• The Korean Journal of Physiology
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• 제23권2호
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• pp.351-361
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• 1989

The contraction of renal arterial strip by no.epineph.me (NE) or 40 mM $K^+$ were Significantly attenuated after histamine $(10^{-5}\;M)-induced$ contraction. The mechanisms of this phenomenon were investigated in the helical strips of isolated renal artery with the measurement of isometric tension. The arterial strip was immersed in the tris-buffered Tyrode's solution which was equilibrated with 100% $O_2\;at\;35^{\circ}C$. The contraction was induced by NE or 40 mM $K^+$ during the recovery from the histamine-induced contraction which lasted for 15 minutes. The contraction by NE was also attenuated in the $Ca^{2+}-free$ Tyrode's solution and the increase of contraction by addition of 2 mM $Ca^{2+}$ was attenuated as well. This attenuation phenomenon was not observed in the presence of low concentration $(3{\times}10^{-7}\;M)$ of histamine. This attenuation was not affected by destruction of endothelium, pretreatment with papaverine or propranolol. This attenuation was partially inhibited by pretreatment of ouabain or in low $K^+(0.5 mM)$ Tyrode's solution. But the attenuation in the $Ca^{2+}-free$ Tyrode's solution was not inhibited. Furthermore this attenuation was completely blocked by pretreatment of djphenhydramine $(H_1-receptor blocker)$ and potentiated by pretreatment of cimetidine $(H_2-receptor\;blocker)$. This attenuation Phenomenon was disappeared after recovery of 1 hour. From the above results, it is suggested that the attenuation phenomenon may be resulted partially from the activation of $Na^+-K^+$ exchange pump and partially from the depletion of intracellular $Ca^{2+}$ pool after the histamine-induced contraction mediated through $H_1-receptor$ function.

• The Korean Journal of Physiology and Pharmacology
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• 제21권6호
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• pp.687-694
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• 2017

Plumbagin, a hydroxy 1,4-naphthoquinone compound from plant metabolites, exhibits anticancer, antibacterial, and antifungal activities via modulating various signaling molecules. However, its effects on vascular functions are rarely studied except in pulmonary and coronary arteries where NADPH oxidase (NOX) inhibition was suggested as a mechanism. Here we investigate the effects of plumbagin on the contractility of skeletal artery (deep femoral artery, DFA), mesenteric artery (MA) and renal artery (RA) in rats. Although plumbagin alone had no effect on the isometric tone of DFA, $1{\mu}M$ phenylephrine (PhE)-induced partial contraction was largely augmented by plumbagin (${\Delta}T_{Plum}$, 125% of 80 mM KCl-induced contraction at $1{\mu}M$). With relatively higher concentrations (>$5{\mu}M$), plumbagin induced a transient contraction followed by tonic relaxation of DFA. Similar biphasic augmentation of the PhE-induced contraction was observed in MA and RA. VAS2870 and GKT137831, specific NOX4 inhibitors, neither mimicked nor inhibited ${\Delta}T_{Plum}$ in DFA. Also, pretreatment with tiron or catalase did not affect ${\Delta}T_{Plum}$ of DFA. Under the inhibition of PhE-contraction with L-type $Ca^{2+}$ channel blocker (nifedipine, $1{\mu}M$), plumbagin still induced tonic contraction, suggesting $Ca^{2+}$-sensitization mechanism of smooth muscle. Although ${\Delta}T_{Plum}$ was consistently observed under pretreatment with Rho A-kinase inhibitor (Y27632, $1{\mu}M$), a PKC inhibitor (GF 109203X, $10{\mu}M$) largely suppressed ${\Delta}T_{Plum}$. Taken together, it is suggested that plumbagin facilitates the PKC activation in the presence of vasoactive agonists in skeletal arteries. The biphasic contractile effects on the systemic arteries should be considered in the pharmacological studies of plumbagin and 1,4-naphthoquinones.

• 대한인간공학회지
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• 제21권2호
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• pp.25-33
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• 2002

The purpose of study is to investigate the relationship between the trunk muscle fatigue and recovery time during repetitive extension by using a surface electromyogram(EMG). Ten healthy subjects particioated in a simulated lifting task with five levels of recovery time and three levels of sub-maximal contraction. EMG signals of the L1(Lumbar 1st Vertebrae) and L3(Lumbar 3rd Vertebrae) level of the erector spinae muscle were recorded. and analyzed in terms of MPF(mean power frequency) parameter to quantify the level of muscle fatigue. It was found that MPF significantly (p<0.05) decreased during repetitive extension task at 50% and 75% sub-maximal contractions. Then it took minutes for the trunk muscle to recover from fatigue during 50% sub-maximal contraction. and it took five minutes during 75% sub-maximal contraction. and it took five minutes during 75% sub-maximal contraction. The recovery time estimated by the maximum force needs to be re-evaluated for the trunk muscle to fully recover from fatigue. In conclusion. the work/rest cycle needs to be studied based upon the information of muscle fatigue in order to prevent workers from musculoskeletal injuries during repetitive lifting task.

• 한국정밀공학회지
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• 제28권6호
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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.

• Biomolecules & Therapeutics
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• 제19권4호
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• pp.460-465
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• 2011

The present study was undertaken to investigate the influence of quercetin on vascular smooth muscle contractility and to determine the mechanism involved. Denuded aortic rings from male rats were used and isometric contractions were recorded and combined with molecular experiments. Quercetin at a low concentration (0.01-0.03 mM) directly and more significantly relaxed fluoride or thromboxane $A_2$-induced vascular contraction than phorbol ester-induced contraction suggesting as a possible anti-hypertensive on the agonist-induced vascular contraction regardless of endothelial nitric oxide synthesis. Furthermore, quercetin more significantly inhibited thromboxane $A_2$-induced increases in pMYPT1 levels than phorbol ester-induced increases. It also more significantly inhibited thromboxane $A_2$-induced increases in pMYPT1 levels than pERK1/2 levels suggesting the mechanism involving the primarily inhibition of Rho-kinase activity and the subsequent phosphorylation of MYPT1. This study provides evidence regarding the mechanism underlying the relaxation effect of quercetin on agonist-induced vascular contraction regardless of endothelial function.

• The Korean Journal of Physiology and Pharmacology
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• 제21권1호
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• pp.91-97
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• 2017

Hyperglycemia is associated with an increased risk of cardiovascular diseases. It has been demonstrated that chronic exposure to high glucose impaired endothelial functions. However, specific effects of short-term exposure to high glucose on vascular reactivity are controversial. Moreover, the combined effects of other metabolic substrates such as free fatty acids (FFA) on vascular reactivity remain poorly understood. Here we investigate the effects of short-term exposure to high glucose with or without other metabolic substrates including FFAs termed "nutrition full" (NF) solution, on mesenteric (MA) and deep femoral arteries (DFA) of rats. Arterial ring segments were mounted in a double-wire myograph. Contraction in response to phenylephrine (PhE) was determined in control (5 mM) and high glucose (23 mM, HG) environments over a 30 min period. In both arteries, PhE-inducedvasocontraction was enhanced by pre-incubation of HG solution. A combined incubation with HG and palmitic acid ($100{\mu}M$) induced similar sensitization of PhE-contractions in both arteries. In contrast, high $K^+$-induced contractions were not affected by HG. Interestingly, pre-incubation with NF solution decreased PhE-induced contraction in MA but increased the contraction in DFA. In NF solution, the HG-induced facilitation of PhE-contraction was not observed in MA. Furthermore, the PhE-induced contraction of DFA was attenuated by HG in NF solution. Our results demonstrate that the sensitization of PhE-induced arterial contraction by HG is differentially affected by other metabolic substrates. The conversation of skeletal arterial contractility by HG in NF solution requires careful interpretation of the previous in vitro studies where only glucose is included in physiological salt solutions. Further studies are required to elucidate the mechanism underlying the inconsistent effect of NF solution on MA and DFA.

• 한국전문물리치료학회지
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• 제14권4호
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• pp.50-57
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• 2007

The purpose of this study was to investigate the relationship between delays in initiation and termination of tibialis anterior contraction through surface electromyographic (sEMG) analysis in adults with hemiplegia and healthy subjects and clinical assessment of lower-limb mobility. EMG activity of 6 long-term survivors of stroke and 5 healthy subjects was recorded during maximal isometric ankle dorsiflexion in 3 seconds beeper signals. It must be done as fast and forcefully as possible. Lower limb mobility was assessed with Modified Emory Functional Ambulation Profile (mEFAP). Delay in initiation and termination of muscle contraction was significantly prolonged in the affected lower limb relative to the unaffected limb. Termination of muscle contraction in the hemiplegic lower limb was significantly delayed than the initiation on the affected sides. Delay in initiation and termination of muscle contraction correlated significantly with a few range of mEFAP. Abnormally delayed initiation and termination of muscle contraction may contribute to hemiparetic lower limb mobility in hemiparetic patients. Consequently, this study showed that abnormal delay of initiation and termination of muscle contraction may contribute to hemiparetic lower limb mobility in adults with hemiplegia. Further studies are needed to demonstrate a treatment effect.

• The Korean Journal of Physiology
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• 제23권1호
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• pp.99-108
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• 1989

The effects of prostaglandin $(PGF_{2{\alpha}})$ on the contractility of vascular smooth muscle were investigated in the helical strip of the rabbit aorta. The aortic strip was immersed in the phosphate-buffered Tyrode's solution which was equilibrated with 100% $O_{2}$ at $35^{\circ}C$ and its isometric tension was measured. The contraction was induced by $(PGF_{2{\alpha}})$, norepinephrine (NE), or potassium (40 mM) in the nomal Tyrode's solution (1 mM, $Ca^{2+}$) or $Ca^{2+}-free$ Tyrode's solution. Effects of verapamil and phentolamine on the contraction were also observed. The aortic strip began to contract at the concentration of $5\;{\mu}g%$ and reached the maximal contraction at the concentration of $150\;{\mu}g%$ $(PGF_{2{\alpha}})$. The maximal contraction was corresponded respectively to $52.2{\pm}3.0%$ and $81.5{\pm}3.5%$ of maximal contraction by NE $(1{\times}10^{-5}M)$ and 40 mM $K^{+}$. And the maximal contractions by $(PGF_{2{\alpha}})$ or NE were induced at the concentration of about 1 mM $Ca^{2+}$. $(PGF_{2{\alpha}})$ induced the contraction of aortic strip even after induction of contraction by 40 mM $K^{+}$ and the contraction by $(PGF_{2{\alpha}})$ was not blocked by the ${\alpha}-receptor$ blocker, phentolamine. And the contraction by the $(PGF_{2{\alpha}})$ was inhibited partially by a verapamil at the concentration of $1{\times}10^{-5}M$ and the contraction began to increase at the concentration of $1{\times}10^{-4}M$ verapamil. Whereas the contraction by NE was completely blocked by verapamil. Though both the $(PGF_{2{\alpha}})$ and NE induced the contraction in the $Ca^{2+}-free$ Tyrode's solution, the peak tension was not maintained. But the rate of tension decline was lower in the contraction by $(PGF_{2{\alpha}})$ than in that by NE. The verapamil did not inhibit the contraction by $(PGF_{2{\alpha}})$ in the $Ca^{2+}-free$ Tyrode's solution and increased the contraction at the concentration of above $1{\times}10^{-4}M$. The NE-induced contraction in the $Ca^{2+}-free$ Tyrode's solution was inhibited completely by a verapamil. From the above results it is suggested that the contraction induced by $(PGF_{2{\alpha}})$ results from the promotion of the both $Ca^{2+}$ influx and the intracellular $Ca^{2+}$ release by different way from NE.

• 산업융합연구
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• 제21권10호
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• pp.57-63
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• 2023

평활근 수축에 대한 감초산(glycyrrhizic acid)의 효과를 연구하고자 하였고 관련 상세 기전을 결정하기 위해 glycyrrhizic acid가 agonist-sensitive하게 평활근 수축한다는 가설을 제시하였다. S/D rats의 평활근을 수조 내 준비하였고 신호 변환기에서 평활근에 의한 운동 신호가 전기적 신호로 변환되어 생리기록기에 표시되는 데이터는 일원배치 분산분석으로 분석하였다. 재미있게도, 감초산은 불화물, 트롬복산 유사체 등 굵은 미세섬유성 조절성 수축제에 의한 평활근 수축을 중등도로 억제하였고 (농도 0.01, 0.03, 0.1 mM 불화물에서 p=0.113, 0.008, 0.004 (Student's t-test), p=0.113, 0.008, 0.004 (One way ANOVA), 그리고 0.01, 0.03, 0.1 mM 트롬복산 유사체에서 p=0.156, 0.004, 0.003 (Student's t-test), p=0.156, 0.004, 0.003 (One way ANOVA)) 포볼 에스테르 등 가는 미세섬유성 조절성 수축제에 의한 평활근 수축에 대해 효과가 소실되었다 (0.01, 0.03, 0.1 mM 포볼 에스테르에서 p=0.392, 0.086, 0.065 (Student's t-test), p=0.392, 0.086, 0.065 (One way ANOVA)). 이러한 결과는 내피 기능이 억제된 평활근에서 감초산은 평활근 내피에서 EDRF (NO) 생성 효과 외에 주로 ROCK 활성 감소 등 평활근에 대한 직접적 효과를 통해 최종적으로 평활근에서 악틴-미오신 상호작용을 제한하여 평활근을 이완시키는 것으로 생각된다.

• The Korean Journal of Physiology
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• 제27권1호
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• pp.27-35
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• 1993

Effects of the endothelium on the contractile responses to norepinephrine (NE) were investigated in isolated helical strips of the proximal and distal coronaries artery of pigs. The helical strips were immersed in Tris-buffered Tyrode's solution equilibrated with 100% $O_2$ at $35^{\circ}C$ and its isometric tension was measured. NE relaxed the strips precontracted with acetylcholine from both the proximal and distal coronary artery. NE-induced relaxation, which might be induced mainly by $\beta$-adrenoceptor function was dominant in the distal coronary arteries. NE-induced relaxation was converted to a contraction after $\beta$-adrenoceptor blockade with propranolol $(3{\times}10^{-6}M)$. ${\alpha}$-adrenoceptor-mediated contraction by NE was greater in the proximal coronary artery than the distal coronary artery. Quantitatively, ${\alpha}_1$-adrenoceptor mediated contraction by NE was greater than ${\alpha}_2$-adrenoceptor mediated contraction by NE in both arteries. NE-induced relaxation was decreased by rubbing of endothelium in both arteries. ${\alpha}_1-and\;{\alpha}_2$-adrenoceptor mediated contraction by NE were potentiated by rubbing of endothelium in both arteries. Pretreatment with methylene blue, an inhibitor of soluble guanylate cyclase, increased ${\alpha}_1-\;and\;{\alpha}_2$-adrenoceptor mediated contraction by NE in both arteries with endothelium. From the above results, we suggest that the effect of activation of $\alpha$-adrenoceptors by NE may be modulated by endothelium in the proximal and distal coronary arteries of pigs. This effect may be mediated via endothelium derived relaxing factor.