Regenerative potentials evoked in circular smooth muscle of the antral region of guinea‐pig stomach

Suzuki, Hiroyoshi; Hirst, G. D. S.

doi:10.1111/j.1469-7793.1999.0563t.x

Cited by 130 publications

(297 citation statements)

References 32 publications

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“…In W/W V mice, which are c-kit gene mutated mice (Huizinga et al, 1997), antral smooth muscles fail to generate unitary potentials and there is associated impairment of the development of ICC-IM, suggesting a causal relationship between these cells and unitary potentials (Dickens et al, 2001). Electrical properties of pacemaker potentials recorded from ICC-MY are similar to those of regenerative slow potentials recorded from circular muscle bundles (Edwards et al, 1999;Suzuki and Hirst, 1999;Hirst and Edwards, 2001;Kito et al, 2002a), suggesting that both of these potentials are formed by similar mechanisms.…”

Section: Introductionmentioning

confidence: 72%

Properties of Unitary Potentials Recorded from Myenteric Interstitial Cells of Cajal Distributed in the Guinea-Pig Gastric Antrum

Kito

Suzuki

Edwards

2002

J Smooth Muscle Res

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Intracellular recordings were made from myenteric interstitial cells of Cajal (ICC-MY) distributed in the guinea-pig gastric antrum to investigate the properties of unitary potentials. In most cells studied, pacemaker potentials with initial fast transient and following plateau components were generated periodically, and intervals between the potentials were quiescent. However, there were few cells (less than 5% of cells examined) which showed discharge of unitary potentials spontaneously in the intervals between pacemaker potentials. The amplitude and frequency of unitary potentials appeared to be random variables, as observed in isolated circular smooth muscle bundles of the guinea-pig gastric antrum. BAPTA-AM (an intracellular Ca 2+ chelator) or papaverine (a non-selective phosphodiesterase inhibitor) reduced the discharge frequency of unitary potentials, with associated decrease in the frequency of pacemaker potentials. These agents finally abolished both unitary potentials and pacemaker potentials. In preparations showing no detectable generation of unitary potentials, depolarization of the membrane with high-K solution ([K + ]o = 10.6 mM) elicited generation of unitary potentials during intervals between pacemaker potentials. Pinacidil (an opener of KATP-channels) hyperpolarized the membrane and increased the frequency and amplitude of unitary potentials with no alteration to the relationship between the amplitudes of unitary potentials and their half-widths. These results suggest that the elevation of intracellular Ca 2+ concentration is causally related to the generation of unitary potentials in pacemaker cells. They are consistent with the proposition that the depolarization produced by a burst of unitary potentials triggers the primary component of pacemaker potentials in ICC-MY, which induces a release of Ca 2+ from inositol 1,4,5-trisphosphate (IP3)-sensitive internal stores and then activates Ca 2+ -sensitive Cl --channels to form the plateau component. Similarities and differences in unitary potentials between circular muscle and pacemaker cells are discussed.

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Section: Introductionmentioning

confidence: 72%

Properties of Unitary Potentials Recorded from Myenteric Interstitial Cells of Cajal Distributed in the Guinea-Pig Gastric Antrum

Kito

Suzuki

Edwards

2002

J Smooth Muscle Res

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“…Thus, in addition to the Ca 2+ inward current, Ca 2+ channels may serve as voltage sensors even in the absence of any Ca 2+ influx. Such a mechanism has been found in visceral [40,41] as well as vascular smooth muscle [42,43] . Although we could not directly test G protein activation in our preparations, our data at least suggest a metabotropic coupling between L-type Ca 2+ channels and IP 3 -mediated Ca 2+ release because DHBP treatment significantly slowed contraction compared with CdCl 2 treatment.…”

Section: Coupling Between Voltage-gated Camentioning

confidence: 98%

High K+-induced contraction requires depolarization-induced Ca2+ release from internal stores in rat gut smooth muscle

et al. 2009

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Aim: Depolarization-induced contraction of smooth muscle is thought to be mediated by Ca 2+ influx through voltage-gated L-type Ca 2+ channels. We describe a novel contraction mechanism that is independent of Ca 2+ entry. Methods: Pharmacological experiments were carried out on isolated rat gut longitudinal smooth muscle preparations, measuring isometric contraction strength upon high K + -induced depolarization. Results: Treatment with verapamil, which presumably leads to a conformational change in the channel, completely abolished K + -induced contraction, while residual contraction still occurred when Ca 2+ entry was blocked with Cd 2+ . These results were further confirmed by measuring intracellular Ca 2+ transients using Fura-2. Co-application of Cd 2+ and the ryanodine receptor blocker DHBP further reduced contraction, albeit incompletely. Additional blockage of either phospholipase C (U 73122) or inositol 1,4,5-trisphophate (IP 3 ) receptors (2-APB) abolished most contractions, while sole application of these blockers and Cd 2+ (without parallel ryanodine receptor manipulation) also resulted in incomplete contraction block. Conclusion: We conclude that there are parallel mechanisms of depolarization-induced smooth muscle contraction via (a) Ca 2+ entry and (b) Ca 2+ entry-independent, depolarization-induced Ca 2+ -release through ryanodine receptors and IP 3 , with the latter being dependent on phospholipase C activation.

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“…The recording chamber was mounted on a stage of an inverted microscope (Nikon IX-70, Tokyo, Japan). These methods were essentially those reported by Suzuki and Hirst (1999) or Kito et al (2002a).…”

Section: Methodsmentioning

confidence: 99%

“…In the guinea-pig, ICC-MY generate driving potentials with initial fast transient (duration, 1-2 s) and subsequent plateau components (duration, 10-15 s), and the potentials are propagated to circular and longitudinal smooth muscle layers in an electrotonic manner through gap junctions (Dickens et al, 1999;Kito et al, 2002b). These slow waves consist of both voltage-sensitive and voltage-insensitive components (Ohba et al, 1975;Tomita, 1981), with only the former easily inhibited by caffeine (Dickens et al, 1999;Suzuki and Hirst, 1999). The driving potential generated in ICC-MY is propagated to circular muscle cells to form a voltage-insensitive component of slow waves, and this potential triggers a voltage-sensitive component (Dickens et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Effects of RHC-80267, an Inhibitor of Diacylglycerol Lipase, on Excitation of Circular Smooth Muscle of the Guinea-Pig Gastric Antrum

Suzuki

Kito

Fukuta

et al. 2002

J. Smooth Muscle Res.

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In small segments of circular smooth muscle isolated from the guinea-pig gastric antrum, the effects of RHC-80267, an inhibitor of diacylglycerol lipase, were investigated both on regenerative slow potentials (either occurring spontaneously or as the result of a depolarizing intracellular current injection) and on the actions of acetylcholine (ACh). As diacylglycerol is a known activator of protein kinase C (PKC), it would therefore be expected that RHC-80267 would activate PKC indirectly. In circular smooth muscle bundles, spontaneously generating slow potentials recorded simultaneously from two given cells were synchronized, indicating that these two cells were electrically coupled. RHC-80267 (0.3-1 µM) increased the frequency of slow potential generation, with no alteration to the amplitude of either the slow potentials or the resting membrane potential. Synchronous electrical activity in a given pair of cells was also unchanged by RHC-80267, indicating that intercellular electrical coupling was not altered. The input resistance of smooth muscle cells calculated from the amplitude of electrotonic potentials produced by injection of current was not significantly altered by RHC-80267. The refractory period for the generation of slow potentials evoked by depolarizing stimuli was about 8 s, and it was decreased to about 5 s by RHC-80267, with no significant alteration to the amplitude of spontaneous or evoked slow potentials. ACh (0.5 µM) depolarized the membrane by about 5 mV and increased the amplitude and frequency of slow potentials. The actions of ACh on the frequency of slow potentials were enhanced by RHC-80267, with no alteration to the amplitudes of both the ACh-induced depolarization and slow potentials. These results support the idea that PKC is involved in determining the frequency of slow potentials, by shortening the refractory period for excitation of gastric smooth muscle cells.

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Regenerative potentials evoked in circular smooth muscle of the antral region of guinea‐pig stomach

Cited by 130 publications

References 32 publications

Properties of Unitary Potentials Recorded from Myenteric Interstitial Cells of Cajal Distributed in the Guinea-Pig Gastric Antrum

Properties of Unitary Potentials Recorded from Myenteric Interstitial Cells of Cajal Distributed in the Guinea-Pig Gastric Antrum

High K+-induced contraction requires depolarization-induced Ca2+ release from internal stores in rat gut smooth muscle

Effects of RHC-80267, an Inhibitor of Diacylglycerol Lipase, on Excitation of Circular Smooth Muscle of the Guinea-Pig Gastric Antrum

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