCIN-INDUCED TYPE 1 DIABETES MELLITUS
AbstractPatients with DM are often afflicted by debilitating urologic complications. The main aim of this study is to investigate the effect of streptozotocin (STZ)-induced type I diabetes on contractile responses to numerous stimuli, intracellular cation concentrations and morphology in the rat. Adult rats (n=12) were humanely killed and detrusor muscles of urinary bladder located and excised rapidly and placed in organ baths. Then urinary bladder detrusor muscles were blotted, weighed and dissolved in concentrated nitric acid for the measurements of cation contents. The diabetic rats had significantly (P<0.05) elevated blood glucose compared to control rats. The contractile responses induced by EFS were significantly (P<0.05) increased in the diabetic urinary bladder tissue in comparison to the control urinary bladder tissue. The increase in the contractile force was calcium-dependent in both control and diabetic urinary bladder tissues. The results also showed no significant differences in the levels of sodium, potassium, calcium, between the diabetic and control urinary bladder (p>0.05). However, there was a significant (P<0.05) decrease in magnesium in the diabetic urinary bladder tissue in comparison to the control urinary bladder tissue. The increased responsiveness of the diabetic urinary bladder tissue compared to the control tissue may be due to either alterations in the intracellular cation concentrations, hypertrophy of the diabetic urinary bladder or calcium sensitivity to the myofilaments. The results also raise the possibility that that these factors, in conjunction with other causes may work in tandem to exacerbate diabetic bladder dysfunction
Article Information
20
2435-43
383
1020
English
IJPSR
V. C. Sangar *, P. Shakil and J. Singh
Department of Virology, Haffkine Institute for Training Research and testing, Parel, Mumbai, India
vikrant.sangar701@gmail.com
19 January, 2016
24 April, 2016
08 May, 2016
10.13040/IJPSR.0975-8232.7(6).2435-43
01 June 2016