Kim, Won-Jae;Lee, Jong-Un;Park, Yong-Hyun;Nam, Sang-Chae
The Korean Journal of Physiology and Pharmacology
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제1권5호
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pp.529-535
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1997
The present study was aimed at investigating whether the vascular calcium regulation is altered in hypertension. Two-kidney, one clip (2K1C) and deoxycorticosterone acetate (DOCA)-salt hypertension were made in rats, and their thoracic aortae were taken 4 weeks later. The isometric contractile response and calcium uptake of the endothelium-denuded aortic preparations were determined. Caffeine ($0.1{\sim}35\;mmol/L$) induced a greater contraction in 2K1C and DOCA-salt hypertension than in normotensive control. When the vascular calcium store was functionally-depleted by a repeated exposure to caffeine, it took longer to reload the store and to resume the initial contraction force in response to caffeine in both 2K1C and DOCA-salt hypertension. The vascular $^{45}Ca$ uptake following the functional depletion of the cellular store was also greater in both models of hypertension than in control. Ryanodine, calcium channel activator of the sarcoplasmic reticulum, attenuated the restoration of caffeine-induced vascular contraction, which was not affected by either 2K1C or DOCA-salt hypertension. Nifedipine, an L-type $Ca^{2+}$ channel blocker, attenuated the restoration of caffeine-induced contraction, which was not affected by DOCA-salt hypertension, but was more pronounced in 2K1C hypertension. Nifedipine also diminished the vascular $^{45}Ca$ uptake, which was not affected by DOCA-salt hypertension, but was more pronounced in 2K1C hypertension. Ouabain, a $Na^+,\;K^+-ATPase$ inhibitor, increased the caffeine-induced contraction by a similar magnitude in control and 2K1C hypertension, which was, however, markedly attenuated in DOCA-salt hypertension. Ouabain enhanced the vascular $^{45}Ca$ uptake, the degree of which was not affected by 2K1C hypertension, but was markedly attenuated in DOCA-salt hypertension compared with that in control. Cyclopiazonic acid, a selective inhibitor of $Ca^{2+}-ATPase$ of the sarcoplasmic reticulum, attenuated the restoration of caffeine-induced contraction, which was not affected by 2K1C hypertension, but was more marked in DOCA-salt hypertension. These results suggest that the increased vascular calcium storage may be attributed to an enhanced calcium influx in 2K1C hypertension, and to an impaired $Na^+-K^+$ pump activity of the cell membrane and subsequently increased calcium pump activity of the cellular store in DOCA-salt hypertension.
본 연구에서는 C2C12 근육 세포에서 IGF-I이 세포골격 연결 단백질인 plectin과 MACF1 유전자 발현에 미치는 영향에 대해 알아보았다. 그 결과 IGF-I이 plectin 유전자의 단백질과 mRNA 발현을 증가시켰으며, MACF1 mRNA 발현을 증가시켰음을 알 수 있었다. 이는 운동에 의해 근육에서 분비가 증가하는 IGF-I이 근육 관련 유전자들의 발현을 조절하여 근부피 유지에 영향을 미친다는 기존의 연구 결과들에서 더 나아가 골격근 구조 안정화 및 근수축 기전에 기여하는 plectin과 MACF1 유전자 발현에도 영향을 미친다는 사실을 증명하였다는데 의의가 있다고 사료된다. 향후 근수축 기전에 있어, 운동 형태, 근섬유의 종류에 따른 세포 골격 단백질의 역할 규명 및 조절자에 관한 연구가 더 수행된다면 운동이 골격근의 생리적 변화에 미치는 영향에 대한 추가적 정보를 제공할 수 있을 것이다.
Tetrahydroisoquinoline (THI) alkaloids can be considered as cyclized derivatives of simple phenylethylamines. Many of them, especially with 6,7-disubstitution, demonstrate a relatively high affinity for catecholamines. Present study examines the pharmacological action of limited series of THI, using rats' isolated atria and aorta. In addition, a $[^3H]$ prazosin displacement binding study with THI compounds was performed, using rat brain homogenates to investigate whether these probes have ?${\alpha}$-adrenoceptor affinity. We also compared the vascular relaxation potency of these probes with dobutamine. YS 49, YS 51, higenamine and dobutamine, concentration-dependently, relaxed endothelium-denuded rat thoracic aorta precontracted with phenylephrine (PE, 0.1 ${\mu}M$) in which $pEC_{50}$ were $5.56{\pm}0.32$ and $5.55{\pm}0.21$, $5.99{\pm}1.16$ and $5.57{\pm}0.34$, respectively. These probes except higenamine also relaxed KCl (65.4 mM)-contracted aorta. In isolated rat atria, all THIs and dobutamine increased heart rate and contractile force. In the presence of propranolol, the concentration response curves of YS 49 and YS 51 shifted to the right and resulted in $pA_2$ values of $8.07{\pm}0.84$ and $7.93{\pm}0.11$, respectively. The slope of each compound was not deviated from unity, indicating that these chemicals are highly competitive at the cardiac ?${\beta}-adrenoceptors$. YS 49, YS 51, and higenamine showed ?${\alpha)-adrenoceptor$ affinity in rat brain, in which the dissociation constant $(K_i)$ was 2.75, 2.81, and 1.02 ${\mu}M$, respectively. It is concluded, therefore, that THI alkaloids have weak affinity to ${\alpha)_1-adrenoceptor$ in rat aorta and brain, respectively, while these probes show relatively high affinity for cardiac ${\beta}-adrenoceptors$. Thus, these chemicals may be useful in the treatment of congestive heart failure.
본 실험실에서는 민간요법으로 말라리아와 성병등의 치료제로 사용되어온 회양목(Buxus microphylla var. koreana Nakai)에서 steroid성 alkaloid인 cyclobuxine D와 nonalkaloid인 buxuletin을 분리하였다. Buxuletin의 가토에 있어서 이뇨작용에 대해서는 본 실험실에서 보고한바 있으며 cyclobuxine D의 약리작용에 대한 보고는 지금까지 전무한 상태이다. 본 실험에서는 새로운 항부정맥 약물의 밭견의 일환으로 cyclobuxine D의 적출 개구리 심장에 대한 작용과 마취시킨 흰쥐의 ECG와 심박동수에 대한 작용을 관찰하였다. Cyclobuxine D는 적출 개구리 심장에 대해 용량의존적 심근 수축력 감소를 나타냈으며 흰쥐에 있어서 현저한 심박동수 감소를 나타냈다. Cyclobuxine D는 흰쥐의 ECG에 있어서 PR interval과 P ${\alpha}T$ interval을 연장시키며, QRS complex와 PR interval의 심박동수에 대한 보상치인 PRc에 대해서는 고용량에서는 연장시키나 그 작용이 현저하지 않다. 이 결과로 보아 cyclobuxine D는 흰쥐의 ECG에서 A-V conduction과 ventricular depolarization에 주로 관여하는 것으로 사료 되며 이는 기존의 antiarrhythmic drugs과 비교해 볼 때 quinidine sulfate와 유사성이 있다고 추정된다.
Kim, Ka Eul;Tae, Hyun-Jin;Natalia, Petrashevskaya;Lee, Jae-Chul;Ahn, Ji Hyeon;Park, Joon Ha;Kim, In Hye;Ohk, Taek Geun;Park, Chan Woo;Cho, Jun Hwi;Won, Moo-Ho
Clinical and Experimental Emergency Medicine
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제3권3호
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pp.175-180
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2016
Objective Combination of ${\beta}_1-adrenergic$ receptor (AR) blockade and ${\beta}_2-AR$ activation might be a potential novel therapy for treating heart failure. However, use of ${\beta}-AR$ agonists and/or antagonists in the clinical setting is controversial because of the lack of information on cardiac inotropic or chronotropic regulation by AR signaling. Methods In this study, we performed hemodynamic evaluation by examining force frequency response (FFR), Frank-Starling relationship, and response to a non-selective ${\beta}-AR$ agonist (isoproterenol) in hearts isolated from 6-month-old transgenic (TG) mice overexpressing ${\beta}_1-$ and ${\beta}_2-ARs$ (${\beta}_1-$ and ${\beta}_2-AR$ TG mice, respectively). Results Cardiac physiologic consequences of ${\beta}_1-$ and ${\beta}_2-AR$ overexpression resulted in similar maximal response to isoproterenol and faster temporary decline of positive inotropic response in ${\beta}_2-AR$ TG mice. ${\beta}_1-AR$ TG mice showed a pronounced negative limb of FFR, whereas ${\beta}_2-AR$ TG mice showed high stimulation frequencies with low contractile depression during FFR. In contrast, Frank-Starling relationship was equally enhanced in both ${\beta}_1-$ and ${\beta}_2-AR$ TG mice. Conclusion Hemodynamic evaluation performed in the present showed a difference in ${\beta}_1-$ and ${\beta}_2-AR$ signaling, which may be due to the difference in the desensitization of ${\beta}_1-$ and ${\beta}_2-ARs$.
Insamjungchuntang has been used in Korea for many centuries as a treatment for respiratory disease. The effect of Insamjungchuntang on tracheal smooth muscle is not known. The purpose of the present study is to determine the effect of Insamjungchuntang on histamine and acetylcholine induced tracheal smooth muscle contraction in rats and guinea pigs. Guinea pig (500 g, male) and Sprague Dawley rats (200 g, male) were killed by $CO_2$ exposure and a segment (8-10 mm) of the thoracic trachea from each rat and guinea pig was cut into equal segments and mounted 'in pairs' in a tissue bath. Contractile force was measured with force displacement transducers under 0.5 g loading tension. The dose of histamine (His) and acetylcholine (Ach) which evoked 50% of maximal response $(ED_{50})$ was obtained from cumulative dose response curves for histamine and acetylcholine$(10^{-7}{\sim}10^{-4}\;M)$. Contractions evoked by His ($ED_{50}$) and Ach $(ED_{50})$ were inhibited significantly by Insamjungchuntang. In guinea pig tracheal smooth muscle, the mean percent inhibition of acetylcholine induced contraction was $38.58\(p<0.05)\;after\;10{\mu}l/ml$ Insamjungchuntang, $90.75\(p<0.01)\;after\;30{\mu}l/ml$. Insamjungchuntang and $133.17\(p<0.01)\;after\;100{\mu}l/ml$ Insamjungchuntang. In rat tracheal smooth muscle, the mean percent inhibition of acetylcholine induced contraction was $10.0\(p<0.05)\;after\;10{\mu}l/ml$ Insamjungchuntang, $80.71\(p<0.01)\;after\;30{\mu}/ml$ Insamjungchuntang and $118.29\(p<0.01)\;after\;100{\mu}l/ml$ Insamjungchuntang. Also, in guinea pig tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was $45.5\(p<0.01)\;after\;10{\mu}l/ml$ lnsamjungchuntang, and $93.17\(p<0.01)\;after\;30{\mu}l/ml$. lnsamjungchuntang $134.50\(p<0.01)\;after\;100{\mu}l/ml$ Insamjungchuntang. In rat tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was $37.83\(p<0.01)\;after\;10{\mu}l/ml$ lnsamjungchuntang, $90.5\(p<0.01)\;after\;30{\mu}l/ml$ Insamjungchuntang and $135.17\(p<0.01)\;after\;100{\mu}l/ml$ Insamjungchuntang. Propranolol $(10^{-7}\;M)$ slightly but significantly attenuated the inhibitory effects of Insamjungchuntang. Following treatment with propranolol, the mean percent inhibition caused by $100{\mu}l/ml$. Insamjungchuntang fell to 46.42% in guinea pig induced by acetylcholine contraction and by $100{\mu}l/ml$ Insamjungchuntang fell to 5.43% (p<0.05) in rat induced by acetylcholine contraction and the mean percent inhibition caused by $100{\mu}l/ml$ Insamjungchuntang fell to 49.0% in guinea pig induced by histamine contraction and by $100{\mu}l/ml$ Insamjungchuntang fell to 48.6% (p<0.05) in rat induced by histamine contraction. Indomethacin and methylene blue $(10^{-7}\;M)$ did not significantly alter the inhibitory effect of lnsamjungchuntang. Also, I could find the effects of lnsamjungchuntang and Insamjungchuntanggamorphine on the tracheal smooth muscle in guinea pig and rat did not change significantly. These results indicate that Insamjungchuntang can relax histamine and acetylcholine-induced contraction of guinea pig and rat tracheal smooth muscle, and that this inhibition involves sympathetic effects.
Chunggeumtang has been used in Korea for many centuries as a treatment for respiratory disease. The effect of Chunggeumtang on tracheal smooth muscle is not konwn. The purpose of the present study is to determine the effect of Chunggeumtang on histamine and acetylcholine induced tracheal smooth muscle contraction in rats and guinea pigs. Guinea pig(500g, male) and Sprague Dawley rats (250g, male) were killed by $CO_2$ exposure and a segment (8-10mm) of the thoracic trachea from each rat and guinea pig was cut into equal swegments and mounted 'in pairs' in a tissue bath. Contractile force was measured with force diplacement transducers under 0.5g loading tension. The dose of histamine (His) and acetylcholine (Ach) which evoked 50% of maximal response ($ED_{50}$) was obtained from cumulative dose response curves for histamine and acetylcholine($10^{-7}{\sim}10^{-4}M$). Contractions evoked by His ($ED_{50}$) and Ach ($ED_{50}$) were inhibited significantly by Chunggeumtang. In guinea pig tracheal smooth muscle, the mean percent inhibition of acetylcholine induced contraction was $6.1%after\;30{\mu}l/ml$ Chunggeumtang, and 49.4% (p<0.01) after $100{\mu}l/ml$ Chunggeumtang. In rat tracheal smooth muscle, the mean percent inhibition of acetylcholine induced contraction was $6.7%\;after\;30{\mu}l/ml$ Chunggeumtang, and $54.2%\;(p<0.01)\;after\;100{\mu}l/ml$ Chunggeumtang. Also, in guinea pig tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was $30.6%\;(p<0.05)\;after\;30{\mu}l/ml$ Chunggeumtang, and $53.0%\;(p<0.01)\;after\;100{\mu}l/ml$ Chunggeumtang. In rat tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was $24.1%\;(p<0.05)\;after\;30{\mu}l/ml$ Chunggeumtang, and $55.3%\;(p<0.01)\;after\;100{\mu}l/ml$ Chunggeumtang. Propranolol and indomethacin($10^{-7}M$) slightly but significantly attenuated the inhibitory effects of Chunggeumtang. Following treatment with propranolol, the mean percent inhibition caused by $100{\mu}l/ml$ Chunggeumtang fell to 27.6% in guinea pig induced by acetylcholine contraction and by $100{\mu}l/ml$ Chunggeumtang fell to 28.7% (p<0.05) in rat induced by acetylcholine contraction and the mean percent inhibition caused by $100{\mu}l/ml$ Chunggeumtang fell to 16.2% in guinea pig induced by histamine contraction and by $100{\mu}l/ml$ Chunggeumtang fell to 28.7% (p<0.05) in rat induced by histamine contraction. Indomethacin, the mean percent inhibition caused by $100{\mu}l/ml$ Chunggeumtang fell to 20.0% in guinea pig induced by acetylcholine contraction and by $100{\mu}l/ml$ Chunggeumtang fell to 16.9% (p<0.05) in rat induced by acetylcholine contraction and the mean percent inhibition caused by $100{\mu}l/ml$ Chunggeumtang fell to 16.4% in guinea pig induced by histamine contraction and by $100{\mu}l/ml$ Chunggeumtang fell to 23.1% (p<0.05) in rat induced by histamine contraction. Methylene blue($10^{-7}M$) did not significantly alter the inhibitory effect of Chunggeumtang. Also, I could find the effects of Chunggeumtang and Chunggeumtanggamorphine on the tracheal smooth muscle in guinea pig and rat did not change significantly. These results indicate that Chunggeumtang can relax histamine and acetylcholine-induced contraction of guinea pig and rat tracheal smooth muscle, and that this inhibition involves sympathetic effects and the release of cyclooxygenase products.
The effects of ouabain on the contractile and electrical activities were investigated in the isolated preparations of guinea-pig taenia coli, and compared with those of vanadate. Spontaneous contractions were recorded with force transducer, and electrical activites were measured by use of suction electrode, or single sucrose-gap technique. The contractions were induced by the electrical stimulation for 5 seconds every 1 minute with alternating current (60 Hz, 3.0 V/cm) through the platinum electrodes located in parallel with the long axis of the preparation. All experiments were performed in tris-buffered Tyrode solution which was aerated with $100%{\;}O_2$ and kept at $35^{\circ}C$. The results obtained were as follows: 1) Responses of spontaneous contractions to ouabain were concentration-dependent; $10^{-7}M$ ouabain caused a rise of basal tone. Above the concentration of $10^{-6}M$ ouabain, an initial increase followed by a decrease in tension was observed. 2) A continuous spike discharge was induced by the administration of $10^{-7}M$ ouabain. Above $10^{-6}M$ ouabain, a transient initial increase followed by a decrease in spike frequency and amplitude was produced, and finally membrane potential was sustained at a certain level without a spike discharge. 3) The characteristic response to $10^{-7}M$ ouabain was not blocked by the pretreatment with $10^{-7}M$ atropine. 4) The electrically induced contractions were completely suppressed at the concentration of $2{\times}10^{-7}M$ ouabain. These contractions were blocked more rapidly in paralled with the increase in ouabain concentration. 5) Effects of vanadate on the spontaneous activities were quite different from those of ouabain; $10^{-6}M$ vanadate increased the amplitude of contractions and $10^{-5}M$ vanadate increased slightly both amplitude and frequency of spontaneous contractions. $10^{-4}M$ vanadate showed irregular phasic contractions superimposed on the increased basal tone. 6) $10^{-5}M$ vanadate depolarized the membrane potential and shortened the interval between the bursts of spike discharge, whereas $10^{-4}M$ vanadate induced continuous spike discharge with membrane depolarization. 7) Vanadate caused a characteristic inhibitory response to the contractions induced by electrical stimulation; An initial rapid inhibition of tension development and then gradual recovery to a certain level. From the above results, the following conclusions could be made: 1) The rise of basal tone at $10^{-7}M$ ouabain is due to continuous spike discharge without a silent period. The continuous spike discharge is likely to be associated with a slight membrane depolarization caused by the blockage of Na pump. 2) The biphasic response induced by above $10^{-6}M$ ouabain seems to occur by the different mechanisms. The initial increase in tension is associated with depolarization along with an increase in spike frquency, whereas the subsequent relaxation occurs through a non-electrical mechanism. 3) The characteristic response to $10^{-7}M$ ouabain is resulted not from the action on intrinsic nerve terminal, but from its direct action on the membrane of smooth muscle cells. 4) The phasic contractions superimposed on the increased basal tone at the concentration of $10^{-4}M$ vanadate is resulted from the continuous spike discharge with membrane depolarization, of which mechanism remains unknown. 5) The inhibitory action of ouabain on the electrically induced contractions suggests that the increasein intracellular Na in some way inhibits the electrically induced $Ca^{2+}$ influx. The mechanism of vanadate action on the induced contractions remains unknown.
Objective : Carthami Flos has been used as a herb to promote blood circulation to remove blood stasis in oriental medicine for many centuries, and Amun(GV15) has been used as a meridian point to treat apoplexy etc. To investigate treatment of cerevral vascular disease(CVA) by promoting blood circulation and removing blood stasis(活血化瘀法), we observed the experimental effects and mechanism of auqa-acupunture of Carthami Flos(ACF) injected into GV15 on cerevral hemodynamics and cardiovascular system of rats. Method : Aqua-acupuncture of Carthami Flos(ACF) was injected into GV15, and then we investigated experimental effects and mechanism of ACF on the cerebral hemodynamics[regional cerebral blood flow(rCBF), pial arterial diameter(PAD), meal arterial blood pressure(MABP)] and cardiovascular system[cardiac muscle contractile force(CMF), heart rate(HR)I by pretreatment with methylene blue(MTB) and indomethacin(IDN). The changes in rCBF, MABP, CMF and HR were tested by Laser Doppler Flowmetry(LDF), and the changes in PAD was determinated by video microscopy methods and video analyzer. Results :The results were as follows in normal rats ; The changes of rCBF and PAD were significantly increased by ACF($120{\mu}{\ell}/kg$) in a injected time-dependent manner, but MABP was not changed by ACF. The changes of cardiovascular system were increased by ACF in a injected time-dependent manner. And pretreatment with MTB was significantly inhibited ACE induced increase of rCBF and PAD, and was decreased ACF induced increase of HR. And pretreatment with IDN was increased ACF induced MABP and CMF. And the results were as follows in cerebral ischemic rats ; The changes of rCBF was increased stabilizly by treatment with ACF($120{\mu}{\ell}/kg$) in during the period of cerebral reperfusion, but pretreatment with MTB was increased ACF induced increase of rCBF during the period of cerebral reperfusion. The results were as follows in normal rats ; The changes of rCBF and PAD were significantly increased by ACF($120{\mu}{\ell}/kg$) in a injected time-dependent manner, but MABP was not changed by ACF. The changes of cardiovascular system were increased by ACF in a injected time-dependent manner. And pretreatment with MTB was significantly inhibited ACF induced increase of rCBF and PAD, and was decreased ACF induced increase of HR. And pretreatment with IDN was increased ACF induced MABP and CMF. And the results were as follows in cerebral ischemic rats ; The changes of rCBF was increased stabilizly by treatment with ACF($120{\mu}{\ell}/kg$) in during the period of cerebral reperfusion, but pretreatment with MTB was increased ACF induced increase of rCBF during the period of cerebral reperfusion Conclusions : In conclusion, ACF causes a diverse response of rCBF, PAD an HR, and action of ACF is mediated by cyclic GMP. I suggested that ACF has an anti-ischemic effect through the improvement of crebral hemodynamics in a transient cerebral ischemia.
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