• The Korean Journal of Pharmacology
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• v.1 no.1 s.1
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• pp.63-65
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• 1965

Rabbit blood pressure showed gradual fall by intraventricular guanethidine (5mg). The pressure rise by carotid occlusion was markedly inhibited or abolished by the guanethidine, while it was enhanced by small dose (2mg). The intraventricular guanethidine did not affect norepinephrine pressor effect, but caused marked inhibition or abolishment of depressor action of serotonin.

• YAKHAK HOEJI
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• v.17 no.1
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• pp.31-39
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• 1973

The influence of guanethidine on the renal function was investigated in the rabbit. Guanethidine, 1-10mg/kg, i.v., produced no marked change in the renal function, while second and successive doses of guanethidine elicited a significant increase in urine flow and electrolyte excretion as well as renal plasma flow and glomerular filtration rate. It was suggested that the diuretic action was brought about by improvement of hemodynamic state in the kidney ; increased filtration as a result of increased renal perfusion. Atropine alone did not significantly influence the renal function but pretreatment of animals with atropine, 4 mg/kg i.v., completely abolished the diuretic action of guanethidine. It is suggested that guanethidine influences the renal function by activating parasympathetic nervous system or some cholinergic mechanism in the kidney.

• Asian-Australasian Journal of Animal Sciences
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• v.9 no.6
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• pp.651-654
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• 1996

The effect of guanethidine on feeding behavior was investigated in the chicken. Graded levels of chronically administered guanethidine, an adrenergic neurone blocker, at 0, 25, 50 and 100 mg/kg body weight, decreased body weight gain and food intake in a dose dependent manner. The effect of acute guanethidine administration on crop emptying rate of the chicken was also investigated. The highest level (10 mg i.v./kg body weight) of guanethidine significantly delayed crop emptying compared with the control. These results suggest that the sympathetic nervous system in the chicken is an important factor for the regulation of feeding behavior associated with food passage from the crop.

• YAKHAK HOEJI
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• v.22 no.3
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• pp.148-156
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• 1978

An influence of bethanidine (B) onpressor effects of norepinephrine (NE) and tyramine (TR) was investigated in the whole rabbits. B, in a dose 1.0, 3.0 and 5.0 mg/kg, i.v., potentiated significantly the pressor effects of NE and TR. Reserpine and desipramine did not increase the NE effect that had been potentiated by B.B also made little modification of NE effect that had been potentiated by reserpine and desipramine. B increased the NE effect that had been potentiated by tranycypromine and guanethidine. The NE pressor effect potentiated by B was decreased by tranylcypromine, but not influenced by guanethidine. The TR pressor effect potentiated by B was not altered by reserpine and guanethidine, but decreased by desipramine and tranylcypromine. B increased the TR pressor effect that had been potentiated by guanethidine. B, when given after administration of reserpine, tranylcypromine or desipramine, exerted little influence on the TR effect. The mechanism of potentiation of NE and TR pressor effects by B seems to be similar to guanethidine, and the potency of B on the influence of NE and TR effects seems to be greater than guanethidine.

• YAKHAK HOEJI
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• v.19 no.4
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• pp.227-233
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• 1975

The diuretic action of guanethidine was investigated in the dogs by means of the stop-flow technique. Guanethidine increased the rejection of sodium in the ascending limb of Henle's loop, as well as in the proximal and distal tubules, resulting in the decrease of the concentrating ability of the kidney, in marked natriuresis and diuresis. It was also effective during an osomotic diuresis, which was induced by infusing 10% mannitol can exhibit its effect even under the diuretic action of mercurophylline, suggesting a different mechanism from that of mercuric iuretics.

• The Korean Journal of Pharmacology
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• v.17 no.1 s.28
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• pp.33-39
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• 1981

In this paper, the influences of adrenergic neuronal blockades of different mode: guanethidine and ${\alpha}$-methyl-para-tyrosine on the changes induced by carbon tetrachloride $(CCl_4)$ of hepatic total lipid, glycogen, and lipid peroxide contents and serum lactic dehydrogenase activity were investigated in male mice. The results obtained were summarized as follows: 1) The hepatic total lipid and lipid peroxide contents and serum lactic dehydrogenase activity were markedly increased by $CCl_4$, but hepatic glycogen content were decreased. 2) The hepatic total lipid and lipid peroxide contents and serum lactic dehydrogenase activity were not significantly changed by guanethidine(20mg/kg) or ${\alpha}$-methyl-para-tyrosine (5 mg/kg) injection. 3) The increase of hepatic total lipid induced by $CCl_4$ was inhibited by the pretreatment of guanethidine or ${\alpha}$-methyl-para-tyrosine, and the increase of hepatic lipid peroxide content induced by $CCl_4$ was slightly inhibited by them. But the decrease of hepatic glycogen content and the increase of serum lactic dehydrogenase activity induced by $CCl_4$ were not affected by them.

• The Korean Journal of Pharmacology
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• v.8 no.1
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• pp.63-65
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• 1972

It is well known that pharmacological actions of bradykinin are smooth muscle dilatation, increase in capillary permeability, accumulation and migration of leucocytes and inducement of pain. The most significant action of bradykinin is the dilatation of blood vessels. The responses of bradykinin (0.5ug/kg, i. v. injection) on blood pressure were observed before and after single i. v. administration of guanethidine (2mg/kg) in the rabbits. The result of experiment was as follows: In the rabbit pretreated with guanethidine, the depressor response of bradykinin was much pronounced in comparison with that of normal rabbit.

• The Korean Journal of Pharmacology
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• v.18 no.2
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• pp.59-67
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• 1982

1) Oxymetazoline, which has been known as an agonist for${\alpha}_1-adrenoceptor$ in various peripheral tissues, caused a pressor response in urethane-anesthetized rabbits when given intra-ventricularly. This pressor response was little affected by pretreatment of rabbits with i.v. guanethidine or chlorisondamine, but it was weakened in rabbits pretreated with either of i.v. phentolamine or guanethidine and chlorisondamine and in guanethidine-pretreated adrenal-ligated rabbits. 2) The pressor to intraventricular oxymetazoline was markedly attenuated by intraventricular pretreatment with prazosin, whereas intraventricular pretreatment with yohimbine or piperoxan did not affect this response. 3) Reserpine-pretreated rabbits also responded with hypertension to intraventricular oxymetazoline, which was markedly diminished by pretreatment with intraventricular prazosin but not affected by yohimbine. 4) Oxymetazoline, given intravenously, produced a pressor response in both whole and spinal rabbits. Intravenous prazosin, phentolamine and yohimbine, in this order, showed greater antagonizing effect to this pressor response. 5) The results indicate that oxymetazoline acts an agonist for ${\alpha}_1-adrenoceptors$ in the rabbit brain participating in the regulation of the blood pressure and in the vasculature of rabbits.

• The Korean Journal of Pain
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• v.3 no.2
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• pp.144-148
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• 1990

정상인에서 Guanethidine Nicardipine Nitroglycerine Prostaglandin $E_1$을 피하주사하고 지속적인 복사열을 주사한 후에 Pain Meter NYT-5를 이용하여 동통역치를 측정하였다. 통증역치는 Guanethidine과 Nicardipine에 의해 상승되었으며 Nitroglycerine에 의해서는 거의 변화가 없고 Prostaglandin $E_1$에 의해서는 감소되었다. 이러한 변화는 지각신경섬유의 말단 감각수용체에 대한 감수성이 이들 혈관확장제에 대하여 서로 다른 작용을 나타내는것 같다.

• The Korean Journal of Pharmacology
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• v.14 no.1_2
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• pp.55-62
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• 1978

Ban formulated the concept of 'sympathetic center' and 'parasympathetic center' in the central nervous system, and Folkow et al. reported that the electric stimulation of the posterior part of hypothalamus induced the marked liberation of catecholamines from the adrenal medulla. Tatum reported that the hyperglycemic action of picrotoxin is contributed to the cathecholamines liberation from adrenal medulla by the excitation of hypothalamus via splanchnic nervous plexus. In this paper, the relationship between the convulsive action and the hyperglycemic effect of picrotoxin was investigated, with references to the influences of several drugs related with adrenergic function and two intravenous anesthetics on the picrotoxin hyperglycemia. The results obtained were summarized as follows; 1) There was no difference between the convulsive dose(1. 5mg/kg) and the subconvulsive dose (0.75mg/kg) of picrotoxin in its hyperglycemic effect that was not affected with the phenobarbital pretreatment, but the efficacy of its hyperglycemic action was more prominent than that of strychnine. 2) The hyperglycemic effect of picrotoxin was markedly suppressed by the pretreatment of thiopental or ketamine. 3) The hyperglycemic effect was not affected by the reserpine pretreatment, but the effect was markedly suppressed by the pretreatment of iproniazid or chlorpromazine. 4) The hyperglycemic effect of picrotoxin was significantly suppressed by the pretreatment of hexamethonium, propranolol or guanethidine, and the order of those suppressing efficacy was propranolol> hexamethonium> guanethidine.