Norepinephrine and GTP-γ-S increase myofilament Ca2+ sensitivity in α-toxin permeabilized arterial smooth muscle

Nishimura, Junji; Kolber, Michael A.; Breemen, Cornelis van

doi:10.1016/s0006-291x(88)80303-6

Cited by 304 publications

(203 citation statements)

References 25 publications

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“…Contractions in Permeabilized Muscle-In ␣-toxin-permeabilized muscle, functional proteins in cytosol are retained, and internal Ca 2ϩ concentrations can be clamped in order to evaluate Ca 2ϩ sensitivity and the contractility of the contractile apparatus (27,28).…”

Section: Resultsmentioning

confidence: 99%

“…Permeabilized Muscle-Permeabilized muscle was prepared by treating the intestinal smooth muscle strips with Staphylococcus aureus ␣-toxin (80 g/ml, 30 min; Sigma), as described previously (27,28 Homogenizing solution to extract CPI-17 and MYPT-1 contained 60 mM ␤-glycerophosphate, 0.5% Nonidet P-40, 0.2% SDS, 1 mM Na 3 VO 4 , 2 mM EGTA, and 50 mM Tris-HCl, pH 8.0. All homogenizing solutions contained 1 mM dithiothreitol (DTT), 1 mM phenylmethanesulfonyl fluoride, 1 mM benzamidine, and 1 g/ml aprotinin.…”

Section: Methodsmentioning

confidence: 99%

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Chronic Treatment with Interleukin-1β Attenuates Contractions by Decreasing the Activities of CPI-17 and MYPT-1 in Intestinal Smooth Muscle

Ohama

Hori

Sato

et al. 2003

Journal of Biological Chemistry

113

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Interleukin-1␤ (IL-1␤) is a proinflammatory cytokine that plays a central role in inflammatory bowel disease (IBD). In order to elucidate the mechanism of motility disorders frequently observed in IBD, we investigated the long term effects of IL-1␤ on rat ileal smooth muscle contractility by using an organ culture system. When ileal smooth muscle strips were cultured with IL-1␤ (10 ng/ml), contractions elicited by high K ؉ and carbachol were inhibited in a time-dependent manner. IL-1␤ more strongly inhibited the carbachol-induced contractions than high K ؉ with decreasing myosin light chain phosphorylation. In the ␣-toxin-permeabilized ileal muscle, carbachol with GTP or guanosine 5 -3-O-(thio)triphosphate increased the Ca 2؉ sensitivity of contractile elements, and this G protein-coupled Ca 2؉ sensitization was significantly reduced in the IL-1␤-treated ileum. Among the functional proteins involved in the smooth muscle Ca 2؉ sensitization, CPI-17 expression was significantly reduced after the culture with IL-1␤, whereas the expressions of RhoA, ROCK-I, ROCK-II, MYPT-1, myosin light chain kinase, and myosin phosphatase (PP1) were unchanged. The phosphorylation level of CPI-17 by carbachol was low in accordance with the decrease in CPI-17 expression due to IL-1␤ treatment. In contrast, constitutively phosphorylated MYPT-1 was also decreased in the IL-1␤-treated muscles. These results suggest that long term treatment with IL-1␤ decreases either CPI-17 expression or MYPT-1 phosphorylation, which may result in an increase in myosin phosphatase activity to reduce force generation. Based on these findings, we consider IL-1␤ to be an important mediator of gastrointestinal motility disorders in IBD, and CPI-17 and MYPT-1 are key molecules in the decreased smooth muscle contractility due to IL-1␤.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Chronic Treatment with Interleukin-1β Attenuates Contractions by Decreasing the Activities of CPI-17 and MYPT-1 in Intestinal Smooth Muscle

Ohama

Hori

Sato

et al. 2003

Journal of Biological Chemistry

113

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“…On the other hand, the application of 10 mM GTPgS or 100 nM endothelin-1 during the 300 nM Ca 2 þ -induced sustained contraction induced a further development of tension and these contractile effects were similar in rings from control animals and those after SAH (Figures 4d and e). GTPgS was used to directly stimulate the G proteins, thereby increasing the Ca 2 þ sensitivity of the contractile apparatus (Smigel et al, 1984;Nishimura et al, 1988).…”

Section: Contractile Response In A-toxin Permeabilized Preparationsmentioning

confidence: 99%

Up‐regulation of proteinase‐activated receptor 1 and increased contractile responses to thrombin after subarachnoid haemorrhage

Maeda

Hirano

Kai

et al. 2007

British J Pharmacology

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Background and purpose: The mechanism for the development of post-haemorrhagic cerebral vasospasm after subarachnoid haemorrhage (SAH) still remains unknown. Experimental approach: We investigated the role of thrombin and its receptor PAR 1 in the development of hyper-contractility of the basilar artery in a rabbit double haemorrhage model, which received two injections of autologous blood into the cisterna magna. Key results: In the basilar artery isolated from the control rabbits, thrombin, only at 10 units ml À1 , induced a transient endothelium-dependent relaxation and a slight smooth muscle contraction. In SAH, the contractile response to thrombin was markedly enhanced, while the endothelium-dependent relaxant effect of thrombin remained unchanged. The enhancement of the contractile responses was also observed in the absence of endothelium and thrombin induced an enhanced contraction at concentrations higher than 0.3 units ml À1 . The contractile response to PAR 1 -activating peptide was also enhanced after SAH. However, the contractile responses to high K þ and endothelin-1, and the myofilament Ca 2 þ -sensitivity remained unchanged after SAH. An immunoblot analysis suggested the up-regulation of PAR 1 in the smooth muscle of the basilar artery. The heparinization of blood before injection prevented the enhancement of the contractile responses to thrombin and PAR 1 -activating peptide. Conclusions and implications:The present study demonstrated, for the first time, that the contractile response of the basilar artery to thrombin was markedly enhanced after SAH. Mechanistically, our findings suggested that the activation of thrombin following hemorrhage up-regulated the expression of PAR 1 , thereby inducing the hyper-responsiveness to thrombin.

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“…In muscle permeabilized with bacterial a-toxin, receptor agonists potentiate Ca2"-induced contraction in the presence of GTP (Nishimura et al, 1988;Kitazawa et al, 1989). Since Ca2" sensitization induced by receptor agonists is accompanied by an increase in MLC phosphorylation in intact and permeabilized smooth muscle preparations (Rembold & Murphy, 1988;Suematsu et al, 1991;Kitazawa et al, 1991;Hori et al, 1992), it has been suggested that an altered balance between the activities of MLC kinase and MLC phosphatase results in the Ca2" sensitization of MLC phosphorylation (Stull et al, 1990;Gong et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Different pathways of calcium sensitization activated by receptor agonists and phorbol esters in vascular smooth muscle

Hori¹,

Sato

Miyamoto

et al. 1993

British J Pharmacology

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1 It has been shown that receptor agonists and activators of protein kinase C, phorbol esters, increase Ca2+ sensitivity of contractile elements in vascular smooth muscle. To discover if protein kinase C is involved in the agonist-mediated Ca2" sensitization, we examined the effects of receptor agonists in the rat isolated aorta in which protein kinase C activity had been diminished by pretreatment with phorbol 12-myristate 13-acetate for 24 h.2 In the aorta with protein kinase C activity, a high concentration (1 gM) of 12-deoxyphorbol 13-isobutyrate induced contraction and a low concentration (100 nM) potentiated high K+-induced contraction. In addition, prostaglandin F2. induced greater contractions than high K+ at a given cytosolic Ca2+ level. The maximally effective concentrations of noradrenaline and endothelin-1 also induced greater contraction than high K+. In the aorta without protein kinase C activity, the contraction induced by 12-deoxyphorbol 13-isobutyrate and its potentiation of the high K+-induced contraction were abolished. However, prostaglandin F2.., noradrenaline and endothelin-1 still induced a greater contraction than high K+.3 In the aorta without protein kinase C activity, noradrenaline, endothelin-l and prostaglandin F2,, but not 12-deoxyphorbol 13-isobutyrate, induced contractions in the presence of the Ca2+ channel blocker, verapamil, or in the absence of external Ca2+, by increasing Ca2+ sensitivify. 4 In the permeabilized preparations, inhibition of protein kinase C activity abolished the effect of potentiation of the Ca2'-induced contraction by 12-deoxyphorbol 13-isobutyrate although the potentiation of the contraction by prostaglandin F2C did not change.5 These results suggest that there are two pathways for Ca21 sensitization in rat aorta; a protein kinase C-dependent pathway which is activated by phorbol esters, and a protein kinase C-independent pathway which is activated by receptor agonists.

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Norepinephrine and GTP-γ-S increase myofilament Ca2+ sensitivity in α-toxin permeabilized arterial smooth muscle

Cited by 304 publications

References 25 publications

Chronic Treatment with Interleukin-1β Attenuates Contractions by Decreasing the Activities of CPI-17 and MYPT-1 in Intestinal Smooth Muscle

Chronic Treatment with Interleukin-1β Attenuates Contractions by Decreasing the Activities of CPI-17 and MYPT-1 in Intestinal Smooth Muscle

Up‐regulation of proteinase‐activated receptor 1 and increased contractile responses to thrombin after subarachnoid haemorrhage

Different pathways of calcium sensitization activated by receptor agonists and phorbol esters in vascular smooth muscle

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