수소이온농도 변화의 수축물질에 따른 가토신동맥 수축에 미치는 영향과 기전

장석종,김세훈,전병화,박해근,Chang, Seok-Jong,Kim, Se-Hoon,Jeon, Byeong-Hwa,Park, Hae-Kun 대한생리학회 1990 대한생리학회지 Vol.24 No.1

The effects of $H^{+}$ on the arterial contraction and their mechanisms were investigated in the renal artery of a rabbit. The helical strips of isolated renal artery were immersed in the HEPES-buffered or $CO_{2}/HCO_{3}^{-}$-buffered Tyrode's solution. The contractions induced by agonists (norepinephrine, histamine, serotonin and angiotensin II) or high $K^{+}$ were observed with change of extracellular or intracellular $H^{+}$ concentration. The contractions induced by norepinephrine, histamine, serotonin, angiotensin II or high $K^{+}$ in HEPES-buffered Tyrode's solution were inhibited by increase in extracellular $H^{+}$ concentration and potentiated by decrease in extracellular $H^{+}$ concentration. The degrees of these effects were most evident in the contraction induced by serotonin and angiotensin II, moderate in those by histamine and high $K^{+}$, and least in those by norepinephrine. Maximal contraction by norepinephrine, histamine and high $K^{+}$ were not influenced by change in extracellular $H^{+}$ concentration, but influenced in those contration by serotonin and angiotensin II. The attenuated contractions by an acidic pH were not returned to the level of contraction at normal pH (7.4) by elevation of extracellular $Ca{2+}$ concentration. The agonists (norepinephrine, histamine and serotonin)-induced contractions in $Ca{2+}$-free Tyrode's solution were also attenuated by increase in extracellular $H^{+}$ concentration and potentiated by decrease in extracellular $H^{+}$ concentration. Elevation of $Pco_{2}$ in the $CO_{2}/HCO_{3}^{-}$-buffered Tyrode's solution, which increase the intracellular $H^{+}$ concentration, at constant extracellular pH (7.4), increased the contraction by 30 mM $K^{+}$. From the above results, it is suggested that the decrease in contractions by increase in extracellular $H^{+}$ concentration may be resulted from that $H^{+}$ make the receptors less sensitive to agonists and cell membrane hyperpolarize and then inhibit the $Ca{2+}$ influx as well as $Ca{2+}$ release from intracellular $Ca{2+}$ storage site.

주가와 거래량의 교호관계가 중,장기 주가행태에 미치는 영향

장영광 ( Young Kwang Chang ),류석종 ( Seok Chong Ryoo ) 韓國金融學會 2007 金融學會誌 Vol.12 No.4

1, 4-Dihydropyridine 칼슘길항제가 유두근의 정상활동전압 및 Ca-dependent, Slow Channel Mediated Action Potential에 미치는 영향

김민형,장석종,Kim, Min-Hyung,Chang, Seok-Jong 대한생리학회 1988 대한생리학회지 Vol.22 No.2

Effects of 1, 4-dihydropyridine compounds, such as nifedipine, nisoldipine, nitrendipine, and nimodipine which were calcium antagonists on the normal and Ca-dependent, slow channel mediated action potentials in the guinea pig's papillary muscle were investigated. The glass microelectrode was impaled into a papillary muscle cell for measurements of potential changes with the simultaneous tracing of isometric contraction. The concentration of Ca antagonists were 1 mg/l (nifedipine and nisoldipine), 2 mg/l (nitrendipine and nimodipine), which showed the maximal inhibition of isometric contraction (above 90%) and simultaneous effects on the normal action potentials and only the halves of those concentrations were sufficient to observe the effects on the calcium action potentials. The data for analysis were only chosen when the microelectrode was maintained in a cell throughout the experiments. 1, 4-Dihydropyridine compounds decreased the action potential duration but did not affect the resting membrane potential, overshoot, and upstroke velocity of the normal action potentials with the decrease in the isometric contraction. And with the decrease in the area and amplitude of isometric contraction, the area, amplitude, upstroke velocity and duration of Ca action potential was decreased. But the differences in the effects of the Ca antagonists were not observed. Therefore it is inferred that the changes in normal and Ca action potential induced by the 1, 4-dihydropyridine compounds with a common chemical structure would be caused by the slow inward Ca-current, not by a fast Na-current.

가토 신동맥 평활근에서 Strontium의 Calcium 대행역할

장윤철(Chang, Yun-Cheol),전병화(Jeon, Byeong-Hwa),장석종(Chang, Seok-Jong) 대한생리학회 1990 대한생리학회지 Vol.24 No.2

The Ca²⁺-substitutional$</TEX> roles of strontium for the contractile processes were investigated in the rabbit renal artery. The contractions induced by either norepinephrine or high K⁺ in the condition which intra- and extracellular Ca²⁺ were replaced by Sr²⁺, i.e. Sr²⁺-mediated contractions, were dose-dependent. And then the maximal amplitude of contraction, as compared with Ca²⁺-mediated contraction, was about 50% in norepinephrine and about 70% in high K⁺. The Sr²⁺-mediated contractions were independent in the contraction by norepinephrine 10^-5M) but dependent in those by high K⁺(100 mM) on the extracellular Sr²⁺ concentration. Also Sr²⁺-mediated contractions induced by norepinephrine were observed in the Sr²⁺-free Tyrode s solution. The Sr²⁺-mediated contractions induced by either norepinephrine or high K⁺ were suppressed by verapamil, a Ca²⁺-channel blocker. By extracellular addition of Sr²⁺, the Ca²⁺-mediated contractions induced by norepinephrine 10^-5M) or 40 mM K⁺ were inhibited but those by high K⁺(100 mM) were increased. And the Sr²⁺-mediated contractions were increased by extracellular addition of Ca²⁺ but did not reach the level of Ca²⁺-mediated contraction. Therfore it is suggested that in the vascular smooth muscle of rabbit renal artery Sr²⁺ could enter the smooth muscle cells easily through the potential-operated calcium channel (POC) but not easily through the receptor-operated calcium channel (ROG), and Sr²⁺ might be stored in the intracellular Ca²⁺-binding site and released by NE and induced the contraction by a way of activating directly the contractile apparatus.

Prostaglandin $F_{2{\alpha}}$가 가토 대동맥 평활근 수축성에 미치는 영향

정수성,김세훈,장석종,박해근,Chung, Soo-Sung,Kim, Se-Hoon,Chang, Seok-Jong,Park, Hae-Kun 대한생리학회 1989 대한생리학회지 Vol.23 No.1

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.

Serotonin에 의한 가토 신동맥 평활근 수축기전

이우영,김세훈,장석종,Lee, Woo-Young,Kim, Se-Hoon,Chang, Seok-Jong 대한생리학회 1990 대한생리학회지 Vol.24 No.1

The contractile mechanisms of serotonin were investigated in the renal artery of a rabbit. The helical strips of isolated renal artery were immersed in the normal or $Ca^{2+}$-free tris-buffered Tyrode's solution, which was equilibrated with 100% $O_{2}$ at $35^{\circ}C$. The contraction by serotonin or norepinephrine (NE) began at $1{\times}10^{-7}\;M$ and reached the maximal contraction at $1{\times}10^{-5}\;M$. The maximal contraction by serotonin corresponded to $58.1{\pm}4.2%$ of maximal contraction by NE. Cyproheptadine, a serotonin receptor blocker, shifted the concentration-response curve to the right without any reduction in the maximum response but shifted that of NE to the right with reduction in maximum response. And phentolamine, an ${\alpha}-receptor$ blocker, shifted the concentration-response curve of serotonin or NE without any reduction in maximum responses. The $pA_{2}$ values for cyproheptadine against serotonin and NE were $10.35{\pm}0.04$ and $8.45{\pm}0.13$, respectively. The $pA_{2}$ values for phentolamine against serotonin and NE were $6.87{\pm}0.04$ and $8.14{\pm}0.08$, respectively. after the pretreatment with 6-hydroxydopamine, the contraction induced by 100 mM $K^{+}$, tyramine and serotonin reduced to $83.0{\pm}2.0$, $26.8{\pm}6.2$ and $82.0{\pm}3.5%$ of control, respectively. The contraction by serotonin in the $Ca^{2+}$-free Tyrode's solution was increased and sustained with the addition of $Ca^{2+}$ extracellulary. The serotonin-sensitive intracellular $Ca^{2+}$ pool was depleted completely by the pretreatment with NE, but the NE-sensitive intracellular $Ca^{2+}$ pool was depleted partially by the pretreatment with serotonin. From the above results, it is suggested that the contraction induced by serotonin in the renal artery of a rabbit may be due to mechanisms in which serotonin acts directly on specific serotonin receptors and also acts indirectly on ${\alpha}-adrenoceptors$ by displacing NE from neuronal stores.

가토 신동맥의 고농도 Histamine에 의한 노아드레날린 유발 수축 및 K-경축 약화 기전

이성우(Lee, Sung-Woo),김세훈(Kim, Se-Hoon),장석종(Chang, Seok-Jong),박해근(Park, Hae-Kun) 대한생리학회 1989 대한생리학회지 Vol.23 No.2

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% O₂ at 35℃. 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 Ca²⁺-free Tyrode s solution and the increase of contraction by addition of 2 mM Ca²⁺ was attenuated as well. This attenuation phenomenon was not observed in the presence of low concentration (3 X 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 Ca²⁺-free Tyrode s solution was not inhibited. Furthermore this attenuation was completely blocked by pretreatment of djphenhydramine (H₁-receptor blocker) and potentiated by pretreatment of cimetidine (H₂-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 Ca²⁺ pool after the histamine-induced contraction mediated through H₁-receptor function.

가토 신동맥 평활근에서 Barium의 수축작용

전병화(Jeon, Byeong-Hwa),김상섭(Kim, Sahng-Seop),김세훈(Kim, Se-Hoon),장석종(Chang, Seok-Jong) 대한생리학회 1990 대한생리학회지 Vol.24 No.2

The contractile action of barium (Ba²⁺) was investigated in the arterial strip of rabbit renal artery. The helical strip of isolated renal artery was immersed in the Tris-buffered Tyrode s solution equilibrated with 100% O² at 37℃ and its isometric tension was measured. Ba²⁺-induced contraction of arterial strip was dose-dependent and its maximal tension corresponded to 92.1±4.5% of tension by K⁺(100 mM). Ba²⁺-induced contraction did not show the tachyphylactic phenomenon in the normal Tyrode s solution. Ba⁺² induced the tonic contraction in the Ca²⁺-free tyrode s solution and that was increased by the extracellula addition of Ca²⁺. During the repeated exposure of the same dose of Ba²⁺ (10 mM) in the Ca²⁺-free Tyrode s solution, Ba²⁺-induced contraction was progressively decreased. Even though the intracellular NE-and caffeine-sensitive Ca²⁺ was depleted, Ba⁺² induced the tonic contraction. After the pretreatment of lanthnum or verapamil, Ba⁺² did not induce contraction. Ba²⁺-inducedcontraction was suppressed by extracellular K⁺ in the normal Tyrode s solution and that was dependent on K⁺ concentration. Suppressive effect of K⁺ (14 mM) on the Ba²⁺-induced contraction was also dependent on the intracellular Ca²⁺ concentration. From the above resuts, it is suggested that Ba⁺² activate indirectly the contractile process by promoting the mobilization of intracellular Ca²⁺ and the influx of extracellular Ca²⁺. It is also suggested that action of Ba⁺² on the Ca²⁺-activated K⁺ channel can result in the depolarization of cell membrane in the rabbit renal artery.

Prostaglandin F_2α가 가토 대동맥 평활근 수축성에 미치는 영향

정수성(Chung, Soo-Sung),김세훈(Kim, Se-Hoon),장석종(Chang, Seok-Jong),박해근(Park, Hae-Kun) 대한생리학회 1989 대한생리학회지 Vol.23 No.1

The effects of prostaglandin (PGF_2α) 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℃ and its isometric tension was measured. The contraction was induced by (PGF_2α), norepinephrine (NE), or potassium (40 mM) in the nomal Tyrode s solution (1 mM, Ca²⁺) or Ca²⁺-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 μg% and reached the maximal contraction at the concentration of 150 μg% (PGF_2α). The maximal contraction was corresponded respectively to 52.2±3.0% and 81.5±3.5% of maximal contraction by NE (1 X 10^-5M) and 40 mM K⁺. And the maximal contractions by (PGF_2α) or NE were induced at the concentration of about 1 mM Ca²⁺. (PGF_2α) induced the contraction of aortic strip even after induction of contraction by 40 mM K⁺ and the contraction by (PGF_2α) was not blocked by the α-receptor blocker, phentolamine. And the contraction by the (PGF_2α) was inhibited partially by a verapamil at the concentration of 1 X 10^-5M and the contraction began to increase at the concentration of 1 X 10^-4M verapamil. Whereas the contraction by NE was completely blocked by verapamil. Though both the (PGF_2α) and NE induced the contraction in the Ca²⁺-free Tyrode s solution, the peak tension was not maintained. But the rate of tension decline was lower in the contraction by (PGF_2α) than in that by NE. The verapamil did not inhibit the contraction by (PGF_2α) in the Ca²⁺-free Tyrode s solution and increased the contraction at the concentration of above 1 X 10^-4M. The NE-induced contraction in the Ca²⁺-free Tyrode s solution was inhibited completely by a verapamil. From the above results it is suggested that the contraction induced by (PGF_2α) results from the promotion of the both Ca²⁺ influx and the intracellular Ca²⁺ release by different way from NE.

심실근의 수축현상에 미치는 O₂, CO₂ 및 pH의 영향

장석종,박해근 충남대학교 의과대학 지역사회의학연구소 1983 충남의대잡지 Vol.10 No.2

It has been well known that increased hydrogen ion concentration causes the negative inotropic effect on the heart. But in the status of acid base imbalance, metabolic or respiratory, the question of which status has more profound effect on the cardiac muscle contractility remains unsolved. Furthermore, whether such effect is attributable to the change of the intracellular pH or the extracellular change is a matter of controversy. In many studies concerning to the effect of carbon dioxide tension on the cardiac contractility, the effect of excess oxygen has been ignored despite of its significant influence upon the cellular function. The author intended to investigate the effects of the change of carbon dioxide tension, which causes the pH change simultaneously, as well as the effect of excess oxygen on the cardiac ventricular contractility. Also, to prove which change, metabolic or respiratory, has more profound effect and which change, intracellulcr or extracellular, has more crucial effect, the author examined the contractility of the ventricle under two different conditions. They were as follows: a) PCO_2 was varying despite of same magnitude of the change in pH. b) pH was varying despite of the same magnitude of the change in PCO_2 Turtle hearts were used and the Langendorf preparations were made. The perfusate was Tris-buffer solution for turtle, saturated with various gases, such as air, pure oxygen, nitrogen, or different concentrations of CO_2 balanced with oxygen or nitrogen. The tension and maximal dT/dt were recorded with the Physiograph and its accessories. The results were summarized as follows. 1. The excess oxygen enhanced the ventricular contractility. 2. Increased carbon dioxide tension, which decreases the pH simultaneously, reduced the ventricular contractility and that was more pronounced when CO_2 was balanced with nitrogen gas rather than with oxygen gas. 3. The relationships among several physiological parameters were estimated as follows: a) Y=1.01X-0.56 X: percent change of the tension Y: percent change of maximal contration dT/dt b) Z=1.06X-4.56 Z: percent change of maximal relation dT/dt The corelation coefficient in a) is 0.939 and in b) is 0.926, being significant statistically (P<0.005). 4. When the change of pH were same but the changes of PCO_2 were different, the change of ventricular contractility was more profound in the respiratory decrease of pH, that was higher PCO_2, more depressing effect (P<0.005) was manifested, than in the case of metabolic origin (p<0.005). 5. When the changes of PCO_2 were same but the changes of pH were different, the influence of the latter parameter on the contractility was not significant (P<0.1). From the above results it was suggested that the increased PCO_2, which also causes the decrease of pH, has negative inotropic effect and excess oxygen has positive inotropic effect on the ventricular muscle of the turtle. The negative inotropic effect of the lowered pH on the ventricular muscle was revealed to be more profound when it was induced by respiratory distress rather than motabolic and may be affected by change of intracellular pH rather than extracellular pH.