• Journal of the Korean Society of Food Science and Nutrition
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• v.14 no.3
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• pp.253-258
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• 1985

It was aimed to elucidate the underlying mechanism which is elevated the systemic arterial blood pressure by cadmium(Cd). By using the isolated vas deferens and tail artery from Cd-poisoned rats, it was undertaken to see whether the ${\alpha}-adrenoceptor$ activity and prostaglandins action on the twitch response to electrical stimulation were altered. It was discussed in relation with sympathetic nerve activity. The response to electrical stimulation in vas deferens from Cd-poisoned rats was much enhanced, and frequency 50(Freq.50) was significantly lowered, comparing to control. However, the response of rat tail artery was attenuated by Cd. Inhibitory action of clonidine on the twitch response of vas deferens to electrical stimulation was decreased by Cd-poisoning. However, the increase in response in the presence of methoxamine was not affected. The inhibitory action of prostaglandin $E_2$ on the twitch response in the vas deferens but not in the tail artery was abolished or rather inverted by Cd-poisoning. In the tail artery from Cd-poisoned rats, the maximum contraction to methoxamine or clonidine was significantly decreased, however, $ED_{50}$ of both agonists was not changed. These results suggest that in vas deferens the autoreceptor of presynaptic membrane is inhibited by Cd-poisoning, by which mechanism the sympathetic activity is being enhanced and this alteration may be causally related to the elevation of arterial pressure.

• YAKHAK HOEJI
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• v.33 no.6
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• pp.333-338
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• 1989

It has been postulated that abnormal characteristics of central noradrenergic nervous system has been implicated in the development and maintenance of hypertension in several modes of experimental hypertension including spontaneously hypertensive rats (SHR). In the present study, we attempt to determine if abnormal characteristics of central noradrenergic nervous system in SHR is caused by genetic factors or hypertensive phenomena by evaluating the changes of central adrenoceptors after long-term treatment of clonidine. Animals were divided into three groups; (1) 14 week-old SHR; (2) age-matched normotensive Wistar rats (NW); (3) DOCA-Salt induced hypertensive rats (DS). Clonidine (100 ug/kg) or vehicle was injected intraperitonealy twice a day for 15 days. Changes of ${\alpha}_1-$ and ${\alpha}_2-receptor$ desities following clonidine treatment were determiend in frontal corte, medulla oblongata and hypothalamus using 3H-WB4101 and 3H-clonidine, respectively. Densities of ${\alpha}_1$ and ${\alpha}_2-receptors$ following clonidine treatment were not changed in frontal cortex and medulla oblongate of SHR as well as DS, but increased in frontal cortex of NW and decreased in medulla oblongata of NW. On the other hand, densities of ${\alpha}_1-receptors$ were increased and densities of ${\alpha}_2-receptors$ were not changed in hypothalamus of SHR but densities of ${\alpha}_1-$ and ${\alpha}_2-receptors$ were decreased in hypothalamus of DS as well as NW. These results suggest that such differences in frontal cortex and medulla oblongata of SHR may be results of hypertensive phenomena whereas those in hypothalamus may be relevant to genetic factors of SHR.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.216-216
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• 1996

The purpose of the present study was to determine whether in vivo noradrenergic neural activity in the locus coeruleus is related to the development of hypertension. Two groups of animals were prepared, 1) young spontaneously hypertensive rats (SHR) and 2) age-matched normotensive wistar kyoto rats (WKY). At il weeks of age, the release of norepinephrine (NE) and 3,4-dihydroxyphenylglycol (DOPEG) from locus coeruleus of young SHR and WKY as an index of neural activity were determined by in vivo microdialysis along with blood pressure (BP) at three conditions : 1) normal; 2) elevated BP by systemic injection of phenylephrine and 3) alpha-1 adrenoceptor stimulated by perfusion of phenylephrine into the locus coeruleus through microdialysis probe. Basal releases of NE and DOPEG from the iocus coeruleus were 0.415+/-0.089pg/20min, 1.311+/-0.293 pg/20min in SHR and 0.204+/-0.078 pg/20min, 1.492+/-0.365 pg/20min in WKY respectively. Basal release of NE from the locus coeruleus of SHR was significantly greater than that of WKY. Phenylephrine systemic injection caused elevation of BP in both SHR and WKY in a dose related manner. Following phenyephrine injection, the releases of NE and DOPEG from the locus coeruleus of SHR were significantly decreased, whereas there were no significant changes in the releases of NE and DOPEG In young WKY. Alpha-1 adrenoceptor stimulation in the locus coeruleus by perfused phenylephrine through microdialysis probe caused pressor responses in both SHR and WKY, but the magnitude of pressor response in SHR was larger compared with that in WKY. The result from the present study suggests that noradrenergic neural activity in locus coeruleus may contribute as one of triggering factors for the expression of hypertension in young SHR.

• Korean Journal of Acupuncture
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• v.25 no.3
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• pp.81-96
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• 2008

Objectives : The purpose of the present study is to determine the effective analgesic parameters of manual acupuncture (MA) and/or electroacupuncture (EA), thus how MA & EA of specific acupoint works after acute ankle sprain in rats. Thus, one series of experiments was designed to analyze the analgesic effects of acupuncture in either the normal or sprained rat, by comparing the behavioral features before and after MA or EA at several acupoints. Methods : Ankle sprain was induced manually by hyper-extension of ligaments of the right ankle in rat. Either MA or EA was applied to the LI4, TE17, 足三里 and SI-6 acupoints at an intensity of 2 mA (1 ms pulse duration) with a frequency of 10 Hz for 30 minutes. Results : Behaviorally, manual acupuncture or electroacupuncture produced potent analgesic effects on acute ankle sprained animals as measured by weight bearing capacity of the affected limb. Furthermore, antinociceptive effect of EA was suppressed by alpha adrenoceptor antagonist phentolamine (5 mg/kg, i.p.) but not by opioid antagonist naltrexone (10 mg/kg, i.p.). Conclusions : It is suggested that acupuncture-induced antinociception may involve the descending inhibition of ${\alpha}2$-adrenoceptor.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.5
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• pp.441-447
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• 2016

Despite the complex vascular effects of dexmedetomidine (DEX), its actions on human pulmonary resistance arteries remain unknown. The present study tested the hypothesis that DEX inhibits vascular tension in human pulmonary arteries through the endothelial nitric oxide synthase (eNOS) mediated production of nitric oxide (NO). Pulmonary artery segments were obtained from 62 patients who underwent lung resection. The direct effects of DEX on human pulmonary artery tension and changes in vascular tension were determined by isometric force measurements recorded on a myograph. Arterial contractions caused by increasing concentrations of serotonin with DEX in the presence or absence of L-NAME (endothelial nitric oxide synthase inhibitor), yohimbine (${\alpha}_2$-adrenoceptor antagonist) and indomethacin (cyclooxygenase inhibitor) as antagonists were also measured. DEX had no effect on endothelium-intact pulmonary arteries, whereas at concentrations of $10^{-8}{\sim}10^{-6}mol/L$, it elicited contractions in endothelium-denuded pulmonary arteries. DEX (0.3, 1, or $3{\times}10^{-9}mmol/L$) inhibited serotonin-induced contraction in arteries with intact endothelium in a dose-dependent manner. L-NAME and yohimbine abolished DEX-induced inhibition, whereas indomethacin had no effect. No inhibitory effect was observed in endothelium-denuded pulmonary arteries. DEX-induced inhibition of vasoconstriction in human pulmonary arteries is mediated by NO production induced by the activation of endothelial ${\alpha}_2$-adrenoceptor and nitric oxide synthase.

• Journal of Pharmacopuncture
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• v.22 no.3
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• pp.122-130
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• 2019

Objectives: The medicinal plants are believed to enhance the natural resistance of the body to infections. Some of the main constituents of the plant and derived materials such as, proteins, lectins and polysaccharides have anti-inflammatory effects. Portulaca oleracea (P. oleracea) were used traditionally for dietary, food additive, spice and various medicinal purposes. This review article is focus on the anti-asthmatic effects of P. oleracea and its constituents. Methods: Various databases, such as the PubMed, Scopus, and Google Scholar, were searched the keywords including "Portulaca oleracea", "Quercetin", "Anti-inflammatory", "Antioxidant", "Cytokines", "Smooth muscle ", and " Relaxant effects " until the end of Jul 2018. Results: P. oleracea extracts and its constituents increased $IFN-{\gamma}$, IL-2, $IFN{\gamma}/IL-4$ and IL- 10/IL-4 ratio, but decreased secretion of $TNF-{\alpha}$, IL-4 and chemokines in both in vitro and in vivo studies. P. oleracea extracts and quercetin also signifcantly decreased production of NO, stimulated ${\beta}$-adrenoceptor and/or blocking muscarinic receptors in tracheal smooth muscles. Conclusion: P. oleracea extracts and quercetin showed relatively potent anti-asthmatic effects due to decreased production of NO, inflammatory cytokines and chemokines, reduced oxidant while enhanced antioxidant markers, and also showed potent relaxant effects on tracheal smooth muscles via stimulatory on ${\beta}$-adrenoceptor or/and blocking muscarinic receptors.

• Korean Journal of Plant Resources
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• v.23 no.6
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• pp.513-518
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• 2010

In the present study, the antinociceptive profiles of Dianthus chinensis L extract were examined in ICR mice. Dianthus chinensis L extract administered orally (200 mg/kg) showed an antinociceptive effect as measured by the tail-flick and hot-plate tests. In addition, Dianthus chinensis L extract attenuated the writhing numbers in the acetic acid-induced writhing test. Furthermore, the cumulative nociceptive response time for intrathecal (i.t.) injection of substance P ($0.7\;{\mu}g$) was diminished by Dianthus chinensis L extract. Intraperitoneal (i.p.) pretreatment with yohimbine ($\alpha_2$-adrenergic receptor antagonist) attenuated antinociceptive effect induced by Dianthus chinensis L extract in the writhing test. However, naloxone (opioid receptor antagonist) or methysergide (5-HT serotonergic receptor antagonist) did not affect antinociception induced by Dianthus chinensis L extract in the writhing test. Our results suggest that Dianthus chinensis L extract shows an antinociceptive property in various pain models. Furthermore, this antinociceptive effect of Dianthus chinensis L extract may be mediated by $\alpha_2$-adrenergic receptor, but not opioidergic and serotonergic receptors.

• YAKHAK HOEJI
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• v.41 no.4
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• pp.498-511
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• 1997

The effects of UK 14,304, an ${\alpha}_2$-adrenergic agonist, on renal function were investigated in dogs. UK 14,304, when given intravenousely($15.0{\mu}g/kg,\;50{\mu}g/kg$), produced the increase of urine flow accompanied with the marked augmentation of free water clearance ($C_{H_2O}$) and reabsorption rates of sodium in renal tubules ($R_{Na}$), and the remarkable decrease of osmolar clearance ($C_{osm}$) and the amounts of sodium excreted in urine ($E_{Na}$). UK 14,304 given into a renal artery($1.5{\mu}g/kg,\;5.0{\mu}g/kg$) elicited the increase of urine flow with the augmentation of $C_{H_2O}$ in both kidney. UK 14,304, when administered into carotid artery($3.0{\mu}g/kg,\;10.0{\mu}g/kg$). exhibited the same aspect as shown in intravenous UK 14.304 at smaller dose than the intravenous dose. Diuretic action of intravenous UK 14,304 were produced together with increase of $C_{H_2O}$ in situation of water diuresis too, changes of renal function in this state were the increase of $C_{osm},\;E_{Na},\;and\;E_K$ (excreted amounts of potassium in urine), and the decrease of $R_{Na}\;and\;R_K$, these were different appearances from situation of saline diuresis. Diuretic action of intravenous UK 14,304 were blocked completely by post or pretreatment of yohim-bine, ${\alpha}_2$-adrenergic blocking agents, and inhibited by pretreatment of vasopressin, antidiuretic hormone. Above results suggest that UK 14,304 produces the diuretic action by the inhibition of vasopressin secretion and suppression of electrolytes reabsorption of electrolytes in renal tubules mediated with central ${\alpha}_2$-adrenoceptor in dog.

• The Korean Journal of Pharmacology
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• v.19 no.2
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• pp.1-8
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• 1983

Prostaglandin(PG) is ubiquitously distributed in most mammalian tissue and their actions are complicated. Especially in autonomic nervous system, there are evidences indicating that PGs act as neuromodulators i.e., PGs, which are released in the vicinity of autonomic neuroeffector junctions, influence the release and the response of the neurotransmitter. Present study was undertaken to elucidate the interrelationship between $PGF_{2\alpha}$ and adrenergic ${\alpha}_2-receptor$ function in electrical field stimulation induced contractile response of vas deferens in rat. Male rat, weighing 150{\sim}200\;g, was sacrificed and vas deferens was obtained. The isolated vas deferens strip was placed between two platinum electrodes in temperature controlled $(37^{\circ}C)$ muscle chamber containing Tyrode's solution and the electrical field stimulation(EFS) induced contraction was recorded with Grass Polygraph(Model 7) via force displacement transducer (FT .03, Grass). The results are summarized as follows: 1) Electrical field stimulation for 1sec( 1 msec, 40 cps) induced contraction of vas deferens was completely blocked by tetrodotoxin. 2) Bretylium caused marked inhibition of the EFS-induced contraction, hut tyramine and cocaine augmented the contraction. 3) EFS-induced contraction was inhibited or little affected in distal portion of vas deferens by norepinephrine or methoxamine, but the contraction was rather augmented by the ${\alpha}-agonists$ in proximal portion. 4) Clonidine inhibited the EFS-induced contraction proportionally to the concentration in distal portion, which was blocked by yohimbine pretreatment, but in the presence of $PGF_{2\alpha}$ the blockade by yohimbine was reversed. 5) Indomethacin pretreatment reduced the effect of clonidine, but addition of $PGF_{2\alpha}$ after washing-out the indomethacin caused the contraction to the control level. From these results it is suggested that PG synthesis is a necessary step and the PG itself has a permissive role in ${\alpha}_2-adrenoceptor$ action in rat vas deferens.

• The Korean Journal of Pharmacology
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• v.25 no.1
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• pp.43-51
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• 1989

Responsiveness of muscarinic and alpha adrenoceptor activation on endothelial cells was studied in isolated canine renal artery rings. Ach (10-100 nM), dose dependently, relaxes endothelial intact rings precontracted with phenylephrine ($IC_{50}$ of Ach was 34.5 nM). Selective mechanical destruction of the endothelium transformed the activity of this substance from vasodilatation to vasoconstriction. Acetylcholine induced relaxations could be selectively inhibited competitively by atropine, but could not be inhibited by cyclooxygenase inhibitor. Methylene blue, however, an inhibitor of soluble guanylate cyclase activity, inhibited Ach as well as sodium nitroprusside (SNP) induced relaxation. Relaxation produced by prostacyclin was not modified by methylene blue. On the other hand, alpha adrenoceptor agonist did not relax but contract canine renal artery rings possessing an intact intima precontracted with U-46619. Clonidine, however, selective alpha-2 adrenergic agonist, is more susceptible than phenylepherine, selective alpha-1 adrenergic agonist, to the inhibitory effect of contraction. These results suggest that in canine renal artery rings, 1) muscarinic receptor is responsible for releasing endothelium dependent relaxation factor (EDRF). 2) alpha-1 and alpha-2 adrenergic receptors are present in canine renal artery. 3) relaxation via EDRF is antagonized by methylene blue, providing further evidence that EDRF acts through a cGMP mechanism.