Effect of pertussis toxin on calcium influx in three contraction models

Grześk, Elżbieta; Tejza, Barbara; Wiciński, Michał; Malinowski, Bartosz; Szadujkis-Szadurska, Katarzyna; Baran, L; Kowal, Elżbieta; Grześk, Grzegorz

doi:10.3892/br.2014.274

Cited by 6 publications

(8 citation statements)

References 21 publications

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“…Our previous studies confirmed that mastoparan-7 is able to increase the calcium load in smooth muscle cytoplasm by activation of calcium influx from intra and extracellular calcium stores in an isolated resistant artery model (20,21). In addition, during ischemia and reperfusion, the pathway associated with direct stimulation of G-proteins remains active (22).…”

Section: Modulatory Effect Of Laser Irradiation On Mastoparan-7-inducsupporting

confidence: 71%

“…Arterial smooth muscle function has been investigated in a number of different studies, involving typical pharmacological stimulation with the use of receptor agonists including α 1 -adrenoceptors, vasopressin type 1 receptors or the L-type calcium channel (20)(21)(22)(23)(24)(25)28,29). Direct stimulation of G-proteins with mastoparan-7 was described in certain studies (20)(21)(22)29,30).…”

Section: Discussionmentioning

confidence: 99%

“…By contrast, inhibition of PLC by mastoparan has been demonstrated in SH-SY5Y human neuroblastoma cells and in human astrocytoma cells (19). In vascular smooth cells, it is able to increase contractility (20)(21)(22).…”

Section: Introductionmentioning

confidence: 97%

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Modulatory effect of laser irradiation on mastoparan‑7‑induced contraction

et al. 2019

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Mastoparan-7 activates guanine nucleotide-binding proteins (G-proteins) and stimulates both apoptosis and increases in cytoplasmic calcium concentration and may induce smooth muscle contraction. The primary aim of the present study was to evaluate the modulatory effect of laser stimulation on vascular smooth muscle contraction induced by direct stimulation of G-protein with mastoparan-7. Experiments were performed on isolated and perfused tail arteries of Wistar rats. Contraction force in the model was measured by increased levels of perfusion pressure with a constant flow. Irradiation treatment was applied directly to the blood vessels. The laser was applied in increasing doses of 10 mW (E=1.8 J), 30 mW (E=5.5 J) and 110 mW (E=19.8 J). Time of exposure was 3 min for each irradiation. In the laser-stimulated arteries, a significant and dose-dependent decrease was observed. The half maximal effective concentration values were 4.43±2.2x10-8 , 2.4±0.56x10-7 , 3.2±0.72x10-7 and 7.7±0.3x10-7 M/l in the control and 10, 30 and 110 mW laser irradiation groups, respectively. Significant (P<0.001) changes were identified for all laser treatment groups in comparison with the control. When analyzing the function of calcium ion (Ca 2+) stores was analyzed, a significant inhibition of influx from both intra-and extracellular Ca 2+ stores was observed. The results from the present study suggested that contraction induced by direct activation of G-protein with mastoparan-7 may by effectively inhibited by laser radiation, and that the effect was associated with an inhibition of Ca 2+ influx from both intracellular and extracellular Ca 2+ stores.

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Section: Modulatory Effect Of Laser Irradiation On Mastoparan-7-inducsupporting

confidence: 71%

Section: Discussionmentioning

confidence: 99%

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Modulatory effect of laser irradiation on mastoparan‑7‑induced contraction

et al. 2019

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“…Activation of PLC smooth muscle leads to an increase in the concentration of IP 3 and DAG, which initiates the increase in the concentration of calcium ions in the cytoplasm as a result of the flow from the intracellular pool, and subsequently out of the extracellular pool (1,6). Non-selective inhibitors of PLC, such as edelfosine-ET-18-OCH3 (7) and U-73122 (8)(9)(10), reduce the efficiency of smooth muscle contraction by reducing the influx of calcium into the cytoplasm. In addition to receptor activation, it is possible to directly activate phospholipase C and this significantly increases the calcium ion concentration in the cytoplasm by 2,4,6-trimethyl-N- [3-(trifluoromethyl) phenyl]benzenesulfonamide (m-3M3FBS) (11,12); however, the selectivity of this action remains controversial (6,13,14).…”

Section: Introductionmentioning

confidence: 99%

Effect of 2,4,6-trimethyl-N-[3-(trifluoromethyl)phenyl]benzene-sulfonamide on calcium influx in three contraction models

et al. 2015

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2,4,6-Trimethyl--[3-(trifluoromethyl)phenyl]benzenesulfonamide (m-3M3FBS) activates phospholipase C and stimulates apoptosis; however, in smooth muscle cells it may increase the perfusion pressure. The main aim of the present study was to evaluate the physiological effect of direct stimulation of phospholipase C on vascular smooth muscle reactivity using three contraction models. Experiments were performed on the isolated and perfused tail artery of Wistar rats. The contraction force in the present model was measured by an increased level of perfusion pressure with a constant flow. Concentration-response curves (CRCs) obtained for phenylephrine, arg-vasopressin, mastoparan-7 and Bay K8644 presented a sigmoidal association. In comparison to the control curves, CRCs in the presence of m-3M3FBS were significantly shifted to the left except for Bay K8644. Analyses of calcium influx suggest that in the presence of m-3M3FBS the calcium influx from intra- and extracellular calcium stores was significantly higher. The results of the present experiments suggest that m-3M3FBS significantly increases the reactivity of vascular smooth muscle stimulated with metabotropic receptors or G-protein by an increase in calcium influx from intra- and extracellular calcium stores. The current knowledge regarding the apoptotic pathway shows the significance of calcium ions involved in this process, thus, m-3M3FBS may induce apoptosis by an increase of cytoplasmic calcium concentration; however, simultaneously, the use of this mechanism in therapy must be preceded by a molecular modification that eliminates a possible vasoconstriction effect.

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“…Perfusion pressure was measured on BPR-01 and BPR-02 transducers (Experimetria Ltd.) connected to a digital recorder (Graphtec midi Logger GL820; Graphtec Corp., Yokohama, Japan). The peristaltic pump, which was used to induce arterial perfusion, was purchased from ZALIMP (Warszawa, Poland) (16,17). All reagents were purchased from Sigma-Aldrich (Merck Millipore, Darmstadt, Germany).…”

Section: Drugs and Solutionsmentioning

confidence: 99%

2,4,6-Trimethyl-N-[3-(trifluoromethyl)phenyl]benzenesulfonamide increases calcium influx in lipopolisaccharide-pre-treated arteries

Grześk

Szadujkis-Szadurska

Bloch-Bogusławska

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. It has been demonstrated that 2,4,6-trimethyl-N-[3-(trifluoromethyl)phenyl]benzenesulfonamide (m-3M3FBS) activates phospholipase C (PLC) and stimulates apoptosis in smooth muscle cells, which may increase vascular reactivity. The primary aim of the present study was to evaluate the physiological effects of the direct stimulation of PLC by m-3M3FBS on vascular smooth muscle reactivity in arteries pre-treated with lipopolysaccharides (LPS) as a model of septic shock. Experiments were performed on isolated and perfused tail arteries of Wistar rats. The contraction force in the model was measured by assessing increases in perfusion pressure at a constant flow. Parameters describing the concentration-response curves (CRCs) obtained for phenylephrine and arginine-vasopressin in the presence of LPS confirmed a decrease in vessels reactivity. In comparison with the controls, m-3M3FBS treatment caused a significant increase in LPS-untreated as well as pre-treated arteries. Furthermore, in the presence of m-3M3FBS, calcium influx from intra-as well as extracellular calcium stores was significantly higher for LPS-untreated and pre-treated arteries. The results of the present study suggested that m-3M3FBS significantly increased the reactivity of vascular smooth muscle cells pre-treated with LPS by increasing the calcium influx from intra-and extracellular calcium stores. Further studies investigating this mechanism are required to evaluate whether this pathway may be a potential therapeutic strategy to treat sepsis. IntroductionNitric oxide synthase (NOS) is an enzyme that catalyzes a reaction which generates nitric oxide in two different stages. The first stage is the oxidation of L-arginine to N-omega-hydroxy-L-arginine, which is degraded to L-citrulline in the second stage by NOS and oxygen, and accompanied by the release of nitric oxide from endothelial cells. There are three main types of nitric oxide synthase: NOS-1, -2 and -3. NOS-2 is localized mainly in macrophages, striated heart muscle, liver, vascular smooth muscle or vascular endothelium, and is activated as a response to infection, inflammation or sepsis following the release of pro-inflammatory cytokines, including interleukin (IL)-1, interferon (IFN)-γ or tumor necrosis factor (TNF)-α. The activated enzyme is active for a few h and synthesizes large quantities of nitric oxide (1). Nitric oxide produced by NOS-3 acts predominantly as a regulator of muscle tension in the local regulation of vascular tone. It is also a factor inhibiting the adhesion and aggregation of platelets, as well as angiogenesis. The role of NOS-3 as part of the initiation of NOS-2 activation in the presence of lipopolysaccharides (LPS) has been investigated over the past decade. The first study suggesting that NOS-3 has a role in the generation of NO-associated hyporeactivity during early sepsis was published in 2001 (2,3). A study on isolated animal tissue treated with short acting LPS (~5 h) showed a statistically significant inhibition of NOS-2 expression following blockad...

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Effect of pertussis toxin on calcium influx in three contraction models

Cited by 6 publications

References 21 publications

Modulatory effect of laser irradiation on mastoparan‑7‑induced contraction

Modulatory effect of laser irradiation on mastoparan‑7‑induced contraction

Effect of 2,4,6-trimethyl-N-[3-(trifluoromethyl)phenyl]benzene-sulfonamide on calcium influx in three contraction models

2,4,6-Trimethyl-N-[3-(trifluoromethyl)phenyl]benzenesulfonamide increases calcium influx in lipopolisaccharide-pre-treated arteries

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