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J Physiol Volume 583, Number 2, 505-519, September 1, 2007 DOI: 10.1113/jphysiol.2007.136697
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CELLULAR

Properties of spontaneous Ca2+ transients recorded from interstitial cells of Cajal-like cells of the rabbit urethra in situ

Hikaru Hashitani1 and Hikaru Suzuki1

1 Department of Regulatory Cell Physiology, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, Japan

Interstitial cells of Cajal-like cells (ICC-LCs) in the urethra may act as electrical pacemakers of spontaneous contractions. However, their properties in situ and their interaction with neighbouring urethral smooth muscle cells (USMCs) remain to be elucidated. To further explore the physiological role of ICC-LCs, spontaneous changes in [Ca2+]i (Ca2+ transients) were visualized in fluo-4 loaded preparations of rabbit urethral smooth muscle. ICC-LCs were sparsely distributed, rather than forming an extensive network. Ca2+ transients in ICC-LCs had a lower frequency and a longer half-width than those of USMCs. ICC-LCs often exhibited Ca2+ transients synchronously with each other, but did not often show a close temporal relationship with Ca2+ transients in USMCs. Nicardipine (1 µM) suppressed Ca2+ transients in USMCs but not in ICC-LCs. Ca2+ transients in ICC-LCs were abolished by cyclopiazonic acid (10 µM), ryanodine (50 µM) and caffeine (10 mM) or by removing extracellular Ca2+, and inhibited by 2-aminoethoxydiphenyl borate (50 µM) and 3-morpholino-sydnonimine (SIN-1; 10 µM), but facilitated by increasing extracellular Ca2+ or phenylephrine (1–10 µM). These results indicated that Ca2+ transients in urethral ICC-LCs in situ rely on both Ca2+ release from intracellular Ca2+ stores and Ca2+ influx through non-L-type Ca2+ channel pathways. ICC-LCs may not act as a coordinated pacemaker electrical network as do ICC in the gastrointestinal (GI) tract. Rather they may randomly increase excitability of USMCs to maintain the tone of urethral smooth muscles.

(Received 17 May 2007; accepted after revision 29 June 2007; first published online 5 July 2007)
Corresponding author H. Hashitani: Department of Regulatory Cell Physiology, Nagoya City University, Graduate School of Medical Sciences, Nagoya 467-8601, Japan. Email: hasitani{at}med.nagoya-cu.ac.jp







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