Expression and angiotensin II‐induced modulation of KCNQ K+ channels in rat visceral sensory neurons

Abstract

Neurons of the nodose ganglion (NG) play an essential role in transmitting barosensory information to the nucleus tractus solitarius (NTS) in the brainstem, a nucleus critical to autonomic cardiovascular regulation. Recently, NG neurons were found to express M‐type (KCNQ) K+ channels (Wladyka et al., 2006; 2007). We now show that KCNQ channels are expressed in the NTS as well. M‐current densities in NTS neurons (at ‐60 mV) were 0.98 ± 0.1 pA/pF (n=3) and immunostaining analysis revealed expression of at least KCNQ2 subunits. In the NG, M‐current densities of A‐type and C‐type neurons were 1.2 ± 0.2 (n=7) and 0.95 ± 0.11 pA/pF (n=12), with time constants of deactivation of 65 ± 12 and 51 ± 8 ms, respectively. Of 16 cells, angiotensin II (AngII, 500 nM) suppressed M‐current amplitude in 7 neurons by 42 ± 9%. AngII caused translocation of the PLC‐PH‐EGFP probe from membrane to cytoplasm, with an increased cytosolic fluorescence of 46 ± 30% (n=4), demonstrating AngII‐induced hydrolysis of PIP2. Ca2+ imaging showed 9 of 40 NG neurons challenged with AngII to respond with substantial [Ca2+]i increases (340 nm/380 nm ratio 0.15 ± 0.01). The Ca2+ imaging results in NG neurons are similar to those obtained from NTS neurons reported earlier (Tolstykh et al., FASEB 2006). Our data suggest an important role of KCNQ K+ channels in autonomic control of the heart and vascular tone. Supported by AHA grant 0865151F (G.T.) and NIH NS043394 (M.S).