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Issue:ISSN 1000-7083
          CN 51-1193/Q
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Your Position :Home->Past Journals Catalog->2018 Vol.37 No.6

In vitro Effect and Mechanism of Anisodine Hydrobromide on Common Carotid Artery of Rats
Author of the article:PAN Yuan, PENG Cheng, JIANG Hongyu, YUE Meiying, TANG Guangmei, XIE Xiaofang*
Author's Workplace:College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu 610075, China
Key Words:anisodine hydrobromide; vascular ring; contraction; diastolic
Abstract:Objective To study the effect and mechanism of anisodine hydrobromide on common carotid artery of rats.Methods The common carotid artery of anesthetized rat was isolated and made into a vascular ring. Potassium chloride (KCl) or phenylephrine (PHE) precontracted rat common carotid artery was then treated by anisodine hydrobromide at a concentration range of 1×10-4-5×10-3 mol·L-1. The nitric oxide synthase inhibitor Nω-nitro-L-arginine methyl ester (L-NAME) or potsssium (K+) channels inhibitors Glyburide (Gly); 4-Aminopyridine (4-AP); Tetraethylammonium chloride (TEA) and BaCl2 were used to study their influence on the anisodine hydrobromide-induced vasorelaxation. Intracellular or extracellular calcium (Ca2+) was used as agonist to deterimine whether contractile response could be affected by anisodine hydrobromide at a concentration of 2×10-3 mol·L-1.Results The constricted common carotid artery ring induced by KCl or PHE could be dilated by anisodine hydrobromide in a concentration range of 1×10-4-5×10-3 mol·L-1 in vitro. In common carotid artery rings precontracted by KCl, anisodine hydrobromide-induced maximal relaxation magnitude (Emsx) was 33.97%±11.53%, and a vasoconstrictor function was observed in the concentration of 1×10-4-1×10-3 mol·L-1 (P<0.01, P<0.05). By contrast, in aortic rings precontracted by PHE, anisodine hydrobromide-induced median effect concentration (EC50) was 5.61 (3.88, 8.10) mmol·L-1, and Emax was 47.93%±18.63%. Compared with the endothelial complete blood vessel ring, there was no significant change in the Emax of anisodine hydrobromide in the de-endothelial common carotid ring pre-contracted by PHE. Moreover, the supplementation of nitric oxide synthase inhibitor L-NAME or K+ channels inhibitors Gly, 4-AP, TEA and BaCl2 had no significant effect on anisodine hydrobromide-induced vasorelaxation. In the absence of Ca2+ solution, PHE-induced transient vasoconstriction could be significantly enhanced by anisodine hydrobromide in a concentration of 2×10-3 mol·L-1 (P<0.01).Conclusion Anisodine hydrobromide can contractile vascular ring at low concentration, and have a concentration dependent diastolic effect on the blood vessel ring of the common carotid artery in rats, and the underlying mechanism is related to the non-endothelium-dependent pathway and calcium release in the sarcoplasmic reticulum.
2018,37(6): 660-666 收稿日期:2018-06-22
分类号:Q95-33
基金项目:四川省科技支撑计划(2016SZ0027)
作者简介:潘媛(1987—),女,博士研究生,实验师,研究方向:中药药效与毒理学,E-mail:panyuan1129@163.com
*通信作者:谢晓芳,副研究员,主要从事中药药理与毒理研究,E-mail:xxf14544@163.com
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