首页> 外文期刊>Regulatory peptides. >Propranolol blocks the tachycardia induced by galanin (1-15) but not by galanin (1-29).
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Propranolol blocks the tachycardia induced by galanin (1-15) but not by galanin (1-29).

机译:普萘洛尔可阻断甘丙肽(1-15)而非甘丙肽(1-29)诱导的心动过速。

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摘要

The efferent pathways involved in the tachycardia induced by intracisternal injections of the N-terminal galanin fragment (1-15) (GAL (1-15)) and galanin (GAL (1-29)) has been evaluated in rats pretreated with the cholinergic antagonist atropine or the beta-antagonist propranolol. The pretreatment with propranolol significantly blocked the tachycardic and vasopressor effect produced by intracisternal injection of GAL (1-15) (p<0.05), but the pretreatment with atropine did not modify these cardiovascular effects. However, the cardiovascular response elicited by GAL (1-29) is modified by the pretreatment with atropine (p<0.05) but not by propranolol. These findings demonstrate that the central cardiovascular action of GAL (1-15), but not GAL (1-29), is mediated by beta-receptor stimulation and this suggests the existence of a different pathway involved in the cardiovascular response produced by the N-terminal galanin fragment as compared with the parent molecule GAL (1-29).
机译:已在接受胆碱能预处理的大鼠中评估了脑池内注射N末端甘丙肽片段(1-15)(GAL(1-15))和甘丙肽(GAL(1-29))诱导的心动过速传出途径拮抗剂阿托品或β-拮抗剂普萘洛尔。普萘洛尔的预处理显着阻断了脑池内注射GAL所产生的心动过速和血管升压作用(1-15)(p <0.05),但阿托品的预处理并未改变这些心血管作用。但是,GAL(1-29)引起的心血管反应可通过阿托品预处理(p <0.05)而不是普萘洛尔进行修饰。这些发现表明,GAL(1-15)而非GAL(1-29)的中枢心血管作用是由β受体刺激介导的,这表明存在由N产生的心血管反应涉及的不同途径-末端甘丙肽片段与亲本分子GAL(1-29)相比。

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