• The Korean Journal of Pharmacology
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• v.20 no.2
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• pp.59-71
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• 1984

To explore the regulatory roles of CNS on the renal function, clonidine, a specific presynaptic ${\alpha}-adrenoceptor$ agonist, was administered into a lateral ventricle of the brain (icv) and the changes of renal function were studies in urethane-anesthetized rabbits. $5{\mu}g/kg$ icv elicited no significant changes in renal function. However, $15{\mu}g/kg$ induced marked natriuresis and kaliuresis for 20 min. Neither RPF nor GFR changed significantly. The fractional sodium reabsorption was significantly reduced, indicating that the renal action was of the tubular origin. Changes of systemic blood pressure were not contributory to the renal action. Yohimbine, a specific antagonist for presynaptic ${\alpha}-adrenoceptor$, when given icv in doses of $100{\mu}g/kg$ 20 min prior to clonidine, completely abolished the renal action of icv clonidine. Yohimbine icv did not produce any significant changes in renal function. Intravenous clonidine, $15{\mu}g/kg$, elicited antidiuresis and decrement of renal function immediately after administration, followed by a slight tendency toward natriuresis, but no natriuresis corresponding to those seen after the icv clonidine were observed, indicating that in the renal action of icv clonidine no direct action is involved. These observations indicate that the central sympathetic tone plays a role in the regulation of renal function in the rabbit.

• Korean Journal of Veterinary Research
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• v.33 no.1
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• pp.71-80
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• 1993

The central nervous system depressant effect of xylazine and xylazine-ketamine was studied in chicken and mice. Intraperitoneal injection of xylazine(1~30 mg/kg) and xylazine(1~30 mg/kg)-ketamine(100 mg/kg) induced a loss of the righting reflex in chicken and mice, respectively. These effects of xylazine were dose-dependent. The results obtained were as follows; 1. The effect of xylazine-induced depression was antagonized by adrenergic antagonists having ${\alpha}_2$-blocking activity(yohimbine, tolazoline, piperoxan and phentolamine). 2. Yohimbine was most effective in the reduction of the CNS depression by xylazine. 3. Phenoxybenzamine and prazosin did not reduced CNS depression by xylazine in both species. 4. Labetalol (${\alpha}_1$, ${\beta}_1$-adrenergic antagonist) and propranolol(${\beta}$-adrenergic blocking agent) were not effective in reducing xylazine induced depression. 5. Cholinergic blocking agents (atropine and mecamylamine), a dopaminergic antagonist (Haloperidol), a histamine $H_1$-antagonist(chlorpheniramine), a histamine $H_2$-antagonist(cimetidine), a serotonergic-histamine $H_1$ antagonist(cyproheptadine) were not effective in reducing xylazine-induced depression. 6. Xylazine-induced depression is mediated by ${\alpha}_2$-adrenergic receptors and appears not to be involved in cholinergic, dopaminergic, serotonergic or histaminergic pathways.

• The Korean Journal of Physiology
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• v.21 no.1
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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.

• Natural Product Sciences
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• v.4 no.2
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• pp.58-61
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• 1998

Eurycoma longifolia Jack was evaluated for aphrodisiac property on sexually naive male mice using the electrical copulation cage. Optimum condition was provided for this study and the male mice were treated with 500 mg/kg of either chloroform, methanol, water or n-butanol fractions from E. longifolia Jack. However, the mice in the yohimbine and control groups received 30 mg/kg and 3 ml/kg of yohimbine and normal saline respectively. The male mice were then conditioned to seek either an estrous female, sexually vigorous male or no mouse, a measurement of right, wrong or no choice respectively. Besides this, hesitation time which was the time spent before the sexually naive male mice crossed the electrical grid (maintained at 0.12 mA) was also determined. Results showed that E. longifolia Jack possesses aphrodisiac property on the sexually naive male mice as shown by the slow and transient reduction in hesitation time and also a similar manner in the increase in the % of sexually naive male mice scoring right choice throughout the investigation period. Hence, this further supports the folkuse of this plant as aphrodisiac.

• Korean Journal of Veterinary Service
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• v.17 no.3
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• pp.255-263
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• 1994

To elucidate the action of the adrenergic nerve on the isolated uterine smooth muscle of the pig, effects of electrical transmural nerve stimulation and norepinephrine were investigated on the pretreatment of phentolamine ； non-selective ${\alpha}$-adrenoceptor blocker, propranolol ; ${\beta}$-adrenoceptor blocker and the yohimbine；${\alpha}_2$-selective adrenoceptor blocker from physiograph. 1. The relaxation response induced by norepinephrine was the concentration of $10^{-6}$ M at first and maximum response was concentration of $10^{-4}$M. 2. The relaxation response induced by norepinephrine was not effected by the pretreatment with non-selective $\alpha$-adrenoceptor blocker, phentolanune ($10^{-6}$ M) but was completely blocked by the pretreatment with ${\beta}$-adrenoceptor blocker, propranolol($10^{-6}$ M). 3. The contractile response induced by electrical transmural nerve stimulation(20V, 10Hz, 0.5msec, 20sec ) was inhibited by the pretreatment with non-selective ${\alpha}$-adrenoceptor blocker, phentolamine($10^{-6}$ M) but was not inhibited and rather increased by the pretreatment ${\beta}$-adrenoceptor blocker, propranolol($10^{-6}$ M), and was not approximately effected by the pretreatment with ${\alpha}_2$-adrenoceptor blocker, yohimbine($10^{-6}$ M). These finding suggest that it was excitatory action by ${\alpha}_1$-adrenergic nerve and inhibitory action by ${\alpha}_2$-adrenergic, ${\beta}$-adrenergic nerve on uterine smooth muscle of the pig.

• Journal of Korean Neurosurgical Society
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• v.47 no.6
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• pp.420-423
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• 2010

Objective : Peripheral nerve injury often leads to neuropathic pain, which is characterized by burning pain, allodynia, and hyperalgesia. The role of the sympathetic nervous system in neuropathic pain is a complex and controversial issue. It is generally accepted that the alpha adrenoreceptor (AR) in sympathetic nerve system plays a significant role in the maintenance of pain. Among alpha adrenoreceptor, alpha-1 receptors play a major role in the sympathetic mediated pain. The primary goal of this study is to test the hypothesis that sympathetically maintained pain involves peripheral alpha-2 receptors in human. Methods : The study was a randomized, prospective, double-blinded, crossover study involving twenty patients. The treatments were : Yohimbine (30 mg mixed in 500 mL normal saline), and Phentolamine (1 mg/kg in 500 mL normal saline) in 500 mL normal saline at 70 mL/hr initially then titrated. The patients underwent infusions on three different appointments, at least one month apart. Thus, all patients received all 2 treatments. Pain measurement was by visual analogue scale, neuropathic pain questionnaire, and McGill pain questionnaire. Results : There were significant decreases in the visual analogue scale, neuropathic score, McGill pain score of yohimnine, and phentolamine. Conclusion : We conclude that alpha-2 adrenoreceptor, along with alpha-2 adrenoreceptor, may be play role in sympathetically maintained pain in human.

• Korean Journal of Veterinary Research
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• v.33 no.2
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• pp.211-216
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• 1993

To elucidate the action of the cholinergic and ${\alpha}_2$-adrenergic nerve on the isolated ileal smooth muscle of the dog, effect a of electrical field stimulation were investigated on the pretreatment of the physostigmine; cholinestrase inhibitor, yohimbine; ${\alpha}_2$-adrenoceptor blocker, atropine ; cholinergic receptor blocker and phentolamine; non-selective $\alpha$-adrenoceptor blocker from physiograph. 1. The contractile response induced by electrical field stimulation was the frequency (2-40 Hz)-dependent manner. 2. The contractile response induced by electrical field stimulation was markedly increased by the pretreatment of physostigmine$(1{\mu}M)$; cholinestrase inhibitor. 3. The contractile response induced by electrical field stimulation was increased by the pretreatment of yohimbine$(1{\mu}M)$; ${\alpha}_2$-adrenoceptor blocker. These finding suggest that it was powerful excitatory action by cholinergic nerve and inhibitory action by ${\alpha}_2$-adrenergic nerve on ileal smooth muscle of the dog.

• YAKHAK HOEJI
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• v.48 no.5
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• pp.285-290
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• 2004

The purpose of this study is to prove how magnetic field (MF) acts on sympathetic neuro-transmissions using thermal response. Mice were divided into two groups and each one was exposed to MF (20 G, 24 hrs) or sham. Every vehicle or drugs were treated a half hour before the thermal response test. The pain threshold was lowered by MF (20 G, 24 hrs) alone. This reduction of pain threshold by MF was not blocked by a single treatment of $\alpha$-receptor antagonist (prazosin), $\alpha$$_2$-receptor agonist (clonidine, guanabenz), $\beta$$_1$-receptor antagonist (atenolol) or $\beta$$_1$,$\beta$$_2$-receptor antagonist (propranolol). But administration of $\alpha$$_2$-receptor antagonist (yohimbine) completely inhibited the decrease in pain threshold by MF. Moreover, it increased by high dose of yohimbine over normal condition. These results suggest that MF acts on sympathetic nerve terminal to induce hyperalgesia, in which pre-synaptic az receptor might be involved.

• The Korean Journal of Pharmacology
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• v.30 no.1
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• pp.29-37
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• 1994

Inhibition of the nociceptive Tail Flick Reflex (TFR) was observed with electrical stimulation of the locus coeruleus/subcoeruleus (LC/SC) in the male Sprague - Dawley rats under light anesthesia, and the involved neurotransmitter (s) were characterized. Electrical stimulation of LC/SC induced the analgesia with the stimulation threshold (intensity of the current, given for 100 usec and in 100 Hz frequency, which caused the TF latency longer than 6.5 sec) around 55 uA. Intrathecal administrations of ${\alpha}_2$ antagonist, yohimbine (30 ug) or opioid antagonist, naloxone (20 ug) increased the stimulation threshold by 147% and 123% respectively (from 55 uA to 135 uA,9 and from 54 uA to 123 uA;P0.01, n=5, each). The basal TF latency without stimulation (3.1 sec) was reduced by the antagonists (to 2.5 sec by yohimbine, p<0.05, n=5; to 2.6 sec by naloxone, p<0.1, n=5), vehicle only did not show any effect. Noradrenaline(NA) in the spinal cord superfusates measured with HPLC was increased by the LC/SC stimulation, from 4.18 ng/ml before to 7.74 ng/ml after stimulation (P<0.05, n=10). The result suggest that analgesia induced by LC/SC stimulation is mediated, at least in part, by the noradrenergic system in which ${\alpha}_2$ receptor is involved, as well as the opioid system.

• The Korean Journal of Pharmacology
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• v.17 no.2
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• pp.23-30
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• 1981

1) Effects of McN-A-343, clonidine and cocaine on the contractile response of the rat and rabbit vas deferens to field stimulation were investigated. The action mechanisms of these drugs have shown to be associated with endogenous norepinephrine(NE). 2) The contractile response to the stimulation of 5-10 Hz was markedly inhibited by the cumulative doses of McN-A-343 (0.003, 0.03, $0.3{\mu}g/ml$), clonidine (0.003, $0.3{\mu}g/ml$) and cocaine $(0.03\;{\mu}g/ml)$. The inhibition was antagonized by yohimbine and pjperoxan. 3) The inhibitory effect of McN-A-343 $(0.03{\mu}g/ml)$ and cocaine $(0.03{\mu}g/ml)$ was markedly enhanced by the same dose of cocaine and McN-A-343, respectively. This enhanced inhibition was also antagonized by yohimbine. 4) The contractile response to the stimulation of 0.01 Hz and 5-10 Hz was markedly potentiated by comparatively large doses of McN-A-343 $(30\;{\mu}g/ml)$ and $(3\;{\mu}g/ml)$. This potentiation was not observed in the presence of thymoxamine. The potentiation by McN-A-343 also did not appear in the presence of atropine. 5) The contractile response to the above stimulation was potentiated by muscarine and the potentiation was markedly attenuated in the presence of thymoxamine and atropine.