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Issue:ISSN 1000-7083
          CN 51-1193/Q
Director:Sichuan Association for Science and Technology
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Effect and Mechanism of Anisodine Hydrobromide on Common Carotid Artery in Rats
Author of the article:PAN Yuan, JIANG Hongyu, YUE Meiying, TANG Guangmei, XIE Xiaofan,PENG Cheng
Author's Workplace:Chengdu University of TCM
Key Words:Anisodine Hydrobromide, Vascular ring, Contraction, Diastolic
Abstract:Objective To observe the effect and mechanism of Anisodine Hydrobromide on common carotid artery in rats. Method After anesthetizing rats, the rat common carotid artery was isolated and made into a vascular ring. Using an isolated vascular ring experiment, the effect of anisodine hydrobromide at a concentration range of 1×10-4-5×10-3 mol/L on the common carotid artery in rats which was precontracted by potassium chloride (KCl) or phenylephrine (PHE) was observed. 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 anisodine hydrobromide-induced vasorelaxation. Intracellular or extracellular calcium (Ca2+) was used as agonists to observe if contractile response was affect by anisodine hydrobromide at a concentration of 2×10-3mol/L. Result The constriction of common carotid artery ring induces by KCl or PHE can be dilated by anisodine hydrobromide in a concentration range of 1×10-4-5×10-3 mol/L in vitro. In common carotid artery rings precontracted by KCl, anisodine hydrobromide -induced the maximal relaxation magnitude (Emsx) were 33.97%±11.53%, and there was a vasoconstrictor function in the low concentration (1×10-4-1×10-3 mol/L) (P<0.01, P<0.05). While in aortic rings pre-contracted by PHE, anisodine hydrobromide-induced EC50 was 5.61(3.88,8.10)mmol/L, and Emax was 47.93%±18.63%. Compared with the Endothelial complete blood vessel ring, there was no significant change in the Emax of the anisodine hydrobromide in the de-endothelial common carotid ring pre-contracted by PHE. There was no significant influence to be observed on anisodine hydrobromide-induced vasorelaxation of the nitric oxide synthase inhibitor L-NAME or K+ channels inhibitors Gly, 4-AP, TEA and BaCl2. In the absence of Ca2+ solution, PHE-induced transient vasoconstriction can be significantly enhanced by anisodine hydrobromide in a concentration of 2×10-3 mol/L (P<0.01) . Conclusion Anisodine hydrobromide can contractile vascular ring at low concentration, and can have a concentration dependent diastolic blood vessel ring of the common carotid artery in rats, which has a dual effect on vascular tension, and its mechanism is related to non endothelium-dependent pathway and calcium release in the sarcoplasmic reticulum.
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