• 약학회지
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• 제41권4호
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• pp.399-406
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• 1997

The effects of different $K^+$ channel blockers were investigated on the non-adrenergic non-cholinergic (NANC) relaxations in the circular muscle of the rabbit proximal stomach. Non-selective blockers of $K^+$ channels, 4-aminopyridine (4-AP, 3~30${\mu}M$) and tetraethylammonium (TEA, 100~1000${\mu}M$) significantly enhanced the NANC relaxations in a concentration-dependent manner. The enhancement was more prominent for the NANC relaxations induced by the electric field stimulation (EFS) with lower frequencies. Blockers of large conductance $Ca^{2+}$-activated $K^+$ channels, charybdotoxin and iberiotoxin, a blocker of small conduntance $Ca^{2+}$-activated $K^+$ channels, apamin and a blocker of ATP-sensitive $K^+$ channels, glibenclamide had no effect on the NANC relaxations, respectively. Exogeneous administration of nitric oxide (NO, 1~30${\mu}M$) caused concentration-dependent relaxations which showed a similarity to those obtained with EFS. None of the $K^+$ channel blockers had an effect on the concentration-dependent relaxation in response to NO. These results suggest that prejunctional $K^+$ channels regulate the release of NO from the NANC nerve in the rabbit proximal stomach as the inhibition of prejunctional $K^+$ channels increases the NANC relaxation induced by the EFS.

• The Korean Journal of Pain
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• 제13권2호
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• pp.156-163
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• 2000

Background: Peripheral nerve injury sometimes leads to chronic neuropathic pain such as causalgia. A subset of patients with causalgia have a sympathetically maintained pain which is often evoked by cooling stimuli. However, our knowledge on adrenergic receptor types responsible for cold-evoked pain that is sympathetically dependent is lacking. The present study was conducted to investigate subtypes of adrenoceptors involved in mediating cold-evoked pain that developed following peripheral nerve injury. Methods: Neuropathic surgery was performed by a unilateral ligation of L5 and L6 spinal nerves of rats. Behavioral sign of cold-evoked pain was examined for 5 min by measuring cumulative duration of time that the rat lifted its foot off a metal plate held at cold temperature ($5^{\circ}C$). Whether cold-evoked pain behavior was affected by antagonists of various subtypes of adrenoceptors, which were administered intraperitoneally before and after the ligation, was investigated. Results: After ligation, duration of foot lifting on the ligated side at cold temperature increased as compared to the pre-operative period. This increase maintained for the entire 40-day test period. Pretreatment with alpha-antagonist phentolamine produced a suppression of cold-evoked pain behavior that was not affected by beta-antagonist propranolol pretreatment. Prazosin, alpha-1 antagonist, suppressed cold- evoked pain behavior when treated either before or after nerve ligation. On the other hand, alpha-2 antagonist yohimbine was without effect on cold-evoked pain behavior whether it was treated before or after the ligation. Conclusions: The results suggest that peripheral nerve injury develops cold-evoked pain that is sympathetically dependent, and that alpha-1 adrenoreceptor plays a critical role for the generation of this type of pain in its initiation as well as maintenance.

• 대한한의학회지
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• 제41권1호
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• pp.11-20
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• 2020

Objectives: We noticed that hyperhidrosis can be differentiated by whether it is topical or systemic in both Korean medicine(KM) and Modern medicine(MM). Comparing between topical and systemic sweating, we will figure out similarity between KM and MM about stimuli on sweat. Methods: All research is done by finding information on text-book, article, books. Results: Hyperhidrosis is differentiated by whether it is topical or systemic in both Korean medicine(KM) and Modern medicine(MM). First, systemic sweating(SS) is affected by body temperature. In KM, Heat and Cold(plus yang deficiency) can make human sweat systemically. In MM, heat is also mentioned as stimulus. Second, topical sweating(TS) can occur on emotionally-stressed situation especially on palms-and-soles. In KM, this phenomenon is explained by heart spirit(心神) and disease transmitted by pericardium meridian(手厥陰心包經 是動病). In MM, anatomically hyperhidrosis on palms-and-soles is generated by adrenergic sympathetic nerve which is involved with stress. Third, sweating on palms-and-soles also can be generated by internal organ. In KM, hyperhidrosis on palms-and-soles is explained as illness on stomach meridian(足陽明胃經). The 70% of parasympathetic nerve is vagus nerve which is located at internal organs-usually gastrointestinal tract. In that point, stomach and parasympathetic nerve seem to be involved in hyperhidrosis on palms-and-soles. Conclusion: Hyperhidrosis is differentiated similarly by whether it is topical or systemic in both Korean medicine and Modern medicine. Conserving each perspective of KM and MM, one perspective can be useful to other by supplementing other's weak point.

• The Korean Journal of Pain
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• 제9권1호
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• pp.26-38
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• 1996

In a normal state, sympathetic efferent activity does not elicit discharges of sensory neurons, whereas it becomes associated with and excites sensory neurons in a pathophysiological state such as injury to a peripheral nerve. Although this sympathetic-sensory interaction is reportedly adrenergic, involved subtypes of adrenoreceptors are not yet clearly revealed. The purpose of this study was to determine which adrenorceptor subtypes were involved in sympathetic-sensory interaction that was developed in rats with an experimental peripheral neuropathy. Using rats that received a tight ligation of one or two of L4-L6 spinal nerves 10~15 days previously, a recording was made from afferent fibers in microfilaments teased from the dorsal root that was in continuity with the ligated spinal nerve. Electrical stimulation of sympathetic preganglionic fibers in T13 or L1 ventral root (50 Hz, 2-5 mA. 0.5 ms pulse duration, 10 sec) was made to see if the activity of recorded afferents was modulated. About half of afferents showing spontaneous discharges responded to sympathetic stimulation, and had the conduction velocities in the A-fiber range. Most of the sympathetically induced afferent responses were excitation. This sympathetically induced excitation occurred in the dorsal root ganglion (DRG), and was blocked by yohimbine (${\alpha}_2$ blocker), neither by propranolol ($\beta$ blocker) not by prazosine (${\alpha}_1$ blocker). The results suggest that after spinal nerve ligation, sympathetic efferents interact with sensory neurons having A-fiber axons in DRG where adrenaline released from sympathetic nerve endings excites the activity of sensory neurons by acting on 2-adrenoreceptors. This 2-adrenoreceptor mediated excitation of sensory neurons may account for sympathetic involvement in neuropathic pain.

• Anatomy and Cell Biology
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• 제51권4호
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• pp.266-273
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• 2018

The ganglion cardiacum or juxtaductal body is situated along the left recurrent laryngeal nerve in the aortic window and is an extremely large component of the cardiac nerve plexus. This study was performed to describe the morphologies of the ganglion cardiacum or juxtaductal body in human fetuses and to compare characteristics with intracardiac ganglion. Ganglia were immunostained in specimens from five fetuses of gestational age 12-16 weeks and seven fetuses of gestational age 28-34 weeks. Many ganglion cells in the ganglia were positive for tyrosine hydroxylase (TH; sympathetic nerve marker) and chromogranin A, while a few neurons were positive for neuronal nitric oxide synthase (NOS; parasympathetic nerve marker) or calretinin. Another ganglion at the base of the ascending aorta carried almost the same neuronal populations, whereas a ganglion along the left common cardinal vein contained neurons positive for chromogranin A and NOS but no or few TH-positive neurons, suggesting a site-dependent difference in composite neurons. Mixtures of sympathetic and parasympathetic neurons within a single ganglion are consistent with the morphology of the cranial base and pelvic ganglia. Most of the intracardiac neurons are likely to have a non-adrenergic non-cholinergic phenotype, whereas fewer neurons have a dual cholinergic/noradrenergic phenotype. However, there was no evidence showing that chromogranin A- and/or calretinin-positive cardiac neurons corresponded to these specific phenotypes. The present study suggested that the ganglion cardiacum was composed of a mixture of sympathetic and parasympathetic neurons, which were characterized the site-dependent differences in and near the heart.

• Applied Microscopy
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• 제26권2호
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• pp.137-155
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• 1996

The development of the ganglia of the trachea was studied by electron microscopy in human fetuses ranging from 40 mm to 260 mm crown rump length. At 40 mm fetus, the tracheal ganglia was observed in the submucosa of the trachea. The primitive ganglia consisted of neuroblasts, undifferentiated cells, and unmyelinated nerve fibers. At 50 mm fetus, the neuroblast and their processes in the tracheal ganglia ware ensheathed by the bodies or processes of satellite cells. The cytoplasm of the neuroblast contained rough endoplasmic reticulum, mitochondria, Golgi complex, and ribosomes. At 70 mm fetus, cholinergic and adrenergic axon terminals were observed. Cholinergic axon terminals with agranular vesicles were abundant in the tracheal ganglia with increasing age. During next prenatal stage from 100 mm fetus, the ganglion cells and its processes were completely covered by a thin processes of the satellite cells. Unmyelinated nerve fibers were also completely ensheathed by processes of Schwann cell. Synaptic contacts between the cholinergic axon and dendrite of ganglion cells and a few dendrodendritic synapses were first observed at 100 mm fetus. The granule-containing cells were first identified in the tracheal ganglia at 200 mm fetus. These findings indicate that tracheal ganglia of human fetus resembles other parasympathetic and sympathetic ganglia, but not the enteric ganglia.

• The Korean Journal of Physiology
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• 제21권1호
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• pp.67-77
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• 1987

Effect of intravenously injected clonidine on the flexion reflex was studied in 15 decerebrated and spinalized cats. The flexion reflex was elicited by electrical stimulation of the tibial nerve or the common peroneal nerve and it was recorded as single unit activity from filaments of the L6 or L7 ventral roots. In order to obtain the late flexion reflex discharges, $A{\delta}$ and C afferent fibers were stimulated with single or train electrical pulses respectively. The flexion reflex, especially the late component, was markedly inhibited after intravenous administration of clonidine. The clonidine-induced inhibition of the flexion reflex was compared before and after treatment of the animals respectively with yohimbine and naloxone. The inhibitory effect on the flexion reflex of clonidine was not altered by naloxone, a ${\mu}-opioid$ receptor blocker, whereas it was completely blocked by yohimbine, an ${\alpha}_2-adrenergic$ antagonist. These results indicate that clonidine inhibits the flexion reflex through excitation of ${\alpha}_2-adrenoceptors$ even at the spinal cord level.

• 약학회지
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• 제21권1호
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• pp.17-25
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• 1977

Intravenous injection of Mori Radicis Cortex Water Extract (MWE) regularly caused the does-related, lowering of blood pressure in the rabbits anesthetized with urethane, and then did not show the cumulative effect and the tachyphylaxis. The hypotensive effects of MWE were inhibited by atropine, chlorisodamine, phentolamine and bethanidine, while not altered by diphenhydramine, propranolol and cyproheptadine. Atropine after chlorisondamine did not alter the effect of MWE. MWE potentiated the pressor effect of nore-pinephrine, but did not carotid occlusion was inhibited by previous administration of MWE. It is conclude that MWE elicits hypotensive action in the rabbit by the centrally induced cholinergic effect and the inhibitation of responses to sypathetic adrenergic nerve activation.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1996년도 춘계학술대회
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• pp.217-217
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• 1996

The putative role of vasoactive intestinal polypeptide (VIP) as non-adrenergic non-cholinergic (NANC) neurotransmitter has been studied in rabbit corpus cavernosum. In the presence of atropine and guanethidine the short and prolonged electrical field stimulation (EFS, 2～16 ㎐) induced a frequency-dependent relaxation which was abolished by tetrodotoxin (0.3 ${\mu}$M), a nerve conductance blocker. The neurogenic relaxant reponses were not affected in the presence of VIP-inactivating peptidase, ${\alpha}$-chymotrypsin (2 units/$m\ell$), whereas VIP-induced relaxation were completely abolished. Inhibition of nitric oxide synthase by N$\^$G/-nitro-L-arginine (10～100 ${\mu}$M) caused concentration-dependent inhibition to the neurogenic relaxant responses and at 100 ${\mu}$M the relaxations were virtually abolished. In contrast NO (3～30 ${\mu}$M) and VIP (0.001～l ${\mu}$M)-induced relaxation were unaffected. The inhibitory effect of L-NNA was reversed in the presence of L-arginine (5 mM), the precursor of the NO biosynthesis. Hemog1obin (20～60 ${\mu}$M), sequestering NO in the extracellular space, abolished the NO-evoked relaxation and also caused a concentration-dependent inhibition to the neurogenic relaxation. These observation indicate that NANC relaxation induced by prolonged EFS of rabbit corpus cavernosum is also mediated mainly by nitric oxide as same as that of short EFS, and suggest that VIP is not involved in NANC relaxation of rabbit corpus cavernosum and NO would not be produced by VIP in this tissue.

• 대한약리학회지
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• 제19권1호
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• pp.85-92
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• 1983

Intestine is innervated by an interconnected plexus of both sympathetic and parasympathetic nerve fibers. Sympathetic influence causes inhibition of intestinal motility mediated by both ${\alpha}-\;and\;{\beta}-adrenergic$ receptors. The mechanism of intestinal relaxation by ${\beta}-receptors$ has been extensively studied, but the function of ${\alpha}-receptors$ in intestinal motility is still unclear. Although it is suggested that catecholamine reduces acetylcholine release and this may play an important role in ${\alpha}-receptor$ mediated intestinal relaxation, there is no definite evidences about the mechanism and site of action of ${\alpha}-receptor$ mediated relaxation. In this experiment, therefore, the effect and site of action of ${\alpha}-receptor$ agonists were investigated in the guinea pig ileum using electrical field stimulation. The results are summarized as follows : 1) Electrical field stimulation elicited tonic contraction in isolated guinea pig ileum ana this contraction was completely inhibited by the pretreatment of tetrodotoxin or atropine. 2) Norepinephrine, epinephrine and dopamine inhibited the contraction induced by electrical field stimulation but methoxamine and phenylephrine had little effects. 3) Inhibitory effects of norepinephrine and dopamine was partially blocked by yohimbine and phentolamine pretreatment. But haloperidol and propranolol pretreatment cause no effects on the electrical field stimulation induced contraction. Inhibitory effect of dopamine was completely blocked by both haloperidol and yohimbine pretreatment. 4) Inhibitory effects of norepinephrine and dopamine were little affected by the pretreatment with hexamethonium. It is suggested that electrical field stimulation causes tonic contraction of guinea pig ileum by releasing acetylcholine from postganglionic fiber, and this release is blocked by presynaptic ${\alpha}-receptor$ activation.