The details and physiologic significance of human renal proximal tubule specific stimulation of Na transport by Angiotensin II

血管紧张素Ⅱ对小鼠近端小管具有双相作用(低浓度刺激和高浓度抑制)，而人血管紧张素Ⅱ单相刺激近曲小管转运。为了阐明这一点，我们测量了人、野生型和cGKII-/-小鼠肾脏PT中NBCe1的活性。在抑制人NO阻断Angii效应的同时，NO供体通过ERK激活NBCe1活性。在野生型小鼠中，高浓度AngII的抑制转变为NO的抑制刺激，而NO供体则抑制NBCe1。提示在人PT中，AngII通过激活NO和ERK而起单相刺激作用，其对血压的调节作用更为重要。

AngII has biphasic effect (stimulation in low concentration and inhibition in high concentration) on mouse proximal tubule (PT) but in human AngII monophasically stimulates PT transport. To clarify this, NBCe1 activity in PT was measured in human, wild-type and cGKII-/- mice kidney. In human inhibition of NO blocked AngII effect, meanwhile NO donor stimulated NBCe1 activity via ERK. In wild-type mice the inhibition by high concentration of AngII changed to stimulation by inhibition of NO, while NO donor suppressed NBCe1. It was suggested that in human PT AngII has monophasic stimulatory effect via NO and consequent ERK activation, and regulation of blood pressure by AngII is more important.