Premium
Changes in T‐type calcium channel and its subtypes in overactive detrusor of the rats with partial bladder outflow obstruction
Author(s) -
Li Longkun,
Jiang Chonghe,
Hao Ping,
Li Weibing,
Fan Lixin,
Zhou Zhansong,
Song Bo
Publication year - 2007
Publication title -
neurourology and urodynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 90
eISSN - 1520-6777
pISSN - 0733-2467
DOI - 10.1002/nau.20392
Subject(s) - overactive bladder , patch clamp , medicine , bladder outlet obstruction , endocrinology , repolarization , calcium channel , myocyte , calcium , electrophysiology , pathology , prostate , alternative medicine , cancer
Aims To investigate the activity of the T‐type calcium channel (TCC) and the expression of its subtypes in overactive detrusor (OD) myocytes in rats after partial bladder outflow obstruction (PBOO). Methods Thirteen male Wistar rats with OD after PBOO (OD group) and eight sham‐operated rats (control group) were studied. The two groups were compared regarding the expression of TCC subtype genes by reverse transcription‐polymerase chain reaction (RT‐PCR) and the TCC kinetics and cell action potential by whole‐cell patch‐clamp. Results The time course and density of the current were significantly higher in the OD cells than those in the control detrusor. Whole‐cell patch‐clamp analysis showed that the activation of TCCs in detrusor myocytes in the OD group was faster than the control group, but inactivation was almost the same in both groups, suggesting a significant enhancement of the Ca 2+ “window” current in the OD group. Patch‐clamp recording of action potentials in the OD cells indicated an increase in excitability and a decrease in the repolarization interval. RT‐PCR assay showed an abnormal expression of α1G subtype in the OD cells. Conclusions TCCs could be one of the crucial factors for the abnormal excitation in OD cells. The development of OD after PBOO presumably relates to the increase in TCC current in the bladder cells, the enhancement of the Ca 2+ “window” current for Ca 2+ inflow, the prolongation of the intracellular calcium oscillations, and the acceleration of the cell depolarization. Neurourol. Urodynam. 26:870–878, 2007. © 2007 Wiley‐Liss, Inc.