NDLI: Dual mechanisms of angiotensin-induced activation of mouse sympathetic neurones

Content Provider	PubMed Central
Author	Bielefeldt, K. Tan, Z. Y. Whiteis, C. A. Abboud, F. M. Chapleau, M. W. Ma, X. Snitsarev, V.
Copyright Year	2006
Abstract	Ang II directly activates neurones in sympathetic ganglia. Our goal was to define the electrophysiological basis of this activation. Neurones from mouse aortic–renal and coeliac ganglia were identified as either ‘tonic’ or ‘phasic’. With injections of depolarizing currents, action potentials (APs) were abundant and sustained in tonic neurones (TNs) and scarce or absent in phasic neurones (PNs). Resting membrane potentials were equivalent in TNs (−48 ± 2 mV, n = 18) and PNs (−48 ± 1 mV, n = 23) while membrane resistance was significantly higher in TNs. Ang II depolarized and increased membrane resistance equally in both TNs (n = 8) and PNs (n = 8) but it induced APs only in TNs, and enhanced current-evoked APs much more markedly in TNs (P < 0.05). The AT1 receptor antagonist losartan (2 μm, n = 6) abolished all responses to Ang II, whereas the AT2 receptor blocker PD123,319 had no effect. The transient K+ current (IA), which was more than twice as large in TNs as in PNs, was significantly inhibited by Ang II in TNs only whereas the delayed sustained K+ current (IK), which was comparable in both TNs and PNs, was not inhibited. M currents were more prominent in PNs and were inhibited by Ang II. The IA channel blocker 4-aminopyridine triggered AP generation in TNs and prevented the Ang II-induced APs but not the depolarization. Blockade of M currents by oxotremorine M or linopirdine prevented the depolarizing action of Ang II. The protein kinase C (PKC) inhibitor H7 (10 μm, n = 9) also prevented the Ang II-induced inhibition of IA and the generation APs but not the depolarization nor the inhibition of M currents. Conversely, the PKC agonist phorbol 12-myristate 13-acetate mimicked the Ang II effects by triggering APs. The results indicate that Ang II may increase AP generation in sympathetic neurones by inducing a PKC-dependent inhibition of IA currents, and a PKC-independent depolarization through inhibition of M currents. The differential expression of various K+ channels and their sensitivity to phosphorylation by PKC may determine the degree of activation of sympathetic neurones and hence may influence the severity of the hypertensive response.
Related Links	http://dx.doi.org/10.1113/jphysiol.2006.106716
Ending Page	63
Page Count	19
Starting Page	45
File Format	PDF
ISSN	00223751
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 1
Volume Number	573
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2006-05-15
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

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