• Korean Journal of Pharmacognosy
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• v.7 no.3
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• pp.215-220
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• 1976

1. Nepetae Herba water extract (NHW) produced a fall of blood pressure in the rabbit. 2. The depressor effect of NHW was inhibited by atropine, but was not affected by propranolol, hexamethonium and diphenhydramine. 3. NHW showed pressor response in the rabbit treated with atropine. 4. The pressor response in the atropine treated rabbit was inhibited by phentolamine and guanethidine.

• The Korean Journal of Pharmacology
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• v.26 no.2
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• pp.177-183
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• 1990

This study was undertaken to confirm whether or not the sympathetic nervous system takes part in the liver regeneration after partial hepatectomy. The male Sprague-Dawley rats were pretreated with I.P. injection of guanethidine 25 mg/kg: single dose (G-1); multiple doses once a day for 3 days (G-3), for 5 days (G-5), or for 6 days (G-6). The rats were subjected to partial hepatectomy $(70.4{\pm}1.99%)$ under light anesthesia of diethyl ether. 1) The systolic blood pressure of control rat was $98.0{\pm}3.9\;mmHg$ and was not affected by G-1. But after the pretreatment with G-3, G-5 or G-6, the pressure was markedly decreased by over 25 %. 2) Both of plasma norepinephrine and epinephrine levels showed the marked increases 3 hrs after the hepatectomy. However, the increases are entirely inhibited by G-1 or G-6. 3) All the liver contents of putrescine, spermidine and spermine showed the significant increases 6 hrs after the hepatectomy and were not affected by G-1 or G-6 with the exception of the inhibition of putrescine increase by only G-6. The present results suggest that the sympathetic activation appeared after partial hepatectomy seems not to play an important role in rat liver regeneration.

• Journal of Pharmaceutical Investigation
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• v.15 no.1
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• pp.22-31
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• 1985

The influence of some sympathetic blocking agents on pressor actions of norepinephrine and angiotensin was investigated in rabbits. 1. Phentolamine, sympathetic ${\alpha}-blocking$ agent, blocked the pressor action of norepinephrine, but did not affect the pressor action of angiotensin 2. Chlorisondamine, autonomic ganglionic blocking agent, potentiated the both actions of norepinephrine and angiotensin. 3. Guanethidine, bethanidine and debrisoquine, sympathetic neuronal blocking agents, potentiated the action of norepinephrine, while diminished that of angiotensin. 4. Reserpine, norepinephrine depleting agent, increased the pressor response of norepinephrine, but did not influence the pressor action of angiotensin.

• The Korean Journal of Pain
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• v.5 no.1
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• pp.85-88
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• 1992

Buerger's disease is a chronic occlusive arterial disease in which a non-arteriosclerotic lesion involves medium-sized arteries, veins, and nerves of the distal leg or arm. Sympathetic interruption is indicated to improve blood flow to the involved extremity, although sympathetic blockade can provide temporally relief of vasospasm and pain. Chemical or surgical sympathectomy has been performed for this purpose and intravenous regional sympathetic block(IRSB) is an alternative. Guanethidine or reserpine has been administered for IRSB. Intraarterial or intravenous systemic administration of prostaglandin E1(PGE1) has been recommended for the treatment of Buerger's disease. We used PGE1 for intravenous regional administration as an IRSB with results as good as that of intraarterial injection. The advantages of the method include that it is less expensive than systemic administration, less invasive than intra-arterial injection, and simple in technical application.

• YAKHAK HOEJI
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• v.23 no.2
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• pp.69-80
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• 1979

Effects of Astragali Radix Water Extract (ARWE) on the blood pressure were investigated in the whole rabbit and the spinalized rabbit. ARWE, when administered into the ear-vein or lateral ventricle, produced a fall in the blood pressure in the whole rabbit, but intravenous ARWE in the spinalized rabbit did not elicite the hypotensive action. Pretreatments with chlorisondamine, guanethidine, phentolamine and cyproheptadine in the whole rabbit weakened the depressor action of ARWE. The hypotensive action of the whole rabbit to ARWE was not influenced by the pretreatment of the animals with diphennylhydramine, propranolol, and vagotomization, whereas inhibited by atropine. ARWE did not affect the pressor response by angiotensin. However, it enhanced the hypertensive action by norepineprine and reduced the elevation in the blood pressure by carotid occlusion in the whole rabbit. These experimental observations suggest that ARWE may cause the depressor response via mechanisms of the central sympathetic blocking action, cholinergic action by peripheral origin and serotonin-like action.

• The Korean Journal of Pain
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• v.10 no.2
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• pp.274-277
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• 1997

The complex regional pain syndrome(CRPS) exhibit symptoms such as: abnormal skin color, temperature change, abnormal pseudomotor activity, edema. If CRPS is not treated appropriately at acute stage, then the affected extremity may become a useless, painful appendage. Treatment of CRPS by sympathetic blockade may be achieved by repeated intravenous regional guanethidine blocks, repeated anesthetic sympathetic blocks, surgical sympathectomy or oral sympatholytic therapy. We treated 29-year-old male patient with CRPS of left upper extremity by continuous cervical epidural blockade. Due to wound infection and dislocation of the epidural catheter, we inserted an implantable port system to inject the mixture of local anesthetics and small amount of morphine. After 10 months of treatment, patient was cured of symptoms and signs of CRPS and was able to resume a normal life.

• Archives of Pharmacal Research
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• v.3 no.1
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• pp.23-30
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• 1980

Berberine, when administered into a ear-vein of the rabbit anesthetized with urethane, produced a long-lasting, dose related fall in blood pressure, but intraventricular berberline did not elicit the hypotensive response. This hypotensive activity of berberine was not influenced by pretreatment of vagotomization and atropine. Depressor responses induced by berberine were not impaired by diphenhydramine, chlorisondamine, guanethidine and propranolol, but reduced significantly by phentolamine pretreatment. Berberine attenuated markedly prossor responses of norepinephrine and epinephrine. These results suggest that berberine causes the hypotensive activity that is attributable to alpha adrenoceptor blockade, but not to a direct relaxant effect upon vascular smooth muscle.

• The Korean Journal of Physiology
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• v.21 no.2
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• pp.225-239
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• 1987

The effects of adenosine on the mechanical contractions and electrical activities were investigated in guinea-pig stomach. Spontaneous contractions of the antral region were recorded with force transducer, and the phasic contractions of fundic region were induced by electrical field stimulation. Electrical responses of smocth muscle cells were recored using glass capillary microelectrodes filled with 3M-KCl. Field stimulation was applied transmurally by using a pair of platinum wire (0.5 mm in diameter) placed on both sides of tissue. All experiments were performed in tris-buffered Tyrode solution which was aerated with 100% $O_2$ and kept at $35^{\circ}C$. The results obtained were as follows. 1) Adenosine suppressed the spontaneous contractions of antrum in a dose-dependent manner. 2) The inhibitory effect on antral spontaneous contractions was not influenced by the administration of guanethidine $(5{\times}10^{-6}\;M)$ and atropine $10^{-6}\;M$, or in the presence of dipyridamole $10^{-7}\;M$. 3) The phasic contractions of fundus induced by electrical field stimulation, which disappeared rapidly by the addition of tetrodotoxin $(3{\times}10^{-7}\;M)$, were potentiated by adenosine in the presence of guanethidine. 4) Adenosine decreased the amplitude and the maximum rate of rise of slow waves, and the increased amplitude and rate of rise evoked in the high calcium solution or in the presence of TEA were decreased by adenosine. 5) The non-adrenergic, non-cholinergic inhibitory junction potential (IJP) was inhibited by adenosine in the antral region, while the excitatory junction potential (EJP) in the fundic region was potentiated. From the above results, the following conclusions could be made. 1) Adenosine suppresses the spontaneous contractions of antrum strip by the decrease in amplitude and rate of rise of slow waves. 2) The release of neurotransmitter(s) from non-adrenergic, non-cholinergic nerve terminals is inhibited by adenosine.

• The Korean Journal of Physiology and Pharmacology
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• v.11 no.4
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• pp.155-161
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• 2007

In order to characterize the role of sympathetic activity in obesity, we repeatedly assessed sympathetic activity via power spectral analyses of heart rate variability in the same subjects at 7, 11, 25, and 60 weeks, using monosodium glutamate (MSG)-induced obese and control rats. The effects of lower sympathetic activity on obesity were also evaluated. Fat mass in MSG rats was already higher at 7 weeks, but the sympathetic activity did not differ between 7 and 25 weeks. Between 25 and 60 weeks, the increase in fat mass, food efficiency, and body weight gain was higher in MSG rats. The increase in sympathetic activity between 25 and 60 weeks and sympathetic activity at 60 weeks were lower in MSG rats. Fat mass at 60 weeks was inversely correlated with changes in sympathetic activity between 25 and 60 weeks. Reduced plasma epinephrine levels by bilateral adrenal demedullation induced increase of fat mass. In, an attenuated increase of sympathetic activity with age may partly be responsible for aggravated obesity in MSG rats. Additionally, reduced sympathetic activity per se induced obesity in rats. These results suggest that lower sympathetic activity contributes to obesity in rats.

• Journal of Pharmaceutical Investigation
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• v.9 no.3
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• pp.27-38
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• 1979

This study was attempted to investigate the pharmacological action, especially depressor action of Phellodendri cortex and to elucidate the mechanism of its action, making use of Phellodendri cortex methanol extract (PCME) because its hypotensive action is not clear. Influence of PCME on the blood pressure of the rabbits and cats were observed in this study. PCME, when given intravenously in the rabbits and cats, elicited the hypotensive action, but intraventricular PCME in the rabbits did not show depressor action. Accumulation and tachyphylaxis by PCME administered into the ear-vein of the rabbits were not shown. Depressor effect of PCME in the rabbits was attenuated significantly by pretreatment with phentolamine, guanethidine, chorisondamine and atropine, but not by propranolol, diphenhydramine, cyproheptadine and vagotomization. The pressor activity of angiotensin was unimpaired after injection of maximal hypotensive doses (100mg/kg) of PCME, but the pressor activity of norepinephrine and carotid occlusion was abolished markedly. In addition, PCME given into jugular vein of the cats weakened norepinephrine pressor responses and caused the reversal of epinephrine pressor responses. These results suggest that the hypotensive action of PCME may be due to dual mechanisms by interference with peripheral sympathetic function, alpha adrenoceptor blocking action, and peripheral parasympathomimetics action, muscarinic action.