• The Korean Journal of Physiology
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• v.29 no.2
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• pp.225-232
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• 1995

The present study was conducted to evaluate the effect of phorbol 12,13-dibutyrate (PDBu) on the contraction of rabbit jugular vein in vitro. PDBu concentrations of greater than 10 nM induced a periodic contraction which was composed of rapid contraction, plateau and slow relaxation. The frequency of periodic contraction increased as PDBu concentration increased. The PDBu-induced contraction was inhibited by staurosporine (100 nM), it was not changed by tetrodotoxin $(1\;{\mu}M).$ In $Ca^{2+}$-free medium, PDBu induced a sustaining contraction, but not periodic contraction. Addition of $Ca^{2+}$ to medium evoked periodic contraction which was inhibited by nifedipine, PDBu concentrations of greater than $0.1\;{\mu}M$ increased ^{45}Ca^{2+}$ uptake without changing $^{45}Ca^{2+}$ efflux. Charybdotoxin and apamin, $Ca^{2+}$-activated K^{+}$ channel blockers, did not affect the PDBu-induced periodic contraction, whereas tetraethylammonium (TEA) abolished the periodicity. Pinacidil $(10\;{\mu}M).$, a potassium channel activator, blocked PDBu induced periodic contraction, which was recovered by glybenclamide $(10\;{\mu}M).$. In high potassium solution, PDBu did not produce the periodic contraction. These results suggest that the PDBu-induced periodicity of contraction is modulated by voltage dependent $Ca^{2+}$ channel and ATP-sensitive $K^{+}$ channel.

• The Korean Journal of Physiology
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• v.26 no.2
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• pp.123-128
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• 1992

The present study was undertaken to examine if endogenous nitric oxide is partly responsible for the high calcium induced vasorelaxation in vitro. Isolated porcine coronary arterial rings were suspended in the tissue chamber and their changes in isometric tension were recorded. KCI little affected the vascular tension in the calcium free media, but subsequent addition of cumulative doses of $CaCl_3$ from 1 to 40 mM caused a contraction followed by complete relaxation. The maximum tension was noted at the calcium concentration in the media of 5 mM, and then the tension progressively declined at 10-40 mM. The relaxation was slightly attenuated in the endothelium-denuded preparation. The relaxation was converted into a contraction by the addition of methylene blue. The relaxation response was not affected in the presence of indomethacin, but was significantly attenuated by $N^w-nitro-L-arginine$ methyl ester pretreatment. These results suggest that the calcium induced vasorelaxation is in part attributable to the release of endogenous nitric oxide.

• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.3
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• pp.593-599
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• 2008

This research was aimed to examine the effect of Polygoni Multiflori Radix extract on the blood pressure in spontaneous hypertensive rat (SHR) and norepinephrine - induced arterial contraction in rabbit. In order to investigate the effect of Polygoni Multiflori Radix on rabbit's contracted vascular ring detached from common carotid artery, vascular ring with intact or damaged endothelium was used for the experiment using organ bath. To analyze the mechanism of Polygoni Multiflori Radix-induced relaxation, Polygoni Multiflori Radix extract was infused into contracted vascular ring which had been pretreated by $N{\omega}$-nitro-L-arginine(L-NNA), Methylene blue(MB), and $Ca^{2+}$ was infused into contracted vascular ring induced by NE after treatment of Polygoni Multiflori Radix extract in $Ca^{2+}$-free solution. The results were as follows: Systolic blood pressure was significantly attenuated by administration of Polygoni Multiflori Radix. Blood flow and aldosterone were significantly decreased, but velocity and renin were not affected by Polygoni Multiflori Radix. Polygoni Multiflori Radix had an effective relaxation to the contracted vascular ring by NE in 0.03 mg/ml, 0.1 mg/ml and 0.3 mg/ml level. Polygoni Multiflori Radix had an effective relaxation to the intact endothelium vascular ring, but when endothelium was removed, vascular ring did not relax. Polygoni Multiflori Radix-induced relaxation was inhibited by the pretreatment of L-NNA and MB. Pretreatment of Polygoni Multiflori Radix extract inhibit the contraction by influx of extra-$Ca^{2+}$ in contracted vascular ring induced by NE in $Ca^{2+}$-free solution. As mentioned above, we suggest that Polygoni Multiflori Radix relaxes vascular ring through suppress influx of extra-cellular $Ca^{2+}$ by the action of nitric oxide from endothelium.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.6
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• pp.1622-1628
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• 2005

This study was undertaken to define the effect of SoPung-Tang extract on hypertension in spontaneous hypertensive rat and norepinephrine- induced arterial contraction in rabbit. In order to investigate the effect of SoPung-Tang extract on contracted rabbit carotid arterial strips, transverse strips with intact or damaged endothelium were used for the experiment using organ bath. To analyze the mechanism of SoPung-Tang extract-induced relaxation, SoPung-Tang extract infused into contracted arterial strips induced by norepinephrine after treatment of indomethacin, Nu-nitro-L-arginine, methylene blue or tetraethylammonium chloride. Blood pressure was significantly decreased five days after administration of SoPung-Tang extract. SoPung-Tang extract relax arterial strip with endothelium contracted by norepinephrine, but in the strips without endothelium, SoPung-Tang extract- induced relaxation was significantly inhibited. SoPung-Tang relax arterial strip contracted by norepinephrine, but in the strips contracted by high $K^+$, SoPung-Tang extract-induced relaxation was significantly inhibited. The endothelium-dependent relaxation induced by SoPung-Tang extract was decreased by the pre-treatment of $N{\omega}$-nitro-L-arginine or methylene blue, but it was not observed in the strips pre-treated with indomethacin or tetraethylammonium chloride. When $Ca^{2+}$ was applied, the strips which were contracted by norepinephrine in a $Ca^{2+}$-free solution, arterial contraction was increased. But pre-treatment of SoPung-Tang extract inhibited contractile response to $Ca^{2+}$. We suggest that SoPung-Tang could be applied effectively for hypertension and may suppress influx of extra-cellular $Ca^{2+}$ through the formation of nitric oxide in the vascular endothelial cells.

• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.3
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• pp.666-671
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• 2008

This study was undertaken to define the effect of ChungGongGo extract on norepinephrine-induced arterial contraction in rabbit. In order to investigate the effect of ChungGongGo extract on rabbit's contracted vascular ring detached from common carotid artery, vascular ring with intact or damaged endothelium was used for the experiment using organ bath. To analyze the mechanism of ChungGongGo extract-induced relaxation, ChungGongGo extract was infused into contracted vascular ring which had been pretreated by $N{\omega}$-nitro-L-arginine(L-NNA), Methylene blue(MB), and $Ca^{2+}$ was infused into contracted vascular ring induced by NE or KCl after treatment of ChungGongGo in $Ca^{2+}$-free solution. The results were as follows: ChungGongGo extract had an effective relaxation to the contracted vascular ring by NE in 1.0mg/ml and 0mg/ml level. ChungGongGo extract had an effective relaxation to the intact endothelium vascular ring, but when endothelium was removed, vascular ring did not relax. ChungGongGo extract-induced relaxation was inhibited by the pretreatment of L-NNA and MB. Pretreatment of ChungGongGo extract inhibit the contraction by influx of extra-$Ca^{2+}$ in contracted vascular ring induced by NE in $Ca^{2+}$-free solution. As mentioned above, we suggest that ChungGongGo relaxes vascular ring through suppress influx of extra-cellular $Ca^{2+}$ by the action of nitric oxide from endothelium.

• The Korean Journal of Physiology
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• v.29 no.2
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• pp.233-241
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• 1995

The nonapeptide bradykinin has been shown to exhibit an array of biological activities including relaxation/contraction of various smooth muscles. In order to investigate the effects of bradykinin on the contractility and the electrical activity of antral circular muscle of guinea-pig stomach, the isometric contraction and membrane potential were recorded. Also, using standard patch clamp technique, the $Ca^{2+}-activated$ K currents were recorded to observe the change in cytosolic $Ca^{2+}$ concentration. $0.4 {\mu}M$ bradykinin induced a triphasic contractile response (transient contraction-transient relaxation-sustained contraction) and this response was unaffected by pretreatment with neural blockers (tetrodotoxin, atropine and guanethidine) or with apamin. Bradykinin induced hyperpolarization of resting membrane potential and enhanced the amplitude of slow waves and spike potentials. The enhancement of spike potentials was blocked by neural blockers. Both the bradykinin-induced contractions and changes in membrane potential were reversed by the selective $B_2$-receptor antagonist $(N{\alpha}-adamantaneacetyl-_{D}-Arg-[Hyp, Thy,_{D}-Phe]-bradykinin)$. In whole-cell patch clamp experiment, we held the membrane potential at -20 mV and spontaneous and transient changes of Ca-activated K currents were recorded. Bradykinin induced a large transient outward current, consistent with a calcium-releasing action of bradykinin front the intracellular calcium pool, because such change was blocked by pretreatment with caffeine. Bradykinin-induced contraction was also blocked by pretreatment with caffeine. From these results, it is suggested that bradykinin induces a calciumrelease and contraction through the $B_{2}$ receptor of guinea-pig gastric smooth muscle. Enhancement of slow wave activity is an indirect action of bradykinin through enteric nerve cells embedded in muscle strip.

• Korean Journal of Oriental Medicine
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• v.11 no.1
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• pp.97-107
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• 2005

Objectives : This experiments were performed to determine the effect of Linderae Radix extract on norepinephrine-induced arterial contraction in rabbit. Methods : In order to investigate the effect of Linderae Radix extract on contracted rabbit carotid arterial strips, transverse strips with intact or damaged endothelium were used for the experiment using organ bath. To analyze the mechanism of Linderae Radix extract-induced relaxation, Linderae Radix extract infused into contracted arterial strips induced by norepinephrine after treatment of indomethacin, tetraethylammonium chloride, $N{\omega}-nitro-L-arginine$ or methylene blue. Results : Linderae Radix extract relax arterial strip with endothelium contracted by norepinephrine, but in the strips without endothelium, Linderae Radix extract-induced relaxation was significantly inhibited. Linderae Radix extract-induced relaxation was decreased by the pre-treatment of $N{\omega}-nitro-L-arginine$ or methylene blue, but it was not observed in the strips pre-treated with indomethacin or tetraethylammonium chloride. When $Ca^{2+}$ was applied, the strips which were contracted by norepinephrine in a $Ca^{2+}$-free solution, arterial contraction was increased. But pre-treatment of Linderae Radix extract inhibited contractile response to norepinephrine and $Ca^{2+}$. Conclusions : We suggest that Linderae Radix may suppress influx of extra-cellular $Ca^{2+}$ through the formation of nitric oxide, and release of intra-cellular $Ca^{2+}$.

• YAKHAK HOEJI
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• v.34 no.3
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• pp.180-191
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• 1990

A comparison was made of the effects of selective ${\alpha_1}-adrenoceptor$ agonist phenylephrine and selective ${\alpha_2}-adrenoceptor$ agonist clonidine on endothelium-containing and endothelium-denuded rings of the rat aorta. In the case of phenylephrine, removal of endothelium increased sensitivity 2.5 fold at $EC_{50}$ level and maximum contractive response 1.4 fold. In the case of clonidine, which gave only 15% of maximum contractive response given to phenylephrine on endothelium-containing rings, removal of the endothelium increased sensitivity 5.6 fold at $EC_{50}$ level and maximum contractive response 5 fold, which was about 55% of that given by phenylephrine. In endothelium-denuded ring, phenylephrine-induced contraction tended to be more increased in tonic contraction than in phasic contraction as compared to that in endothelium-containing ring, while clonidine-induced contraction was monophasic and was increased only in tonic contraction. In the calcium-free solution or in the presence, of verapamil, contraction stimulated by clonidine was almost abolished while that stimulated by phenylephrine produced only phasic contraction. The depression of sensitivity to these agonists in rings with endothelium appeared to be due to the vasodepressor action of endothelium derived relaxing factor (EDRF), because hemoglobin, a specific blocking agent of EDRF, abolished this depression. It is unlikely that the endothelium-dependent relaxation was due to stimulation of release of EDRF, because clonidine did not produce endothelium-dependent relaxation in 5-hydroxytryptamine-precontracted ring even when its contractile action was blocked by the ${\alpha_1}-adrenoceptor$ antagonist, prazosin. When the efficacy of phenylephrine was reduced to about the initial efficacy of clonidine by pretreatment with dibenamine, the contraction-response curves for phenylephrine became very similar to the corresponding curves obtained for clonidine before receptor inactivation. In the dibenamine-treated rings, contraction of phenylephrine was abolished in calcium-free solution or in the presence of verapamil like that obtained for clonidine before receptor inactivation. These results suggest that EDRF spontaneously released from endothelium depress contraction more profoundly in a case of an agonist with low efficacy and the phenylephrine-induced contraction was totally dependent on extracellular calcium as was that obtained for clonidine when the efficacy of phenylephrine was reduced to that of clonidine by irreversible inactivation of ${\alpha_1}-adrenoceptor$ with dibenamine.

• Journal of Korean Medicine Rehabilitation
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• v.18 no.1
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• pp.125-140
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• 2008

Objectives : The purpose of this study was to investigate the effect of Progressive Muscle Relaxation(PMR) on stress and muscle relaxation in healthy people. Methods : Sample group of 14 healthy subjects had been treated by progressive muscle relaxation for 10 days. Control group of 14 healthy subjects were not treated during the same period. Outcomes were assessed by Meridian-Electromyograph(MEMG), Heart Rate Variability(HRV), Stress Reaction Inventory(SRI). Results : The contraction and fatigue of erector spinae muscle by MEMG had decreased significantly in Sample group. There was no significant difference between two groups in the HRV and SRI. Conclusions : Further studies analysing PMR effect on stress and muscle relaxation are needed.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.3
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• pp.257-262
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• 2015

It is well known that cigarette smoke can cause erectile dysfunction by affecting the penile vascular system. However, the exact effects of nicotine on the corpus cavernosum remains poorly understood. Nicotine has been reported to cause relaxation of the corpus cavernosum; it has also been reported to cause both contraction and relaxation. Therefore, high concentrations of nicotine were studied in strips from the rabbit corpus cavernosum to better understand its effects. The proximal penile corpus cavernosal strips from male rabbits weighing approximately 4 kg were used in organ bath studies. Nicotine in high concentrations ($10^{-5}{\sim}10^{-4}M$) produced dose-dependent contractions of the corpus cavernosal strips. The incubation with $10^{-5}M$ hexamethonium (nicotinic receptor antagonist) significantly inhibited the magnitude of the nicotine associated contractions. The nicotine-induced contractions were not only significantly inhibited by pretreatment with $10^{-5}M$ indomethacin (nonspecific cyclooxygenase inhibitor) and with $10^{-6}M$ NS-398 (selective cyclooxygenase inhibitor), but also with $10^{-6}M$ Y-27632 (Rho kinase inhibitor). Ozagrel (thromboxane $A_2$ synthase inhibitor) and SQ-29548 (highly selective TP receptor antagonist) pretreatments significantly reduced the nicotine-induced contractile amplitude of the strips. High concentrations of nicotine caused contraction of isolated rabbit corpus cavernosal strips. This contraction appeared to be mediated by activation of nicotinic receptors. Rho-kinase and cyclooxygenase pathways, especially cyclooxygenase-2 and thromboxane $A_2$, might play a pivotal role in the mechanism associated with nicotine-induced contraction of the rabbit corpus cavernosum.