Journal
NEUROPEPTIDES
Volume 43, Issue 3, Pages 193-199Publisher
CHURCHILL LIVINGSTONE
DOI: 10.1016/j.npep.2009.04.003
Keywords
Spike frequency accommodation; Potassium current; Patch clamp; Action potential; Blood pressure
Categories
Ask authors/readers for more resources
The octapeptide angiotensin II (ANG II) plays a pivotal role in the maintenance of blood pressure by activating ANG II receptors located in variety of cell types including neurons housed in the central nervous system (CNS) and in the peripheral nervous system (PNS). ANG II (100 nM) blocked spike frequency accommodation (SFA) recorded with whole-cell patch technique in acutely isolated nodose ganglion neurons (NGN) from adult rats. ANG II increased the frequency of action potentials (AP) produced by supra-maximal 500 ms depolarizing currents recorded in both tonic (16 Hz vs. 58 Hz, control vs. ANG II perfusion respectively, n = 9) and phasic (1 Hz vs. 38 Hz, n = 13) NGNs. ANG II produced no significant changes in: the resting membrane potential (-51 mV vs. -50 mV, n = 65), AP overshoot (46 mV vs. 41 mV, n = 25). AP undershoot (-65 mV vs. -61 mV, n = 25), AP duration (1 ms vs. 1.2 ms, n = 25), and AP threshold (-40 mV vs. -43 mV, n = 19). CV-11974 (600 nM), a specific AT1 receptor antagonist, prevented ANG II-evoked changes SFA (n = 10). ANG II (100 nM) had no significant effect on total outward potassium current (I-K) but inhibited a fast activating and fast inactivating I-K recorded in the presence of TEA. A kinetically similar I-K was also inhibited by 4-AP (3 mM). In phasic NGNs, 4-AP occluded the effects of 100 nM ANG II on SFA. Our results indicate that ANG II can block an A-type of I-K and that this effect may underlie the ANG II-mediated change in SFA. (C) 2009 Published by Elsevier Ltd.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available