Dynamics and contribution of mechanisms mediating renal blood flow autoregulation

Dynamics and contribution of mechanisms mediating renal blood flow autoregulation
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DOI:
10.1152/ajpregu.00766.2002
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发表时间:
2003-09-01
影响因子:
2.8
通讯作者:
Arendshorst, WJ
Arendshorst, WJ
中科院分区:
医学3区
文献类型:
--
作者:
Just, A;Arendshorst, WJ

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我们研究了大鼠肾血流量(RBF)自动调节的动态特征以及自动调节压力范围内潜在机制的相对贡献。肾上主动脉缩窄60 s后迅速释放肾动脉压(RAP)。在快速阶跃降低和RAP升高后评估肾血管阻力(RVR)的变化。作为对升高的反应,RVR最初下降5-10%,随后增加约20%,反映了93%的自动调节效率(AE)。在最初的7-9秒内,RVR上升到总响应的55%,提供37%的AE,在2.2秒时达到最大速度。第二次RVR增加开始于7-9秒,并在10-15秒达到最大速度。反应时间表明,初始RVR反映了肌源性反应和次级肾小管肾小球反馈(TGF)。在呋塞米抑制TGF时,AE为64%。最初的RVR上升加速和增强,提供49%的AE,但它只占总数的88%。剩下的12%表示第三个监管组成部分。当RAP的增加开始低于自动调节范围时,后者的贡献高达50%。乙酰唑胺增加TGF既不影响AE也不影响相对肌源性贡献。地尔硫卓可明显抑制AE和原发性和继发性RVR的增加,但留下一个缓慢的组成部分。在响应RAP减少,初始血管舒张占总反应的73%,但不受呋塞米。第三部分的贡献率为9%。因此,RBF自动调节主要是由于肌源性反应和TGF,对RAP升高的反应贡献55%和33-45%,对RAP降低的反应贡献73%和18-27%。这些数据表明TGF和肌源性反应之间的相互作用影响RAP上升期间肌源性反应的强度和速度。数据表明,第三种监管体系有助于
We investigated dynamic characteristics of renal blood flow (RBF) autoregulation and relative contribution of underlying mechanisms within the autoregulatory pressure range in rats. Renal arterial pressure ( RAP) was reduced by suprarenal aortic constriction for 60 s and then rapidly released. Changes in renal vascular resistance (RVR) were assessed following rapid step reduction and RAP rise. In response to rise, RVR initially fell 5-10% and subsequently increased similar to20%, reflecting 93% autoregulatory efficiency (AE). Within the initial 7-9 s, RVR rose to 55% of total response providing 37% AE, reaching maximum speed at 2.2 s. A secondary RVR increase began at 7-9 s and reached maximum speed at 10-15 s. Response times suggest that the initial RVR reflects the myogenic response and the secondary tubuloglomerular feedback (TGF). During TGF inhibition by furosemide, AE was 64%. The initial RVR rise was accelerated and enhanced, providing 49% AE, but it represented only 88% of total. The remaining 12% indicates a third regulatory component. The latter contributed up to 50% when the RAP increase began below the autoregulatory range. TGF augmentation by acetazolamide affected neither AE nor relative myogenic contribution. Diltiazem infusion markedly inhibited AE and the primary and secondary RVR increases but left a slow component. In response to RAP reduction, initial vasodilation constituted 73% of total response but was not affected by furosemide. The third component's contribution was 9%. Therefore, RBF autoregulation is primarily due to myogenic response and TGF, contributing 55% and 33-45% in response to RAP rise and 73% and 18-27% to RAP reduction. The data imply interaction between TGF and myogenic response affecting strength and speed of myogenic response during RAP rises. The data suggest a third regulatory system contributing