AT2R and Sympathetic Outflow

Role of AT 2 R (Angiotensin Type 2 Receptor) in Maintaining Sodium-Potassium Balance

“…Compared to that discussing the role of AT 2 R in Na + excretion, literature describing the effect of AT 2 R on the K + channel is limited only to neuronal cells 3 and the renal outer medullary K + channel 4 in the cortical collecting duct. Wu et al 5 reported important and relevant information in the field of AT 2 R and K + excretion through a patch-clamp and renal clearance study published in the current issue of Hypertension .…”

“…They showed that AT 2 R activation by the AT 2 R agonist, CGP42112a, inhibited the activity of the basolateral 40-pS K + channel (a Kir4.1/Kir5.1 heteromer) in the DCT (Fig.1), and the AT 2 R antagonist, PD123319, stimulated the activity of this K + channel. The inhibitory effect of AT 2 R on the K + channel activity would be definite if the CGP42112a response was blocked by PD123319 or by an inhibitor of Src homology region 2 domain-containing phosphatase-1 (SHP-1), which is a downstream signaling component of AT 2 R. Furthermore, ang-II inhibited the K + channel only when AT 1 R was blocked, 3 although it is surprising that ang-II alone had no effect on the channel activity. Another study 6 performed on the thick ascending limb revealed that there was no effect of ang-II on the 50-pS K + channel activity while AT 1 R was blocked with losartan.…”