• Molecules and Cells
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• v.27 no.2
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• pp.191-198
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• 2009

The present study was undertaken to determine whether treatment with genistein, the plant-derived estrogen-like compound influences agonist-induced vascular smooth muscle contraction and, if so, to investigate related mechanisms. The measurement of isometric contractions using a computerized data acquisition system was combined with molecular experiments. Genistein completely inhibited KCl-, phorbol ester-, phenylephrine-, fluoride- and thromboxane $A_2$-induced contractions. An inactive analogue, daidzein, completely inhibited only fluoride-induced contraction regardless of endothelial function, suggesting some difference between the mechanisms of RhoA/Rho-kinase activators such as fluoride and thromboxane $A_2$. Furthermore, genistein and daidzein each significantly decreased phosphorylation of MYPT1 at Thr855 had been induced by a thromboxane $A_2$ mimetic. Interestingly, iberiotoxin, a blocker of large-conductance calcium-activated potassium channels, did not inhibit the relaxation response to genistein or daidzein in denuded aortic rings precontracted with fluoride. In conclusion, genistein or daidzein elicit similar relaxing responses in fluoride-induced contractions, regardless of tyrosine kinase inhibition or endothelial function, and the relaxation caused by genistein or daidzein was not antagonized by large conductance $K_{Ca}$-channel inhibitors in the denuded muscle. This suggests that the RhoA/Rho-kinase pathway rather than $K^+$- channels are involved in the genistein-induced vasodilation. In addition, based on molecular and physiological results, only one vasoconstrictor fluoride seems to be a full RhoA/Rho-kinase activator; the others are partial activators.

• Journal of International Academy of Physical Therapy Research
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• v.9 no.4
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• pp.1614-1618
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• 2018

The purpose of this study was to evaluate the effect of joint mobilization and manual stretching exercises in patients with hallux valgus. Twenty-three participants were divided into two groups; joint mobilization (n=11) and manual stretching exercises (n=12). The subjects participated in the experiment for 15minutes, three times a week, four weeks. The joint mobilization (Grade III, Maitland) was performed to experimental group for a minute and then rested for 10 seconds for each set. The manual stretching was performed to control group with three exercise session (preparatory and finishing exercises, agonist contraction exercises, agonist contraction and hold-relax exercises). In the results of the study, intragroup comparison of the deformity angles (DA) was shown to decrease from $15.18^{\circ}$ to $13.09^{\circ}$ in the joint mobilization group (p<.05) and from $19.00^{\circ}$ to $16.83^{\circ}$ in the stretching exercises group (p<.05). However, left static foot pressure (LSFP), right static foot pressure (RSFP), left dynamic foot pressure (LDFP) and right dynamic foot pressure (RDFP) did not significantly increase or decrease after the experiment. Intergroup differences also were not statistically significant in all variables (p>.05). The current study suggests that JM and MSE are effective in decreasing the DA in patients with hallux valgus.

• Journal of Korean Physical Therapy Science
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• v.11 no.1
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• pp.20-27
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• 2004

It is widely accepted that smooth muscle contraction is triggered by intracellular $Ca^{2+}$ ($[Ca^{2+}]_i$) released from intracellular $Ca^{2+}$ stores such as sarcoplasmic reticulum (SR) and from the extracellular space, The increased $[Ca^{2+}]_i$ can phosphorylate the 20-kDa myosin light chain ($MLC_{20}$) by activating MLC kinase (MLCK), and this initiates smooth muscle contraction. In addition to the $[Ca^{2+}]_i$-MLCK-tension pathway, a number of intracellular signal molecules, including mitogen-activated protein kinase (MAPK), protein kinase C (PKC), phosphatidylinositol 3-kinase (PI3K), and Rho-associated coiled coil-forming protein kinase (ROCK), play important roles in the regulation of smooth muscle contraction. However, the mechanisms regulating contraction of caldesmon (CaD), actin-binding protein, are not entirely elucidated in the presence of $Ca^{2+}$. It is known that CaD tightly interacts with actin and inhibits actomyosin ATPase activity. Therefore, the purpose of the present study was to investigate the roles of $Ca^{2+}$-dependent CaD in smooth muscle contraction. Endothelin-1 (ET-1), G-protein coupled receptor agonist and vasoconstrictor, increased both vascular smooth contraction and phosphorylation of CaD in the presence of $Ca^{2+}$. These results suggest that ET-1 induces contraction and phosphorylation of CaD in rat aortic smooth muscle, which may he mediated by the increase of $[Ca^{2+}]_i$.

• Journal of the Korean Society for Precision Engineering
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• v.28 no.6
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• pp.670-677
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• 2011

This study is to estimate the joint torques without torque sensor using the EMG (Electromyogram) signal of agonist/antagonist muscle with Neural Network Back Propagation Algorithm during the elbow motion. Command Signal can be guessed by EMG signal. But it cannot calculate the joint torque. There are many kinds of field utilizing Back Propagation Learning Method. It is generally used as a virtual sensor estimated physical information in the system functioning through the sensor. In this study applied the algorithm to obtain the virtual senor values estimated joint torque. During various elbow movement (Biceps isometric contraction, Biceps/Triceps Concentric Contraction (isotonic), Biceps/Triceps Concentric Contraction/Eccentric Contraction (isokinetic)), exact joint torque was measured by KINCOM equipment. It is input to the (BP)algorithm with EMG signal simultaneously and have trained in a variety of situations. As a result, Only using the EMG sensor, this study distinguished a variety of elbow motion and verified a virtual torque value which is approximately(about 90%) the same as joint torque measured by KINCOM equipment.

• YAKHAK HOEJI
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• v.53 no.3
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• pp.156-160
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• 2009

The present study was undertaken to determine whether transgelin participates in the regulation of vascular smooth muscle contraction and, if so, to investigate the mechanism. By PCR homology cloning, the cDNA sequence of ferret transgelin was determined and phosphorothioate antisense and random oligonucleotides were synthesized and introduced into strips of ferret aorta by a chemical loading procedure. Treatment of ferret aorta with transgelin antisense oligonucleotides resulted in a significant decrease in protein levels of transgelin to sham- or random sequence-loaded muscles, but no change in the protein levels of actin. Contraction in response to a phorbol ester was significantly decreased in antisense-treated muscles compared to sham- or random sequence-loaded controls. Neither basal intrinsic tone nor the contraction in response to phenylephrine was significantly affected by the antisense treatment. The data indicate that transgelin plays a significant role in the regulation of contraction and suggest that in a tonically active smooth muscle transgelin may function as a signalling protein to facilitate PKC or ERK-dependent signalling rather than thick filament regulation including $Ca^{2+}$ or calmodulin dependent regulation of myosin light chain kinase.

• YAKHAK HOEJI
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• v.35 no.5
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• pp.416-426
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• 1991

The effects of an irreversible or a reversible $\alpha_1$-adrenoceptor antagonist (dibenamine or prazosin) on $\alpha_1$-adrenoceptor-mediated vasoconstrictions were studied in the endothelium-denuded rat aorta. In these experiments, the mobilization of intracelluier calcium and translocation of extracellular calcium were also studied. To exclude the modulation of endothelium releasing EDRF and EDCF, the endothelium was removed in all rat aortas. Contraction induced by phenylephrine (a full $\alpha_1$-adrenoceptor agonist) was separated into a fast phasic component of the response due to the release of intracellular calcium and a slow tonic one due to the influx of extracellular calcium. Pretreatments with increasing doses of reversible $\alpha_1$-adrenoceptor antagonist prazosin, as well as irreversible $\alpha_1$-adrenoceptor antagonist dibenamine, inhibited the phasic component of phenylephrine-induced contraction more effectively than the tonic one. Pretreatment of dibenamine (0.2 $\mu{M}$) or prazosin (10 nM) to the rat aorta abolished phasic response but remained tonic one about 41% and 51%, respectively. These results suggest that as the efficiency of phenylephrine was progressively reduced by pretreatments with increasing doses of an irreversible or a reversible $\alpha_1$-adrenoceptor antagonist (dibenamine or prazosin), the contraction induced by phenylephrine became progressively more dependent on the influx of extracellular calcium.

• The Korean Journal of Pharmacology
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• v.30 no.2
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• pp.181-190
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• 1994

In rat atrium the characteristics of purinergic receptors were investigated by observing the effects of some purinergic receptor agonists and antagonists on action potential and contractile force. The statistically significant effects of $ATP(10^{-6}{\sim}10^{-3}M)$ and adenosine $(10^{-6}{\sim}10^{-3}M)$ on normal action potential characteristics were a dose-dependent shortening of action potential duration $(APD_{90})$ by both agents and hyperpolarization by $ATP(10^{-4},10^{-3}M)$. $CAP(10^{-8}{\sim}10^{-4}M)$, an $A_1$ adenosine receptor agonist, shortened $(APD_{90})$ markedly in a dose-dependent manner and these effects were almost abolished by $DPCPX\;(10^{-6}\;M), an $A_1$, adenosine receptor antagonist, but not affected by $DMPX(2{\times}10^{-6}\;M)$, an $A_2$ adenosine receptor agonist. On the other hand, CGS $21680(10^{-7}{\sim}10^{-4}M)$, an $A_2$ adenosine receptor agonist, elicited a slight shortening of $(APD_{90})$ and these effects were inhibited by DPCPX but persisted in the presence of DPMX. Adenosine $(10^{-6}{\sim}10{\-4}\;M)$ decreased the basal contraction of atrial muscle in a dose-dependent manner and these effects were not inhibited by DMPX but by DPCPX. These results suggests that purinergic receptor agonists depress the cardiac activity by a short ening of action potential duration and this effect is mostly mediated by $A_1$ adenosine receptors in rat atrium.

• Archives of Pharmacal Research
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• v.18 no.2
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• pp.129-132
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• 1995

Intravenous administration of O-acetyliervine (an alkaloid from Vertrum album) produced a dose-dependent (10-100 .mu.g/kg) fall in blood pressure and tachycardia in anaesthetized normotensive rats. Pretreatment of animals with propranolol (1mg/kg) abolished these cardiovascular responses of O-acetyljervine similar to that of isoprenaline $(1\mu/ml)$. In isolated tissue experiments, O-acetyljervine $(10-100\mu/ml)$ produced a dose-dependent relaxation of phenylephrine-induced contraction of the rabbit aorta. In guinea-pig spontaneously beating atria, it caused positive inotropic and chronotorpic responses in a dose-dependent fashion $(10-100\mu/ml)$. These responses were abolished in the presence of propranolol $(1\mu/ml)$ similar to that of isoprenaline. These results indicate that O-accetyljervine is adrenoceptor stimulant $(\beta_1\; and\;beta_2)$ like isoprenaline.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.164.2-165
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• 2003

Chronic exposure of arsenic is well known to be the cause of cardiovascular disease such as hypertension. In order to investigate the effect of arsenic on blood vessels. we examined whether arsenic affected agonist-induced contraction of aortic rings in isolated organ bath system. Treatment with arsenite increased vasoconstriction induced by phenylephrine or serotonin in a concentration-dependent manner. (omitted)

• Biomolecules & Therapeutics
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• v.18 no.4
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• pp.442-447
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• 2010

This study was conducted to determine whether treatment with the anti-inflammatory eupatilin influences intestinal smooth muscle contraction stimulated by carbachol and, if so, to investigate the related mechanism. Denuded ileal or colonic muscles from Sprague-Dawley rats were used for the study and measurements of isometric contractions were obtained using a computerized data acquisition system; this data was also combined with results from molecular experiments. Eupatilin from Artemisia asiatica Nakai significantly decreased carbachol-induced contractions in both ileal and colonic muscles. Interestingly, eupatilin decreased carbachol-induced phosphorylation of ERK1/2 more significantly than that of MYPT1 at Thr855 in ileal and colonic muscles. However, eupatilin significantly decreased phosphorylation of MYPT1 at Thr855, but only in ileal muscle. Therefore, thin filament regulation, including MEK inactivation and related phospho-ERK1/2 decrease, is mainly involved in the eupatilin-induced decrease of intestinal contraction induced by carbachol. In conclusion, this study provides the evidence and a possible related mechanism concerning the inhibitory effect of the flavonoid as an antispasmodic on the agonist-induced contractions in rat ileum and colonic muscles.