• The Korean Journal of Physiology
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• v.25 no.2
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• pp.147-158
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• 1991

The effects of noradrenaline on the spontaneous contraction recorded from a strip of mucosa-free antral circular muscle were studied in the guinea-pig stomach, and the changes in slow waves and membrane resistance were analyzed in order to elucidate the mechanism for the excitatory response to noradrenaline. Electrical responses of circular muscle cells were recorded using glass microelectrodes filled with 3 M KCI. Electrotonic potentials were produced to estimate membrane resistance by the partition stimulating method. 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) The spontaneous contractions were potentiated dose-dependently by the application of noradrenaline. 2) Through the experiments using adrenoceptor-blockers, the strong excitatory effect via $[\alpha}-adrenoceptors$ and the weak inhibitory efffect via ${\beta}-adrenoceptors$ were noted. 3) Noradrenaline produced hyperpolarization of membrane potential, and increases in the amplitude and the maximum rate of rise of slow waves. 4) In the presence of apamin, Ca-dependent K channel blocker, the characteristic hyperpolarization was not developed. However, the excitatory effect of noradrenaline on spontaneous contraction remained. 5) Membrane resistance was reduced during the hyperpolarized state by the application of noradrenaline, and the change of membrane resistance and the hyperpolarized state were completely abolished by apamin. From the above results, following conclusions could be made: Excitatory responses to noradrenaline result from the dominant ${\alpha}-excitatory$, and the weak ${\beta}-inhibitory$ action of noradrenaline. Hyperpolarization of membrane potential by noradrenaline is due to the activation of Ca-dependent K channel.

• Journal of International Academy of Physical Therapy Research
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• v.9 no.4
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• pp.1571-1575
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• 2018

The purpose of this study was to investigate the effect of somatotype on the $VO_2max$ and hormone (adrenaline and noradrenaline) during treadmill walking. Forty healthy men participated and were randomized to four groups: Male 1 (M1) group, Male 2 (M2) group, Male 3 (M3) group, and Male 4 (M4) group. M4 group is the largest body type, and M1 group is the smaller the body type. Participants walked at a speed of 3.5 km/h for five minutes at an incline angle of $0^{\circ}$, $5^{\circ}$, and $10^{\circ}$ in the treadmill. Maximum oxygen consumption and hormone (adrenaline and noradrenaline) were measured. In the results, $VO_2max$ has significantly increased according to the degree of the treadmill inclination, and M4 group (larger body type) consumed more oxygen than the M1 group (smaller body type). In the hormone, there was a significant increase in adrenaline concentration after walking in all groups, and there was a significant difference in M1-M4, M2-M4 and M3-M4. The noradrenaline concentration significantly increased after treadmill gait in all groups, and there was no significant difference in noradrenaline between groups. This study suggests that the larger body type consumes more oxygen during walking, and treadmill walking contributes to an increase in the concentration of adrenaline and noradrenaline.

• The Korean Journal of Physiology
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• v.23 no.2
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• pp.277-289
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• 1989

The effects of noradrenaline on the contractile and electrical activities were investigated using the circular muscle strips with intact mucosa prepared from the antrum and fundus of guinea-pig stomach. Electrical responses of circular muscle cells were recorded using glass capillary microelectrodes filled with 3 M KCI. 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) The spontaneous contractions recorded from the antral and fundic circular muscle strips with intact mucosa were suppressed dose-dependently by the application of noradrenaline, whereas those recorded from the mucosa-free strips were potentiated in a dose-dependent manner. 2) The inhibitory influences on the contractile activities in the normal intact strips were developed via both ${\alpha}-adrenoceptors\;and\;{\beta}-adrenoceptors$, while the excitatory influences in the mucosa-free strips resulted from the strong excitatory effect via ${\alpha}-adrenoceptors$ and the weak inhibitory effect via ${\beta}-adrenoceptors$. 3) Noradrenaline produced hyperpolarization of membrane potential, and increased the amplitude and the maximum rate of rise of slow waves in the mucosa-free strips of antral and fundic circular muscle. 4) Apamin blocked the appearance of the component of initial suppression of spontaneous phasic contractions observed in the mucosa-free strips of antral circular muscle after the application of noradrenaline. 5) The inhibitory influences on the contractile activities in the normal strips with intact mucosa remained unaffected even in the strip with separate mucosa, in which mucosa and muscle layer were mechanically disconnected . From the above results, following conclusions could be made. (1) There are no regional differences between the effects of noradrenaline on the antral circular muscle and those on the fundic circular muscle. (2) Excitatory responses to noradrenaline observed in the mucosa-free strip result from the dominant ${\alpha}-excitatory$ and tile weak ${\beta}-inhibitory$ action of noradrenaline. (3) Inhibitory responses to noradrenaline in the normal strips with intact mucosa develop via both ${\alpha}-inhibitory\;and\;{\beta}-inhibitory$ actions.

• The Korean Journal of Pharmacology
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• v.6 no.1
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• pp.15-22
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• 1970

The present study is concerned with the demonstration of the relationship between the behavior and the brain concentration of noradrenaline resulted from pretreatment of amphetamine in isolated or aggregated rats. The experimental subjects were rats weighing from 120g to 200g housed 1, 2, and 6 in a cage. Analeptic activity of amphetamine was measured by determining the sleeping time induced by pentobarbital sod. The noradrenaline content in brain was determined with Aminco-Bowmann's spectro-photofluorometer by Lee's modification of Shore and Olin method. Results: 1) The analeptic activity of amphetamine on the sleeping time induced by pentobarbital sod. was more increased in the grouped rats than in isolated animal. 2) In being isolated and grouped rats, the sleeping time induced pentobarital sod, was markedly prolonged by pretreatment of amphetamine. 3) Means of housing rats, e.g., isolation or aggregation did not seem to affect the brain noradrenaline depleting action. 4) Repeated daily parenteral administration of amphetamine sulfate for a period 1 to 3 weeks resulted in decrement of brain noradrenaline concentration in being isolated and grouped rats. 5) The prolongation of sleeping time of the isolated or aggregated rats, when pretreated with amphetamine, compared with that of stock rats, seems to be attributable rather to the means of housing than the variation of the noradrenaline caused by amphetamine.

• The Korean Journal of Physiology
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• v.27 no.2
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• pp.115-122
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• 1993

There is evidence that noradrenaline enhances spontaneous contractions dose-dependently in guinea-pig antral circular muscle. To investigate the mechanism of this excitatory action, slow waves and membrane currents were recorded using conventional microelectrode techniques in muscle strips and the whole cell patch clamp technique in isolated gastric myocytes. On recording slow waves, noradrenaline $(10^{-5}\;M)$ induced the hyperpolarization of the membrane potential, although the shape of the slow waves became tall and steep. Also, spike potentiaIs occurred at the peaks of slow waves. These changes were completely reversed by administration of phentolamine $(10^{-5}\;M),\;an\;{\alpha}-adrenoceptor$ blocker. Noradrenaline-induced hyperpolarization was blocked by apamin $(10^{-7}\;M)$, a blocker of a class of $Ca^{2+}\;-dependent\;K^+$ channels. To investigate the mechanisms for these effects, we performed whole cell patch clamp experiments. Norndrenaline increased voltage-dependent $Ca^{2+}$ currents in the whole range of test potentials. Noradrenaline also increased $Ca^{2+}\;-dependent\;K^+$\;currents, and this effects was abolished by apamin. These results suggest that the increase in amplitude and the generation of spike potentials on slow waves was caused by the activation of voltage-dependent $Ca^{2+}$ channel via adrenoceptors, and hyperpolarization of the membrane potential was mediated by activation of apamin-sensitive $Ca^{2+}\;-dependent\;K^+\;channels$.

• The Korean Journal of Pain
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• v.28 no.2
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• pp.96-104
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• 2015

Background: The present experiment was conducted to identify the cooperative effect of serine histogranin (SHG) and noradrenaline in alleviating peripheral neuropathic pain. Methods: Chronic constriction injury of the right sciatic nerve was used to induce chronic neuropathic pain. For drug delivery, a PE10 tube was inserted into the subarachnoid space. Acetone drops and a $44^{\circ}C$ water bath were used to evaluate the cold and heat allodynia, respectively. Placing and grasping reflexes were used to assess the locomotor system. Results: SHG at 0.5 and $1{\mu}g$significantly (P < 0.05) decreased the thermal allodynia. The cold allodynia was also significantly reduced by intrathecal injections of 0.5 (P < 0.05) and $1{\mu}g$(P < 0.001) of SHG. $1{\mu}g$of noradrenaline, but not $0.5{\mu}g$, significantly alleviated the cold (P < 0.01) and thermal (P < 0.05) allodynia. The ameliorating effect of noradrenaline or SHG disappeared when the two compounds were administrated in equal concentrations. A significant difference (P < 0.01 in the acetone and P < 0.05 in the heat) was observed in the groups under equal doses of the two compounds, with a lower effectiveness of the combination therapy. Conclusions: Our findings suggest that the simultaneous administrations of noradrenaline and SHG do not result in synergistic analgesia, and combination therapy may not be a good approach to the treatment of chronic neuropathic pain syndrome.

• 경락경혈학회:학술대회논문집
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• 2006.11a
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• pp.139-139
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• 2006

• The Korean Journal of Physiology
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• v.21 no.2
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• pp.191-200
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• 1987

The activation mechanism of the sustained contractions induced by norepinephrine and K-depolarization was studied in renal vascular muscle. Helical strips of arterial muscle were prepared from rabbit renal arteries. All experiments were performed in Tris-buffered Tyrode solution which was aerated with 100% $O_2$ and kept at $35^{\circ}C$. Renal arterial muscles developed a contracture rapidly when exposed to a 40 mM K-Tyrode solution. In the absence of external $Ca^{2+}$, however, no K-contracture appeared. The contracture induced by K-depolarization was abolished by the treatment with $Ca^{2+}-antagonist\;(verapamil)$ or lanthanum $(La^{3+})$. From these results, it is obvious that K-contracture of renal arterial strip required $Ca^{2+}$ in the medium and this contracture was developed by the increased $Ca^{2+}-influx$ due to K-depolarization. Noradrenaline (5 mg/l) induced also a similar sustained contraction rapidly in all strips. Even on the K-contracture and in $Ca^{2+}-free$ Tyrode solution and also in the Tyrode solution pretreated with verapamil or $La^{3+}$, noradrenaline produced a contraction. However, the contraction in $Ca^{2+}-free$ Tyrode solution was not sustained and decreased gradually. The amplitude of noradrenaline-induced contracture was dependent on external $Ca^{2+}$; The contracture increased dose-dependently, but over 3 mM $Ca^{2+}$, decreased. The results of this experiment suggest that K-contracture was developed by an increased $Ca^{2+}-influx$ due to membrane depolarization, while noradrenaline-induced contracture was developed by both transmembrane $Ca^{2+}-influx$ and the mobilizaiton of cellular $Ca^{2+}$

• Journal of Ginseng Research
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• v.15 no.3
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• pp.179-182
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• 1991

The relationship between the brain monoamines and morphine tolerance was examined in ginseng total saponins treated mice. Ginseng total saponins (100 mg/kg, i.p.) did not antagonize morphine (10 mg/kg, s.c.) analgesia in mice. Daily treatment with ginseng total saponins (100 mg/kg) did not affect the brain levels of noradrenaline, dopamine and serotonin for 5 days but inhibited the development of morphine tolerance. This inhibition of the development of morphine tolerance was not attributed to the reductions of brain noradrenaline, dopamine and serotonin in mice treated with ginseng total saponins (100 mg/kg) daily. This result suggest that a newly equilibrated state of neurologic function may involve an underlying mechanism in mice treated with ginseng total saponins.

• Anxiety and mood
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• v.2 no.1
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• pp.17-21
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• 2006

SSRIs have been considered as the first line of treatment for patients with panic disorder since 1990s along with cognitive behavioral treatments. High potency benzodiazepines (e.g. alprazolam, clonazepam) have had advantages in anti-panic effects. However, these drugs have limitations of treating panic disorder because of their dependency, tolerance and withdrawal. Serotonin and noradrenaline reuptake inhibitors (SNRIs) such as venlafaxine were introduced as antidepressants since 1990s. Recently, it is confirmed that SNRIs have the remarkable anti-panic effects although some concerns about its cost, tolerance, withdrawal, side effects such as dry mouth, constipation, and hypertension have emerged. In this regard, further study is required to confirm the efficacy of long term treatment of panic disorder. Despite these concerns, venla-faxine extended-release is an effective treatment in patients with panic disorder.