scholarly journals Calcium oscillations in interstitial cells of the rabbit urethra

2005 ◽  
Vol 565 (2) ◽  
pp. 449-461 ◽  
Author(s):  
L. Johnston ◽  
G. P. Sergeant ◽  
M. A. Hollywood ◽  
K. D. Thornbury ◽  
N. G. McHale
2002 ◽  
Vol 283 (3) ◽  
pp. C885-C894 ◽  
Author(s):  
G. P. Sergeant ◽  
K. D. Thornbury ◽  
N. G. McHale ◽  
M. A. Hollywood

Freshly dispersed interstitial cells from the rabbit urethra were studied by using the perforated-patch technique. When cells were voltage clamped at −60 mV and exposed to 10 μM norepinephrine (NE) at 80-s intervals, either large single inward currents or a series of oscillatory inward currents of diminishing amplitude were evoked. These currents were blocked by either phentolamine (1 μM) or prazosin (1 μM), suggesting that the effects of NE were mediated via α1-adrenoceptors. NE-evoked currents were depressed by the blockers of Ca2+-activated Cl− currents, niflumic acid (10 μM), and 9-anthracenecarboxylic acid (9-AC, 1 mM). The reversal potential of the above currents changed in a predictable manner when the Cl− equilibrium potential was altered, again suggesting that they were due to activation of a Cl−conductance. NE-evoked currents were decreased by 10 μM cyclopiazonic acid, suggesting that they were dependent on store-released Ca2+. Inhibition of NE-evoked currents by the phospholipase C inhibitor 2-nitro-4-carboxyphenyl- N, N-diphenylcarbamate (100 μM) suggested that NE releases Ca2+ via an inositol 1,4,5-trisphosphate (IP3)-dependent mechanism. These results support the idea that stimulation of α1-adrenoceptors releases Ca2+ from an IP3-sensitive store, which in turn activates Ca2+-activated Cl− current in freshly dispersed interstitial cells of the rabbit urethra. This elevates slow wave frequency in these cells and may underlie the mechanism responsible for increased urethral tone during nerve stimulation.


2006 ◽  
Vol 574 (3) ◽  
pp. 651-661 ◽  
Author(s):  
E. Bradley ◽  
M. A. Hollywood ◽  
L. Johnston ◽  
R. J. Large ◽  
T. Matsuda ◽  
...  

2015 ◽  
Vol 593 (15) ◽  
pp. 3333-3350 ◽  
Author(s):  
Bernard T. Drumm ◽  
Roddy J. Large ◽  
Mark A. Hollywood ◽  
Keith D. Thornbury ◽  
Salah A. Baker ◽  
...  

2014 ◽  
Vol 2 (1) ◽  
pp. e00203 ◽  
Author(s):  
Bernard T. Drumm ◽  
Gerard P. Sergeant ◽  
Mark A. Hollywood ◽  
Keith T. Thornbury ◽  
Toshio T. Matsuda ◽  
...  

2005 ◽  
Vol 289 (3) ◽  
pp. C625-C632 ◽  
Author(s):  
Eamonn Bradley ◽  
Mark A. Hollywood ◽  
Noel G. McHale ◽  
Keith D. Thornbury ◽  
Gerard P. Sergeant

The aim of the present study was to investigate the properties and role of capacitative Ca2+ entry (CCE) in interstitial cells (IC) isolated from the rabbit urethra. Ca2+ entry in IC was larger in cells with depleted intracellular Ca2+ stores compared with controls, consistent with influx via a CCE pathway. The nonselective Ca2+ entry blockers Gd3+ (10 μM), La3+ (10 μM), and Ni2+ (100 μM) reduced CCE by 67% ( n = 14), 65% ( n = 11), and 55% ( n = 9), respectively. These agents did not inhibit Ca2+ entry when stores were not depleted. Conversely, CCE in IC was resistant to SKF-96365 (10 μM), wortmannin (10 μM), and nifedipine (1 μM). Spontaneous transient inward currents were recorded from IC voltage-clamped at −60 mV. These events were not significantly affected by Gd3+ (10 μM) or La3+ (10 μM) and were only slightly decreased in amplitude by 100 μM Ni2+. The results from this study demonstrate that freshly dispersed IC from the rabbit urethra possess a CCE pathway. However, influx via this pathway does not appear to contribute to spontaneous activity in these cells.


2003 ◽  
Vol 285 (2) ◽  
pp. C327-C333 ◽  
Author(s):  
M. A. Hollywood ◽  
G. P. Sergeant ◽  
N. G. McHale ◽  
K. D. Thornbury

Interstitial cells were isolated from strips of rabbit urethra for study using the amphotericin B perforated-patch technique. Depolarizing steps to -30 mV or greater activated a Ca2+ current ( ICa), followed by a Ca2+-activated Cl- current, and, on stepping back to -80 mV, large Cl- tail currents were observed. Both currents were abolished when the cells were superfused with Ca2+-free bath solution, suggesting that Ca2+ influx was necessary for activation of the Cl- current. The Cl- current was also abolished when Ba2+ was substituted for Ca2+ in the bath or the cell was dialyzed with EGTA (2 mM). The Cl- current was also reduced by cyclopiazonic acid, ryanodine, 2-aminoethoxydiphenyl borate (2-APB), and xestospongin C, suggesting that Ca2+-induced Ca2+ release (CICR) involving both ryanodine and inositol 1,4,5-trisphosphate receptors contributes to its activation.


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