Laboratory of Tissue Biology and Therapeutic Engineering, UMR 5305 CNRS, University Lyon 1, France.
Laboratory of Tissue Biology and Therapeutic Engineering, UMR 5305 CNRS, University Lyon 1, France; Institute of Pharmaceutical and Biological Sciences, University Lyon 1, France.
Microvasc Res. 2018 Jan;115:44-51. doi: 10.1016/j.mvr.2017.08.007. Epub 2017 Aug 30.
We have reported a novel relationship involving mechanical stimulation and vasodilation in rodent and human skin, referred to as pressure-induced vasodilation (PIV). It is unknown whether this mechanism exists in kidney and reflects the microcirculation in deep organs. Therefore, we compared the skin and kidney PIV to determine whether their changes were similar.
In anesthetized mice fed a normal salt-diet, laser Doppler flux (LDF) signals were measured when an increase in local pressure was applied to the surface of the head skin with the rate of 2.2Pa/s (1mmHg/min) and to the left kidney with a rate of 4.4Pa/s (2mmHg/min). The mechanism underlying renal PIV was also investigated. The skin and kidney PIV were also compared during salt load (4% NaCl diet).
The kidney had higher baseline LDF and vascular conductance compared to those of the skin. Pressure application increased the LDF in the kidney as well as in the skin with a comparable maximal magnitude (about 25% from baseline value), despite different kinetics of PIV evolution. As we previously reported in the skin, the kidney PIV response was mediated by the activation of transient receptor potential vanilloid type 1 channels, the release of calcitonin gene-related peptide, and the participation of prostaglandins and nitric oxide. In the absence of hypertension, high salt intake abolished the cutaneous PIV response and markedly impaired the renal one.
PIV response in the mouse kidney results from a neuro-vascular interaction. Despite some differences between the skin and the kidney PIV, the similarities in their response and signaling mechanisms suggest that the cutaneous microcirculation could reflect, in part, the microcirculation of the renal cortex.
我们曾报道过一种涉及啮齿动物和人类皮肤的机械刺激和血管舒张的新型关系，称为压力诱导的血管舒张（PIV）。目前尚不清楚该机制是否存在于肾脏中并反映深部器官的微循环。因此，我们比较了皮肤和肾脏 PIV，以确定它们的变化是否相似。
在给予正常盐饮食的麻醉小鼠中，当以 2.2Pa/s（1mmHg/min）的速率向头部皮肤表面施加局部压力增加（1mmHg/min），或以 4.4Pa/s（2mmHg/min）的速率向左侧肾脏施加局部压力增加时，测量激光多普勒通量（LDF）信号。还研究了肾脏 PIV 的发生机制。在盐负荷（4%NaCl 饮食）期间还比较了皮肤和肾脏 PIV。
与皮肤相比，肾脏具有更高的基线 LDF 和血管传导率。与皮肤相比，尽管 PIV 演变的动力学不同，但施加压力会增加肾脏和皮肤中的 LDF，其最大幅度相当（约为基线值的 25%）。与我们之前在皮肤中报道的情况一样，肾脏 PIV 反应是由瞬时受体电位香草酸型 1 通道的激活、降钙素基因相关肽的释放以及前列腺素和一氧化氮的参与介导的。在没有高血压的情况下，高盐摄入会消除皮肤 PIV 反应，并显著损害肾脏 PIV 反应。
小鼠肾脏的 PIV 反应是神经血管相互作用的结果。尽管皮肤和肾脏 PIV 之间存在一些差异，但它们的反应和信号机制的相似性表明，皮肤微循环在一定程度上反映了肾脏皮质的微循环。
