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Study on the catechol somatostatin on effect and mechanism of vascular rings isolated from rats

Author: ZhaoZhuangQin
Tutor: WangWeiShu
School: Shanxi Medical
Course: Geriatrics
Keywords: Blood vessels rings Catestatin Nitric oxide
CLC: R96
Type: Master's thesis
Year: 2013
Downloads: 7
Quote: 0
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Abstract


ObjectiveBy measuring the tension of isolated thoracic aortic rings, observe the effects of CST in the tension of that induced by PE and the change following administration of L-Nitro-Arginine-Methyl ester(L-NAME),compared with acetylcholine (Ach) and sodium nitroprusside(SNP), to investigate the effects of catestatin and to deduce the mechanisms of CST.Methods①Prepare the isolated vascular rings of rat, record the tension change after using the phenylephrine (PE) with Powerlab system.②Observe the effects of CST at various concentrations in the tension of isolated thoracic aortic rings induced by PE.③Observe the effect change of CST following administration of L-Nitro-Arginine-Methyl ester(L-NAME),Compared with the classic endothelium dependent and independent reagents:acetylcholine (Ach) and sodium nitroprusside(SNP), to deduce the mechanisms of CST.Results①PE(10-9-10-5mmol/L) elicited isolated thoracic aortic rings contraction in rats in a concentration-dependent manner.②CST, when administered at the concentration of10-8to10-4mol/L, caused vasodilation depending on its concentration that counteracted the vasoconstriction induced by PE (10-6mmol/L). This vasodilation effect was less competent than that of acetylcholine(Ach) and sodium nitroprusside(SNP) at the same concentration.③The vasodilation effect of CST was significantly suppressed by L-NAME. that of Ach was disappeared, and of SNP was not obviously influenced.Conclusion①CST counteract the vasoconstriction effect of PE in a concentration-dependent fashion. ②The mechanism of CST is different from the fully endothelial dependent reagent Ach and the fully endothelial independent reagent SNP.③The effect of CST may be partly interpreted by the release nitric oxide induced by the endothelium.

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