Sensitization of the contractile system of canine colonic smooth muscle by agonists and phorbol ester.

Sato, Koichi; Leposavic, R; Publicover, Nelson G.; Sanders, Katherine; Gerthoffer, William T.

doi:10.1113/jphysiol.1994.sp020473

Cited by 31 publications

(27 citation statements)

References 29 publications

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“…These results clearly indicated that NKA activates G-proteins and consequently induces an increase in the Ca 2+ sensitivity of the contractile apparatus. This ®nding is consistent with previous reports which showed that NKA induced Ca 2+ sensitization of the contractile element of canine colonic smooth muscle (Sato et al, 1994). It is thus concluded that NKA induces the contraction of the rat myometrium not only by increasing [Ca 2+ ] i but also by increasing the Ca 2+ sensitivity of the contractile apparatus.…”

Section: Discussionsupporting

confidence: 82%

Mechanisms underlying the neurokinin A‐induced contraction of the pregnant rat myometrium

Shintani

Nishimura

Niiro

et al. 2000

British J Pharmacology

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1 Using fura-PE3¯uorimetry and a-toxin permeabilization, the characteristics of the contractile responses to neurokinin A (NKA) were determined in the pregnant rat myometrium. 2 NKA induced contractions in rat myometrium in a concentration-dependent manner. There were no signi®cant dierences in the maximum contractions and EC 50 values between the pregnant and non-pregnant myometrium, however, the contraction of only the former was greatly enhanced in the presence of phosphoramidon (PPAD), an endopeptidase inhibitor. -sensitizing eect by NKA was also observed in the a-toxin permeabilized myometrium. 6 These results indicated that in the pregnant rat myometrium: (1) the responsiveness to NKA increased, although it was masked by the increase in the endopeptidase activity; (2) NKA induced contractions of the myometrium by increasing both [Ca 2+ ] i and the myo®lament Ca 2+ sensitivity and (3) The NKA-induced [Ca 2+ ] i elevation was partly due to the intracellular Ca 2+ release and mainly due to the Ca 2+ in¯ux, which was thought to be through both voltage dependent calcium channels and non-speci®cation channels.

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Section: Discussionsupporting

confidence: 82%

Mechanisms underlying the neurokinin A‐induced contraction of the pregnant rat myometrium

Shintani

Nishimura

Niiro

et al. 2000

British J Pharmacology

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“…These results suggest that a rho-mediated pathway contributes to Ca 2 þ sensitization by activation of muscarinic receptors in ileal smooth muscle. Sato et al (1994) showed Ca 2 þ sensitization in canine colonic smooth muscle induced by acetylcholine, histamine and neurokinin A. However, the intracellular mechanism that connects activation of muscarinic receptors to Ca 2 þ sensitization in colonic smooth muscle remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms involved in carbachol‐induced Ca²⁺ sensitization of contractile elements in rat proximal and distal colon

Takeuchi

Kushida

Hirayama

et al. 2004

British J Pharmacology

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1 Mechanisms involved in Ca 2 þ sensitization of contractile elements induced by the activation of muscarinic receptors in membrane-permeabilized preparations of the rat proximal and distal colon were studied. 2 In a-toxin-permeabilized preparations from the rat proximal and distal colon, Ca 2 þ induced a rapid phasic and subsequent tonic component. After Ca 2 þ -induced contraction reached a plateau, guanosine 5 0 -triphosphate (GTP) and carbachol (CCh) in the presence of GTP further contracted preparations of both the proximal and distal colon (Ca 2 þ sensitization). 3 Y-27632, a rho-kinase inhibitor, inhibited GTP plus CCh-induced Ca 2 þ sensitization more significantly in the proximal colon than in the distal colon. Y-27632 at 10 mM had no effect on Ca 2 þ -induced contraction or slightly inhibited phorbol-12,13-dibutyrate-induced Ca 2 þ sensitization in either proximal or distal colon. Chelerythrine, a protein kinase C inhibitor, inhibited GTP plus CChinduced Ca 2 þ sensitization in the distal colon, but not in the proximal colon. The component of Ca 2 þ sensitization that persisted after the chelerythrine treatment was completely inhibited by Y-27632. 4 In b-escin-permeabilized preparations of the proximal colon, C3 exoenzyme completely inhibited GTP plus CCh-induced Ca 2 þ sensitization, but PKC(19-31) did not. In the distal colon, C3 exoenzyme abolished GTP-induced Ca 2 þ sensitization. It inhibited CCh-induced sensitization by 50 % and the remaining component was inhibited by PKC(19-31). 5 These results suggest that both protein kinase C and rho pathways in parallel mediate the Ca 2 þ sensitization coupled to activation of muscarinic receptors in the rat distal colon, whereas the rho pathway alone mediates this action in the proximal colon.

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“…PDBu has been demonstrated to be a potent specific PKC activator, without any alteration in intracellular Ca 2+ concentration (Ozaki et al, 2003;Sato et al, 1994), that has been widely used to activate PKC and to study the PKC signaling pathway. PKC isoforms are classified into three (Salamanca and Khalil, 2005).…”

Section: Discussionmentioning

confidence: 99%

Augmented PDBu-mediated contraction of bronchial smooth muscle of mice with antigen-induced airway hyperresponsiveness

Sakai

Kurihara

Hashimoto

et al. 2010

J. Smooth Muscle Res.

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To explore the role of protein kinase C (PKC) in the augmented bronchial smooth muscle (BSM) contraction observed in the antigen-induced airway hyperresponsive (AHR) mice, the effects of a PKC activator, phorbol 12,13-dibutylate (PDBu), on BSM contraction were compared between the AHR and control mice. Actively sensitized mice were repeatedly challenged by antigen inhalation. Twenty-four hours after the final antigen challenge the isometrical contractions of the BSMs were measured. The BSM contraction induced by acetylcholine, but not high K + depolarization, was significantly augmented in the AHR mice. In BSMs of control mice, PDBu caused a significant increase in tension when the tissues were precontracted with high K + , although PDBu itself had no effect on basal tone. The PDBu-mediated contraction was markedly augmented in BSMs of the AHR mice. These findings suggest that an increase in the PKC-mediated signaling is involved in the augmented contraction of BSMs in the antigen-induced AHR mice.

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Sensitization of the contractile system of canine colonic smooth muscle by agonists and phorbol ester.

Abstract: 4. The results suggest that endogenous agonists acting via G-proteins sensitize the contractile element of colonic smooth muscle in part by activation of protein kinase C.

Cited by 31 publications

References 29 publications

Mechanisms underlying the neurokinin A‐induced contraction of the pregnant rat myometrium

Mechanisms underlying the neurokinin A‐induced contraction of the pregnant rat myometrium

Mechanisms involved in carbachol‐induced Ca²⁺ sensitization of contractile elements in rat proximal and distal colon

Augmented PDBu-mediated contraction of bronchial smooth muscle of mice with antigen-induced airway hyperresponsiveness

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Sensitization of the contractile system of canine colonic smooth muscle by agonists and phorbol ester.

Abstract: 4. The results suggest that endogenous agonists acting via G-proteins sensitize the contractile element of colonic smooth muscle in part by activation of protein kinase C.

Cited by 31 publications

References 29 publications

Mechanisms underlying the neurokinin A‐induced contraction of the pregnant rat myometrium

Mechanisms underlying the neurokinin A‐induced contraction of the pregnant rat myometrium

Mechanisms involved in carbachol‐induced Ca2+ sensitization of contractile elements in rat proximal and distal colon

Augmented PDBu-mediated contraction of bronchial smooth muscle of mice with antigen-induced airway hyperresponsiveness

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Mechanisms involved in carbachol‐induced Ca²⁺ sensitization of contractile elements in rat proximal and distal colon