• YAKHAK HOEJI
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• v.35 no.5
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• pp.394-400
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• 1991

A question whether abnormal responsiveness of hypothalamic catecholaminergic nervous system to ovarian steoid hormones in spontaneously hypertensive rats (SHR) exist was investigated. Four groups of experimental animals were prepared for SHR and normotensive Wistar rats (NW) respectively: 1) intact, 2) ovariectomized (OVX+V), 3) ovariectomized and estrogen treated (OVX+E), 4) ovariectomized and estrogen plus progesterone treated (OVX+E+P) groups. Hypothalami from experimental animals were dissected out and used for determination of .alpha.-adrenergic receptor binding characteristics and catecholamine contents. Norepinephrine(NE) content and B$_{max}$ of $\alpha_1$-adrenergic receptors in hypothalami were greater in intact SHR than in intact NW, but dopamine(DA) content was lower in SHR than in NW. Neither contents of NE and DA nor binding characteristics of $\alpha_1$-adrenergic receptors were different in OVX+V and OVX+E group from intact group of both SHR and NW. Kd and B$_{max}$ of $\alpha_1$-adrenergic receptors in OVX+E+P was lower than that in intact SHR but not in NW. DA content was lower in OVX+E+P than in intact group of SHR and NW. The result of the present study indicates that there is an abnormal responsiveness of hypothalamic catecholaminergic nervous system to ovarian steroid hormones in SHR which may be one of genetically-determined factors probably not responsible for the development of hypertension.

• Korean Journal of Veterinary Research
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• v.33 no.4
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• pp.617-622
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• 1993

The preliminary studies on the localization of adrenoceptors were performed on smooth muscle strips of bovine esophageal groove. The mechanical activity of the muscle strip was recorded isometrically in vitro.w In the bottom circular muscle strips. the excitatory ${\alpha}-adrenergic$ responses were not blocked by tetrodotoxin$(2.1{\times}10^{-6}M)$ and denervation which was carried by cold storage of strips for 48 hrs in Tyrode's solution at $5-6{^{\circ}C}$ without oxygen supply. These excitatory ${\alpha}-adrenergic$ responses were partially blocked by atropine. In the lip longitudinal muscle strips, the inhibitory${\beta}-adrenergic$ responses were not blocked by pretreatment of tetrodotoxin and atropine. The results suggest that ${\beta}-adrenergic$ receptors mediating relaxations are located on the postsynaptic smooth muscle cells, whereas ${\beta}-adrenergic$ receptors mediating contractions are located both in the smooth muscle cells and in the cholinergic neurones.

• Biomolecules & Therapeutics
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• v.1 no.1
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• pp.1-8
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• 1993

It has been known that calcium antagonists also inhibit the radioligand binding to muscarinic and $\alpha$-adrenergic receptors and, in case of verapamil, these inhibitions may play a role in the effects of verapamil on the heart. In this study, the effects of nicardipine, nifedipine, nimodipine, diltiazem and verapamil on the binding of [$^3H$]dihydroalprenolol (DHA) to dog cardiac ${\beta}$-adrenergic receptors were examined. A single uniform [$^3H$]DHA binding site ($K_D/= 5nM\;and\;B_{max}=2600$ fmol/mg protein) was identified in dog cardiac sarcolemma. [$^3H$]DHA binding was not affected by the usual therapeutic concentrations of these calcium antagonists (nanomolar range) but in the "nonspecific"concentration ranges ($28-180{\mu}m$) these drugs inhibited [$^3H$]DHA binding to $\beta$-adrenergic receptors. Nicardipine, nifedipine, nimodipine and diltiazem competed for [$^3H$]DHA binding to ${\beta}$-adrenergic receptors with dissociation constants ($K_i$) of $28{\mu}m,\' 74{\mu}m, 39{\mu}m \;and \;35{\mu}m,$ respectively. Verapamil ($K_i=176.5 {\mu}m$) was less potent inhibitor than other drugs and this inhibition was noncompetitive; the maximal binding capacity ($B_{max}$) $300 {\mu}m$ verapamil without change in the apparent dissociation constant (4K_D$) for DHA. These results indicate that the inhibitory action of calcium antagonists at high concentrations on ${\beta}$-adrenergic receptors is not involved in the therapeutic effects of these drugs by the calcium channel blocking action.

• Journal of Korean Biological Nursing Science
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• v.10 no.1
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• pp.80-87
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• 2008

Purpose: Hypoestrogenism caused by ovariectomy, disease, or menopause is associated with increased obesity in women. Altered fat distribution and weight gain are consequences of menopausal hypoestrogenism, but the mechanisms responsible are not completely known. This study examined the effect of estrogen on obesity in ovariectomized rats. Method: The groups of female rats were 4 weeks post ovariectomy (OVX) or, 4 weeks post-sham operation (SHAM), and 2 weeks post ovariectomy followed by 2 weeks replacement with estradiol benzoate (ER-$16{\mu}g$/kg, subq, qd). Serum ghrelin level was measured by radioimmunoassay (RIA). The expression of adrenergic receptors in adipose tissue was measured by Western blotting assay. Result: OVX significantly increased body weight, serum cholesterol. Two weeks estrogen replacement reduced body weight accompanied by the increment of serum ghrelin and the reduction of the receptor ratio of adrenergic ${\alpha}_{2A}/{\beta}_1$, and ${\alpha}_{2A}/{\beta}_3$. Conclusion: We provide evidence that estrogen reduces obesity through the altered receptor ratio of adrenergic ${\alpha}_{2A}/{\beta}_1$, and ${\alpha}_{2A}/{\beta}_3$ in adipose tissue in ovariectomized rats.

• YAKHAK HOEJI
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• v.32 no.6
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• pp.428-434
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• 1988

The effects of calcium and calcium antagonist, nifedipine on the adrenergic receptor-stimulated glycogenolysis were investigated in isolated rat hepatocytes. The hepatic glycogenolysis induced by alpha-adrenergic receptor stimulation depended on calcium ions, and beta-adrenergic activation was unrelated to calcium ions. Nifedipine decreased the alpha-adrenergic agonist-induced glucose release significantly and the decrease was depended on calcium ions. The glucose release induced by beta-adrenergic agonist was not inhibited by nifedipine.

• The Korean Journal of Pharmacology
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• v.2 no.1 s.2
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• pp.41-48
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• 1966

The author studied the adrenotropic receptors of the non-pregnant uteri of the rabbit and rat, using epinephrine (alpha and beta activator), phenoxybenzamine(alpha blocking agent) and nethalide (beta blockade), and obtained the following results: 1. The spontaneous motility of isolated non-pregnant uteri from rabbits were stimulated by epinephrine, whereas that of isolated non-pregnant rat uterus was inhibited by epinephrine. 2. Both alpha and beta adrenergic receptors were present in the uterine muscle of both animals. 3. In the non-pregnant rabbit uterus, alpha receptors were predominant, whereas in the non -pregnant rat uterus, beta receptors preponderated over alpha receptors.

• The Korean Journal of Pain
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• v.21 no.1
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• pp.27-32
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• 2008

Background: Experimental evidence indicates that ginseng modulate the nociceptive transmission. Authors examined the role of adrenergic and cholinergic receptors on the antinociceptive action of Korean red ginseng against the formalin-induced pain at the spinal level. Methods: Catheters were inserted into the intrathecal space of male Sprague-DawIey rats. Fifty ${\mu}l$ of 5% formalin solution was injected to the hindpaw for induction of pain and formalin-induced pain (flinching response) was observed. The role of spinal adrenergic and cholinergic receptors on the effect of Korean red ginseng was assessed by antagonists (Prazosin, yohimbine, atropine and mecamylamine). Results: Intrathecal Korean red ginseng produced a dose-dependent suppression of the flinching response in the rat formalin test. All of prazosin, yohimbine, atropine and mecamylamine antagonized the antinociception of Korean red ginseng. Conclusions: Spinal Korean red ginseng is effective against acute pain and facilitated pain state evoked by formalin injection. All of alpha 1, alpha 2, muscarinic and nicotinic receptors may play an important role in the antinociceptive action of Korean red ginseng at the spinal level.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.3
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• pp.149-155
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• 2003

The aim of the present study was to examine the effects of platycodin D and $D_3$, which are active components derived from the roots of Platycodon grandiflorum A. DC., on the contractile force of the i3olated rat aorta and blood pressure of the anesthetized rat, and also to elucidate its mechanism of action. Both phenylephrine (an adrenergic ${\alpha}1$-receptor agonist) and high potassium (a membranedepolarizing agent) caused great contractile responses in the isolated aortic strips. Platycodin D at high concentration $(24{\mu}g/ml)$ inhibited contractile responses induced by phenylephrine $(10^{-5}\;M)$ and high potassium $(5.6{\times}10^{-2}\;M)$, while low concentrations of platycodin D $(4{\sim}8{\mu}g/ml$) did not affect those responses. However, platycodin $D_3\;(8{\sim}32{\mu}g/ml)$ did not alter the contractile responses evoked by phenylephrine and high $K^+$. Interestingly, the infusion of platycodin $D_3$ (1.0 mg/kg/30 min) significantly reduced the pressor responses induced by intravenous norepinephrine. However, platycodin $D_3$ (1.0 mg/kg/30 min) did not affect them. Taken together, these results show that intravenously administered platycodin D depresses norepinephrine-induced pressor responses in the anesthetized rat, at least partly through the blockade of adrenergic ${\alpha}1$-receptors. Platycodin D also caused vascular relaxation in the isolated aortic strips of the rat via the blockade of adrenergic ${\alpha}1$-receptors, in addition to an unknown direct mechanism. However, platycodin $D_3$ did not affect both norepinephrine-induced pressor responses and the isolated rat aortic contractile responses evoked by phenylephrine and high potassium. Based on these results, there seems to be much difference in the mode of action between platycodin D and platycodin $D_3$.

• 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.

• 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.