Effects of substance P on rate and perfusion pressure in the isolated guinea pig heart.
Effects of substance P on rate and perfusion pressure in the isolated guinea pig heart.
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发表时间：
1990
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通讯作者：
D. Hoover
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作者：
D. Hoover
本文观察了豚鼠离体心脏对P物质（SP）的负性变时反应和舒张反应。推注2.5，25和125 nmol的SP引起剂量依赖性心动过缓，最大剂量降低心率的53%的基线。1 μ M阿托品预处理阻断了对25 nmol SP的负性变时反应。0.5 μ M新斯的明预处理降低了基线心率并增强了对25 nmol SP的负性变时反应。在用1 μ M [Arg8]加压素或40 mM KCl升高基线灌注压后，证明了对SP的有效血管扩张反应。SP的血管扩张作用具有剂量依赖性，并且在比影响心率所需的剂量低得多的剂量下发生。两种制剂的血管舒张ED 50均小于1 pmol。在心脏血管紧张度增加的加压素，阿托品（1 μ M）减少了最大的血管扩张反应，SP的23%，但无论是阿托品也没有组合的10 μ M西咪替丁和1 μ M扑尔敏影响的ED 50为SP。这些结果表明，SP引起心动过缓刺激胆碱能神经元和冠状动脉血管扩张的一些机制，不涉及乙酰胆碱或组胺。然而，乙酰胆碱可能有助于对SP的最大血管扩张反应。
Negative chronotropic and vasodilator responses of the isolated perfused guinea pig heart to substance P (SP) were evaluated. Bolus injections of 2.5, 25 and 125 nmol of SP caused a dose-dependent bradycardia, with the largest dose decreasing heart rate by 53% of base line. Pretreatment with 1 microM atropine blocked the negative chronotropic response to 25 nmol of SP. Pretreatment with 0.5 microM neostigmine lowered base-line heart rate and potentiated the negative chronotropic response to 25 nmol of SP. A potent vasodilator response to SP was demonstrated after elevation of base-line perfusion pressure with 1 microM [Arg8]vasopressin or 40 mM KCl. The vasodilator effect of SP was dose-dependent and occurred at much lower doses than required to affect heart rate. The ED50 for vasodilation was less than 1 pmol in both preparations. In hearts with vascular tone increased by vasopressin, atropine (1 microM) decreased the maximum vasodilator response to SP by 23%, but neither atropine nor a combination of 10 microM cimetidine and 1 microM chlorpheniramine affected the ED50 for SP. These results suggest that SP causes bradycardia by stimulating cholinergic neurons and coronary vasodilation by some mechanism not involving either acetylcholine or histamine. Acetylcholine may, however, contribute to the maximum vasodilator response to SP.