The change of signaling pathway on the electrical stimulated contraction in streptozotocin-induced bladder dysfunction of rats.
10.4196/kjpp.2018.22.5.577
- Author:
Jong Soo HAN
1
;
Young Sil MIN
;
Gil Hyung KIM
;
Sang hyun CHAE
;
Yoonjin NAM
;
Jaehwi LEE
;
Seok Yong LEE
;
Uy Dong SOHN
Author Information
1. Department of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul 06974, Korea. udsohn@cau.ac.kr
- Publication Type:Original Article
- Keywords:
Bladder;
Contractility;
Diabetes;
Phospholipase C;
Smooth muscle
- MeSH:
Animals;
Atropine;
Diabetes Mellitus;
Muscle, Smooth;
Phosphotransferases;
Prazosin;
Rats*;
Rats, Sprague-Dawley;
Streptozocin;
Type C Phospholipases;
Urinary Bladder*;
Verapamil
- From:The Korean Journal of Physiology and Pharmacology
2018;22(5):577-584
- CountryRepublic of Korea
- Language:English
-
Abstract:
Bladder dysfunction is a common complication of diabetes mellitus (DM). However, there have been a few studies evaluating bladder smooth muscle contraction in DM in the presence of pharmacological inhibitors. In the present study, we compared the contractility of bladder smooth muscle from normal rats and DM rats. Furthermore, we utilized pharmacological inhibitors to delineate the mechanisms underlying bladder muscle differences between normal and DM rats. DM was established in 14 days after using a single injection of streptozotocin (65 mg/kg, intraperitoneal) in Sprague-Dawley rats. Bladder smooth muscle contraction was induced electrically using electrical field stimulation consisting of pulse trains at an amplitude of 40 V and pulse duration of 1 ms at frequencies of 2–10 Hz. In this study, the pharmacological inhibitors atropine (muscarinic receptor antagonist), U73122 (phospholipase C inhibitor), DPCPX (adenosine A₁ receptor antagonist), udenafil (PDE5 inhibitor), prazosin (α₁-receptor antagonist), verapamil (calcium channel blocker), and chelerythrine (protein kinase C inhibitor) were used to pretreat bladder smooth muscles. It was found that the contractility of bladder smooth muscles from DM rats was lower than that of normal rats. In addition, there were significant differences in percent change of contractility between normal and DM rats following pretreatment with prazosin, udenafil, verapamil, and U73122. In conclusion, we suggest that the decreased bladder muscle contractility in DM rats was a result of perturbations in PLC/IP₃-mediated intracellular Ca²⁺ release and PDE5 activity.
