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The effects of oxymatrine, an alkaloidal component of Sophora flavescens, on the cardiovascular system of anesthetized rats
Oxymatrine (OM) , an alkaloidal component of Sophora flavescens, produced a transient decline in blood pressure and bradycardia. The threshold dose for the depressor effect was about 1.25 mg/kg, and maximal response was observed with about 5 mg/kg. There was no difference between responses to supram...
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Published in: | Japanese Journal of Pharmacology 1986, Vol.40 (suppl), p.175-175 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Online Access: | Get full text |
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Summary: | Oxymatrine (OM) , an alkaloidal component of Sophora flavescens, produced a transient decline in blood pressure and bradycardia. The threshold dose for the depressor effect was about 1.25 mg/kg, and maximal response was observed with about 5 mg/kg. There was no difference between responses to supramaximal doses and those to 5 mg/kg for the degree of depressor effect except for duration. The effects of OM were not inhibited by propranolol or methysergide, suggesting that the response to OM was not mediated through the β-adrenoceptor or 5-HT receptor. Although pretreatment with antihistamines attenuated the decline in blood pressure by OM, OM itself did not have the histamine-releasing activity from peritoneal mast cells, suggesting that the inhibitory effect of antihistamines on OM may be ascribed to their anticholinergic properties. The bradycardia and depressor effect caused by OM was diminished by vagotomy and atropine treatment. From all results, it was suggested that the effects of OM on the cardiovascular system were largely mediated through the vagus cholinergic nerve, and it was assumed that the fall in blood pressure caused by OM may be due to decreased cardiac output. The facts that OM did not act directly on the thracic aorta and that intracerebroventricular injection of OM did not influence the blood pressure, imply that OM may produce its effect reflexively. |
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ISSN: | 0021-5198 1347-3506 |
DOI: | 10.1016/S0021-5198(19)59271-X |