Zhang Zhong, Payne Kristie, Pallone Thomas L
Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland.
Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland
Am J Physiol Renal Physiol. 2014 Jul 1;307(1):F41-52. doi: 10.1152/ajprenal.00178.2014. Epub 2014 Apr 30.
Using dual cell patch-clamp recording, we examined pericyte, endothelial, and myoendothelial cell-to-cell communication in descending vasa recta. Graded current injections into pericytes or endothelia yielded input resistances of 220 ± 21 and 128 ± 20 MΩ, respectively (P < 0.05). Injection of positive or negative current into an endothelial cell depolarized and hyperpolarized adjacent endothelial cells, respectively. Similarly, current injection into a pericyte depolarized and hyperpolarized adjacent pericytes. During myoendothelial studies, current injection into a pericyte or an endothelial cell yielded small, variable, but significant change of membrane potential in heterologous cells. Membrane potentials of paired pericytes or paired endothelia were highly correlated and identical. Paired measurements of resting potentials in heterologous cells were also correlated, but with slight hyperpolarization of the endothelium relative to the pericyte, -55.2 ± 1.8 vs. -52.9 ± 2.2 mV (P < 0.05). During dual recordings, angiotensin II or bradykinin stimulated temporally identical variations of pericyte and endothelial membrane potential. Similarly, voltage clamp depolarization of pericytes or endothelial cells induced parallel changes of membrane potential in the heterologous cell type. We conclude that the descending vasa recta endothelial syncytium is of lower resistance than the pericyte syncytium and that high-resistance myoendothelial coupling also exists. The myoendothelial communication between pericytes and endothelium maintains near identity of membrane potentials at rest and during agonist stimulation. Finally, endothelia membrane potential lies slightly below pericyte membrane potential, suggesting a tonic role for the former to hyperpolarize the latter and provide a brake on vasoconstriction.
我们采用双细胞膜片钳记录技术,研究了直小血管降支中周细胞、内皮细胞和肌内皮细胞之间的细胞间通讯。向周细胞或内皮细胞注入分级电流,测得其输入电阻分别为220±21 MΩ和128±20 MΩ(P<0.05)。向内皮细胞注入正向或负向电流,分别使相邻内皮细胞去极化和超极化。同样,向周细胞注入电流会使相邻周细胞去极化和超极化。在肌内皮细胞研究中,向周细胞或内皮细胞注入电流会使异源性细胞的膜电位发生微小、可变但显著的变化。配对的周细胞或配对的内皮细胞膜电位高度相关且相同。异源性细胞静息电位的配对测量也具有相关性,但内皮细胞相对于周细胞有轻微超极化,分别为-55.2±1.8 mV和-52.9±2.2 mV(P<0.05)。在双记录过程中,血管紧张素II或缓激肽刺激周细胞和内皮细胞膜电位发生时间上相同的变化。同样,对周细胞或内皮细胞进行电压钳去极化会在异源性细胞类型中诱导膜电位的平行变化。我们得出结论,直小血管降支的内皮细胞合体的电阻低于周细胞合体,并且还存在高电阻的肌内皮耦合。周细胞和内皮细胞之间的肌内皮通讯在静息状态和激动剂刺激期间维持膜电位接近相同。最后,内皮细胞膜电位略低于周细胞膜电位,表明前者对后者有超极化的张力作用,并对血管收缩起到制动作用。