• Asian-Australasian Journal of Animal Sciences
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• v.7 no.3
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• pp.397-400
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• 1994

The effect of xylazine administration on plasma cortisol, prolactin, glucose and packed cell volume (PCV) responses to immobilization and heat stress was investigated. Immobilization of rats for 2 hours by ligation of the fore and hind legs strongly caused approximately two-fold increase in plasma cortisol and prolactin levels. Plasma glucose and PCV were not significantly changed. Pretreatment of immobilized rats with xylazine (20 mg/kg body weight i.m.) resulted in approximately 20% reduction in both plasma cortisol and prolactin concentrations. A marked hyperglycemia and increase in the PCV value was observed. On the other hand, rats exposed to acute heat stress ($40^{\circ}C$, and 60% relative humidity) for 2 hours, also developed two fold increase in both plasma cortisol and prolactin concentrations and the pretreatment with xylazine caused a 20% reduction in the levels of both hormones. Plasma glucose level was not significantly changed in heat stressed rats but it was markedly increased after pretreatment with xylazine. PCV was significantly incrcased under heat stress and pretreatment with xylazine induced a pronounced elevation in this value. It was suggested that stimulation of cortisol and prolactin secretion in response to immobilization or heat stress can be partially reduced by an alpha 2-adrenergic agonist.

• Biomolecules & Therapeutics
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• v.10 no.1
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• pp.50-58
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• 2002

lt had been reproted previously that (${\pm}$)6-chloro-7,8-dihydroxy-1-phenyl 2,3,4,5-tetra-hydro -lH-3benzazepine (SKF 81297), dopamine $D_1$ receptor agonist, produced diuresis by both Indirect action through central function and direct action being induced in kidney. This study was attempted in order to examine the diuresis mechanism of such SKF 81297 Diuretic action of SKF 81297 given into the vein or the carotid artery was not affected by renal denervation, whereas diuretic action of SKF 81297 administered into a renal artery was blocked completely by renal denervation, and then diuretic action of SKF 81297 injected into carotid artery was inhibited by SCH 23390, dopamine $D_1$ receptor antagonist, given into carotid artery. Above results suggest that indirect diuretic action of SKF 81297 elicites through central dopamine $D_1$ receptor and direct diuresis in kidney by influence of renal nerves.

• Korean journal of applied entomology
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• v.31 no.4
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• pp.475-479
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• 1992

The non-steroidal ecdysone agonist RH 5849 showed almost similar LC.o values( 18.1-26.5 ppm) at all stages of larval development of the tobacco cutworm, Spodoptera litura, when treated by a leaf-disk dipping method. The feeding-inhibition rate for the 4th instar larvae was dose-dependent, and simultaneously the weight gain of 3rd instar larvae ceased within 48 hour after feeding of the cabbage leafdisk dipped into RH 5849 4.2 ppm solution. The systemic larvicidal effect of RH 5849 was compared at cabbage and tobacco whole plant test. The $LC_{50}$ values below 20 ppm(mg/kg soil) was lasted for 15 days in cabbage, 30 days in tobacco respectively.

• Biomolecules & Therapeutics
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• v.24 no.3
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• pp.291-297
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• 2016

Cytisine (CYT), a partial agonist of ${\alpha}4{\beta}2-nicotinic$ receptors, has been used for antidepressant efficacy in several tests. Nicotinic receptors have been shown to be closely associated with depression. However, little is known about the effects of CYT on the depression. In the present study, a mouse model of depression, the unpredictable chronic mild stress (UCMS), was used to evaluate the activities of CYT. UCMS caused significant depression-like behaviors, as shown by the decrease of total distances in open field test, and the prolonged duration of immobility in tail suspension test and forced swimming test. Treatment with CYT for two weeks notably relieved the depression-like behaviors in the UCMS mice. Next, proteins related to depressive disorder in the brain region of hippocampus and amygdala were analyzed to elucidate the underlying mechanisms of CYT. CYT significantly reversed the decreases of 5-HT1A, BDNF, and mTOR levels in the hippocampus and amygdala. These results imply that CYT may act as a potential anti-depressant in the animals under chronic stress.

• The Korean Journal of Pain
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• v.12 no.2
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• pp.177-182
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• 1999

Background: Clonidine, an ${\alpha}_2$ adrenergic agonist blocks nerve conduction. However, in our previous experiment we found that adrenaline neither blocks nerve conduction by itself nor augment nerve conduction blockade by lidocaine near clinical concentrations. Possible explanations are: 1) there may be antagonism between some of adrenergic receptors, 2) clonidine may block nerve conduction via non-adrenergic mechanism. The purpose of this study is to obtain dose-response curves of several different forms of adrenergic receptor agonist to see the relative potencies of each adrenergic receptors to block nerve conduction. Methods: Recordings of compound action potentials of A-fiber components (A-CAPs) were obtained from isolated sciatic nerves of adult male Sprague-Dawley rats. Nerve sheath of the sciatic nerve was removed and desheathed nerve bundle was mounted on a recording chamber. Single pulse stimuli (0.5 msec, supramaximal stimuli) were repeatedly applied (2Hz) to one end of the nerve and recordings of A-CAPs were made on the other end of the nerve. Dose-response curves of epinephrine, phenylephrine, isoproterenol, clonidine were obtained. Results: $ED_{50}$ of each adrenergic agonist was: $4.51\times10^{-2}$ M for epinephrine; phenylephrine, $7.74\times10^{-2}$ M; isoproterenol, $9.61\times10^{-2}$ M; clonidine, $1.57\times10^{-3}$ M. Conclusion: This study showed that only clonidine, ${\alpha}_2$ adrenergic agonist, showed some nerve blocking action while other adrenergic agonists showed similar poor degree of nerve blockade. This data suggest that non-effectiveness of epinephrine in blocking nerve conduction is not from the antagonism between adrenergic receptors.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.1
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• pp.45-53
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• 2005

The present study was designed to examine the effect of d-amphetamine on CA release from the isolated perfused model of the rat adrenal gland, and to establish its mechanism of action. Damphetamine $(10{\sim}100{\mu}M$), when perfused into an adrenal vein of the rat adrenal gland for 60 min, enhanced the CA secretory responses evoked by ACh ($5.32{\times}10^{-3}$ M), excess $K^+$ ($5.6{\times}10^{-2}$ M, a membrane depolarizer), DMPP ($10^{-4}$ M, a selective neuronal nicotinic $N_n-receptor$ agonist) and McN-A-343 ($10^{-4}$ M, a selective $M_1-muscarinic$ agonist) only for the first period (4 min), although it alone has weak effect on CA secretion. Moreover, d-amphetamine ($30{\mu}M$) in to an adrenal vein for 60 min also augmented the CA release evoked by BAY-K-8644, an activator of the dihydropyridine L-type $Ca^{2+}$ channels, and cyclopiazonic acid, an inhibitor of cytoplasmic $Ca^{2+}$ ATPase only for the first period (4 min). However, in the presence of high concentration ($500{\mu}M$), d-amphetamine rather inhibited the CA secretory responses evoked by the above all of secretagogues. Collectively, these experimental results suggest that d-amphetamine at low concentrations enhances the CA secretion from the rat adrenal medulla evoked by cholinergic stimulation (both nicotininc and muscarinic receptors) as well as by membrane depolarization, but at high concentration it rather inhibits them. It seems that d-amphetamine has dual effects as both agonist and antagonist at nicotinic receptors of the isolated perfused rat adrenal medulla, which might be dependent on the concentration. It is also thought that these actions of d-amphetamine are probably relevant to the $Ca^{2+}$ mobilization through the dihydropyridine L-type $Ca^{2+}$ cha$N_n$els located on the rat adrenomedullary chromaffin cell membrane and the release of $Ca^{2+}$ from the cytoplasmic store.

• Asian-Australasian Journal of Animal Sciences
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• v.12 no.5
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• pp.788-793
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• 1999

To determine the interrelationship between thyroid status and the reparitioning action of clenbuterol (CLE) in broilers, two-week-old female chickens were fed diets containing an antithyroid substance, propylthiouracil (PTU, 0 or 0.3%), CLE (0 to 1 mg/kg), or both for 18 days in a $2{\times}2$ factorial design experiment. Muscle weights (breast muscle, gastrocnemius and peroneus longus) increased only in the normal chickens fed CLE. As absolute mass, protein of leg muscle quantitatively increased in the CLE-fed normal birds. In contrast, inhibition of the CLE-induced protein accretion, especially of peroneus longus, occurred in the PTU group. A quantitative increase in DNA was observed in leg muscles of the normal chickens, but no DNA response to CLE was shown in the PTU-treated chickens. The decreased RNA in leg muscles of the PTU group was more reduced by CLE feeding. Although not statistically significant, the reduced degradation rate of whole muscle protein in normal chickens fed CLE was not confirmed in the PTU-fed group. The present study, therefore, concluded that metabolic action of thyroid hormones was a prerequisite for the hypertrophic effect of ${\beta}$-agonist in broilers.

• 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.

• YAKHAK HOEJI
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• v.34 no.3
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• pp.180-191
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• 1990

A comparison was made of the effects of selective ${\alpha_1}-adrenoceptor$ agonist phenylephrine and selective ${\alpha_2}-adrenoceptor$ agonist clonidine on endothelium-containing and endothelium-denuded rings of the rat aorta. In the case of phenylephrine, removal of endothelium increased sensitivity 2.5 fold at $EC_{50}$ level and maximum contractive response 1.4 fold. In the case of clonidine, which gave only 15% of maximum contractive response given to phenylephrine on endothelium-containing rings, removal of the endothelium increased sensitivity 5.6 fold at $EC_{50}$ level and maximum contractive response 5 fold, which was about 55% of that given by phenylephrine. In endothelium-denuded ring, phenylephrine-induced contraction tended to be more increased in tonic contraction than in phasic contraction as compared to that in endothelium-containing ring, while clonidine-induced contraction was monophasic and was increased only in tonic contraction. In the calcium-free solution or in the presence, of verapamil, contraction stimulated by clonidine was almost abolished while that stimulated by phenylephrine produced only phasic contraction. The depression of sensitivity to these agonists in rings with endothelium appeared to be due to the vasodepressor action of endothelium derived relaxing factor (EDRF), because hemoglobin, a specific blocking agent of EDRF, abolished this depression. It is unlikely that the endothelium-dependent relaxation was due to stimulation of release of EDRF, because clonidine did not produce endothelium-dependent relaxation in 5-hydroxytryptamine-precontracted ring even when its contractile action was blocked by the ${\alpha_1}-adrenoceptor$ antagonist, prazosin. When the efficacy of phenylephrine was reduced to about the initial efficacy of clonidine by pretreatment with dibenamine, the contraction-response curves for phenylephrine became very similar to the corresponding curves obtained for clonidine before receptor inactivation. In the dibenamine-treated rings, contraction of phenylephrine was abolished in calcium-free solution or in the presence of verapamil like that obtained for clonidine before receptor inactivation. These results suggest that EDRF spontaneously released from endothelium depress contraction more profoundly in a case of an agonist with low efficacy and the phenylephrine-induced contraction was totally dependent on extracellular calcium as was that obtained for clonidine when the efficacy of phenylephrine was reduced to that of clonidine by irreversible inactivation of ${\alpha_1}-adrenoceptor$ with dibenamine.

• Applied Microscopy
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• v.39 no.4
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• pp.301-309
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• 2009

Estrogens induce pronounced structural and functional changes in male and female reproductive system, but the exact mechanisms of estrogen are not fully understood. In relation to estrogen's function, the present study was designed to identify effects of estrogen receptor agonist, 4,4',4"- (4-propyl-[1H]-pyrazole-1,3,5-triyl)tris phenol (PPT) in the reproductive organ of the female mouse. The PPT was subcutaneously given to adult female mice at a weekly dosage of 3 mg in a volume 0.06 mL of vehicle for 3, 5 or 8 weeks whereas controls received weekly injections of the castor oil vehicle. Effects of PPT on reproductive organs were analyzed using a light microscope. PPT induced decreases of body, ovary and adipose tissue weights with experimental time. Ovary diameter of PPT treatment group was reduced as compared with control group. The number of Graffian follicle and corpus luteum was reduced in PPT treatment group. The luminal diameter of uterus was increased in relation with decrease of myometrium and endometrium height by PPT administration. The number of uterine glands was decreased by PPT treatment. These data indicate that PPT treatment induced morphological change of female reproductive organs resulting in alteration of fertility.