实验性肾衰竭中保留内皮依赖性但受损的β -肾上腺素能松弛血管。

Pasi Jolma, Jarkko Kalliovalkama, Jari-Petteri Tolvanen, Peeter Kööbi, Mika Kähönen, Heikki Saha, Ilkka Pörsti
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引用次数: 11

摘要

慢性肾衰竭与心血管发病率增加和动脉弹性降低有关。关于尿毒症对耐药动脉的功能影响的资料很少。因此,我们研究了肾功能衰竭对大鼠肠系膜小血管的影响。在5/6肾切除术或假手术后6周用Mulvany肌图观察动脉环的反应。肾大部切除术导致血浆尿素氮升高1.9倍,但对血压无显著影响。在尿毒症大鼠的抵抗血管中,主要通过动脉K(+)通道介导的内皮依赖性松弛得以保留。通过外源性一氧化氮和atp敏感的K(+)通道打开介导的内皮非依赖性血管松弛也没有变化。然而,异丙肾上腺素诱导的反应略有减弱,表明实验性肾功能衰竭时β -肾上腺素受体的松弛功能受损。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Preserved endothelium-dependent but impaired beta-adrenergic relaxation of the resistance vessels in experimental renal failure.

Chronic renal failure is associated with increased cardiovascular morbidity and reduced arterial elasticity. Only little information is available on the functional effects of uraemia on resistance arteries. Therefore, we studied the influence of renal failure on rat small mesenteric vessels. The responses of arterial rings were investigated in a Mulvany myograph 6 weeks after 5/6 nephrectomy or sham operation. The subtotal nephrectomy resulted in a 1.9-fold elevation of plasma urea nitrogen but was without significant effect on blood pressure. Endothelium-dependent relaxations, largely mediated via arterial K(+) channels, were preserved in the resistance vessels of uraemic rats. Endothelium-independent vasorelaxations, mediated via exogenous nitric oxide and the opening of ATP-sensitive K(+) channels, were also unchanged. However, the responses induced by isoprenaline were slightly reduced, indicating impaired relaxation via beta-adrenoceptors in experimental renal failure.

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