2-Aminoethoxydiphenyl borate causes dissociation between membrane electrical and mechanical activity in guinea-pig urinary bladder smooth muscle

Imai, Tamaki; Tanaka, Yoshio; Okamoto, Takao; Horinouchi, Takahiro; Tanaka, Hikaru; Koike, Kenichi; Shigenobu, Koki

doi:10.1007/s00210-002-0596-0

Cited by 9 publications

(10 citation statements)

References 9 publications

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“…9) In the present study, the spontaneous contraction of guinea pig UBSM was also suppressed significantly by U-73122 and NCDC. Diminishment of UBSM contraction by the IP 3 receptor antagonist (2-APB) and PLC inhibitors (U-73122 and NCDC) strongly suggests a role for the activation of PLC and subsequent IP 3 -induced Ca 2ϩ release mechanism in the spontaneous mechanical activity of this smooth muscle.…”

Section: Discussionmentioning

confidence: 62%

“…8,9) Our present findings indicate the possibility that the alteration in PLC activity also functions as a triggering mechanism to evoke spontaneous muscle contraction in this type of muscle tissue. Vol.…”

Section: Discussionmentioning

confidence: 82%

“…3,12) For intracellular recordings, a thin layer of muscle bundles (three to five bundles) was prepared (1-3 mm in widthϫ3-6 mm in length). 8,9) Measurement of Spontaneous Rhythmic Contraction of UBSM Spontaneous rhythmic contractions were recorded as reported previously. 3,8) Tension changes were isometrically recorded with a force-displacement transducer (TB-612T, Nihon-Kohden, Tokyo, Japan) connected to a minipolygraph (Signal Conditioner: Model MSC-2, Labo Support, Co., Ltd., Osaka, Japan).…”

Section: Methodsmentioning

confidence: 99%

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Phospholipase C Inhibitors Suppress Spontaneous Mechanical Activity of Guinea Pig Urinary Bladder Smooth Muscle

Tanaka

Okamoto

Imai

et al. 2003

Biological & Pharmaceutical Bulletin

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Urinary bladder smooth muscle (UBSM) exhibits spontaneous rhythmic contraction. This spontaneous mechanical activity is generated in the presence of neuronal blockade and thus is myogenic in origin. The spontaneous myogenic contraction of UBSM may be the fundamental determinant of the physiological functions of the urinary bladder to store and excrete urine. Although the mechanisms by which UBSM generates spontaneous contraction have not been completely ascertained, its induction has been suggested to be intimately associated with smooth muscle cell action potentials to enhance extracellular Ca(2+) influx through voltage-gated L-type Ca(2+) channels. However, the alteration of membrane electrical activity does not seem to be the exclusive trigger mechanism for the generation of the spontaneous contraction. In the present study, we show that spontaneous mechanical activity of guinea pig UBSM is substantially diminished by an inhibitor of phospholipase C (PLC), U-73122, but is not affected by its inactive form, U-73343. Significant attenuation of the mechanical activity can be also obtained with another PLC inhibitor 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate. Our present findings suggest a significant role for the activation of PLC and subsequent inositol 1,4,5-trisphosphate-induced Ca(2+) release mechanism as an alternative triggering system for inducing spontaneous mechanical activity of UBSM. The present results support the idea that the action potential is not the sole pacemaker mechanism by which spontaneous contraction is induced in UBSM.

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Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 82%

Section: Methodsmentioning

confidence: 99%

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Phospholipase C Inhibitors Suppress Spontaneous Mechanical Activity of Guinea Pig Urinary Bladder Smooth Muscle

Tanaka

Okamoto

Imai

et al. 2003

Biological & Pharmaceutical Bulletin

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“…2-APB has been shown to block slow calcium waves in myometrial (Ascher-Landsberg et al, 1999), intestinal (Hirst et al, 2002;Varro et al, 2004), and urinary bladder (Imai et al, 2002) smooth muscle, to decrease spontaneous calcium elevations in astrocytes in slice preparations (Parri and Crunelli, 2003), and to reduce spinal cord damage in response to injury (Thorell et al, 2002). Although each of these findings has been interpreted in the context of blockade of the IP 3 receptor, it should be noted that each result might be expected as a consequence of gap junction channel blockade.…”

Section: -Apb Selectively Blocks Gap Junction Channels Formed Of Difmentioning

confidence: 99%

Block of Specific Gap Junction Channel Subtypes by 2-Aminoethoxydiphenyl Borate (2-APB)

Bai

Corsso

Srinivas

et al. 2006

J Pharmacol Exp Ther

105

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2-Aminoethoxydiphenyl borate (2-APB), an inositol 1,4,5-triphosphate receptor modulator, inhibits capacitive current transients measured in normal rat kidney and human embryonic kidney 293 cells, an indication of blocking gap junction channels between these cells. Here, we used the dual whole-cell patch-clamp method to study the actions of 2-APB on gap junction channels formed by selected connexins expressed in a communication-deficient neuroblastoma cell line (N2A). 2-APB dose-dependently and reversibly blocked junctional currents of connexin (Cx) 50 gap junction channels. The concentrationinhibition curve of 2-APB on the junctional current indicated an IC 50 of 3.7 M, lower than that of most gap junction inhibitors. At a concentration of 20 M, 2-APB also significantly blocked junctional conductance in cell pairs coupled by Cx26, Cx30, Cx36, Cx40, and Cx45 but did not appreciably affect coupling in cell pairs expressing Cx32, Cx43, and Cx46. Although concentration inhibition curves of 2-APB on Cx36 channels were similar to Cx50 (Cx36; IC 50 , 3.0 M), IC 50 values were higher for Cx43 (51.6 M), Cx45 (18

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“…Additionally, 2-APB has also been reported to inhibit Ca 2+ entry through store-operated channels (SOCs) in liver cells [36]. Recently, ryanodine and 2-APB have been shown to induce membrane depolarization and increase the frequency of action potential, respectively [39,40]. Depletion of intracellular Ca 2+ stores by ryanodine is also sufficient for depolarization of plasma membrane [41].…”

Section: Discussionmentioning

confidence: 97%

Involvement of Ca2+ signaling in tachykinin-mediated contractile responses in swine trachea

2005

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Neuropeptide tachykinins, present within sensory nerves, have been implicated as neurotransmitters involved in nonadrenergic and noncholinergic airway muscle contraction. The signal transduction pathways of tachykinins on muscle contraction and Ca2+ mobilization were investigated in swine trachea. Tachykinins, substance P (SP) and neurokinin A (NKA), concentration (1 nM to 1 microM)-dependently induced contractile responses with removal of epithelium, whereas neurokinin B (NKB) did not alter the muscle tension. The SP- and NKA-evoked muscle contractions were inhibited by NK1-R antagonist L732138, but not by either NK2-R antagonist MDL29913 or NK3-R antagonist SB218795. Consistently, SP-elicited increase in [Ca2+]i was abolished by NK1-R antagonist, neither by NK2-R nor NK3-R antagonists. The SP-induced muscular responses were significantly inhibited by L-type Ca2+ channel blocker verapamil and withdrawal of external Ca2+. Caffeine (10 mM) or ryanodine (50 microM) also partly suppressed the SP-induced muscle responses. Inhibition of inositol 1,4,5-trisphosphate (InsP3) receptor with 2-APB (75 microM) potently attenuated SP-evoked Ca2+ mobilization and muscle contraction, which was further inhibited by 2-APB under Ca2+-free external solution, but not completely. Unexpectedly, simultaneous blockade of InsP3 receptor and ryanodine receptor (RyR) by 2-APB and ryanodine enhanced SP-evoked muscle contraction and Ca2+ mobilization. This potentiation was virtually abolished by removal of external Ca2+, suggesting native Ca2+ channels may contribute to this phenomenon. These results demonstrate that tachykinins produce a potent muscle contraction associated with Ca2+ mobilization via tachykinin NK1- R-dependent activation of multiple signal transduction pathways involving Ca2+ influx and release of Ca2+ from InsP3- and ryanodine-sensitive Ca2+ stores. Blockade of both InsP3 receptor and RyR enhances the Ca2+ influx through native Ca2+ channels in plasma membrane, which is crucial to Ca2+ signaling in response to NK1 receptor activation.

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2-Aminoethoxydiphenyl borate causes dissociation between membrane electrical and mechanical activity in guinea-pig urinary bladder smooth muscle

Cited by 9 publications

References 9 publications

Phospholipase C Inhibitors Suppress Spontaneous Mechanical Activity of Guinea Pig Urinary Bladder Smooth Muscle

Phospholipase C Inhibitors Suppress Spontaneous Mechanical Activity of Guinea Pig Urinary Bladder Smooth Muscle

Block of Specific Gap Junction Channel Subtypes by 2-Aminoethoxydiphenyl Borate (2-APB)

Involvement of Ca2+ signaling in tachykinin-mediated contractile responses in swine trachea

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