首页> 外文期刊>Life sciences >Beta1-adrenergic receptor activation decreases ANP release via cAMP-Ca2+ signaling in perfused beating rabbit atria.
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Beta1-adrenergic receptor activation decreases ANP release via cAMP-Ca2+ signaling in perfused beating rabbit atria.

机译:Beta1肾上腺素受体激活通过灌注的跳动兔心房通过cAMP-Ca2 +信号传导减少ANP释放。

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AIMS: Although a beta-adrenoceptor (beta-AR) blockade-induced increase in plasma atrial natriuretic peptide (ANP) levels is implicated in the therapeutic significance of beta-AR antagonists, the role of beta-AR in the regulation of ANP release is not clearly defined. The purpose of the present study was to define the role of beta-AR subtypes and the mechanisms responsible for regulation of atrial ANP release. MAIN METHODS: Experiments were performed in isolated perfused beating rabbit atria, including measurement of atrial contractile response, cAMP efflux, and atrial myocyte ANP release. KEY FINDINGS: beta-AR activation with (-)-isoproterenol decreased ANP release concomitantly with increases in cAMP efflux concentration, atrial dynamics, stroke volume and pulse pressure in a concentration-dependent manner. The ANP response was inversely related to the change in cAMP efflux concentrations. The isoproterenol-induced decrease in ANP release was inhibited by beta(1)-AR blockade with CGP 20712A but not by beta(2)-AR blockade with ICI 118551. The isoproterenol-induced decrease in ANP release was attenuated by the L-type Ca(2+) channel antagonist nifedipine and the cAMP-dependent protein kinase inhibitor KT5720. SIGNIFICANCE: These findings suggest that beta(1)-AR activation decreases ANP release via cAMP- and Ca(2+)-dependent mechanisms.
机译:目的:尽管β-肾上腺素受体(β-AR)阻断引起的血浆心钠素水平升高与β-AR拮抗剂的治疗意义有关,但β-AR在调节ANP释放中的作用是没有明确定义。本研究的目的是确定β-AR亚型的作用以及负责调节心房ANP释放的机制。主要方法:实验是在孤立的灌注搏动的兔心房中进行的,包括测量心房收缩反应,cAMP外排和心房肌细胞ANP释放。主要发现:(-)-异丙肾上腺素的β-AR激活以浓度依赖的方式随着cAMP外排浓度,心房动力学,中风量和脉压的增加而降低了ANP的释放。 ANP反应与cAMP外排浓度的变化成反比。异丙肾上腺素诱导的ANP释放减少受到CGP 20712A的beta(1)-AR阻断的抑制,但不受ICI 118551的beta(2)-AR阻断的抑制。L型减弱了异丙肾上腺素诱导的ANP释放的降低。 Ca(2+)通道拮抗剂硝苯地平和cAMP依赖性蛋白激酶抑制剂KT5720。意义:这些发现表明,β(1)-AR激活通过cAMP-和Ca(2+)依赖性机制降低ANP释放。

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