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首页> 外文期刊>American Journal of Physiology >Frequency modulation of renal myogenic autoregulation by perfusion pressure.
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Frequency modulation of renal myogenic autoregulation by perfusion pressure.

机译:灌注压力对肾脏肌原性自动调节的频率调节。

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Recent studies of renal autoregulation have shown modulation of the faster myogenic mechanism by the slower tubuloglomerular feedback and that the modulation can be detected in the dynamics of the myogenic mechanism. Conceptual and empirical considerations suggest that perfusion pressure may modulate the myogenic mechanism, although this has not been tested to date. Here we present data showing that the myogenic operating frequency, assessed by transfer-function analysis, varied directly as a function of perfusion pressure in the hydronephrotic kidney perfused in vitro over the range from 80 to 140 mmHg. A similar result was obtained in intact kidneys in vivo when renal perfusion pressure was altered by systemic injection of N(G)-nitro-L-arginine methyl ester (L-NAME). When perfusion pressure was not allowed to increase, L-NAME did not affect the myogenic operating frequency despite equivalent reduction of renal vascular conductance. Blood-flow dynamics were assessed in the superior mesenteric artery before and after L-NAME. In this vascular bed, the operating frequency of the myogenic mechanism was not affected by perfusion pressure. Thus the operating frequency of the renal myogenic mechanism is modulated by perfusion pressure independently of tubuloglomerular feedback, and the data suggest some degree of renal specificity of this response.
机译:肾自调节的最新研究表明,较慢的肾小管肾小球反馈调节了较快的肌发生机制,并且该调节可在肌发生机制的动力学中检测到。从概念和经验上的考虑,尽管目前尚未进行测试,但灌注压力可能会调节肌源性机制。在这里,我们提供的数据显示,通过传递功能分析评估的成肌操作频率直接随灌注压力在80到140 mmHg范围内直接变化为在体外肾积水的肾功能。当通过全身性注射N(G)-硝基-L-精氨酸甲酯(L-NAME)改变肾脏灌注压力时,在体内完整肾脏中获得了相似的结果。当不允许增加灌注压力时,尽管肾脏血管传导相应降低,但L-NAME并未影响成肌操作频率。在L-NAME之前和之后评估肠系膜上动脉的血流动力学。在该血管床中,成肌机制的操作频率不受灌注压力的影响。因此,由灌注压力独立于肾小球肾小球反馈调节肾肌发生机制的工作频率,并且数据表明该反应的某种程度的肾特异性。

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