HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Supplemental Data Supplemental Data All Versions of this Article: 564/2/475    most recent jphysiol.2004.080960v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jiang, Z.-G. Articles by Yang, Y.-Q. Search for Related Content PubMed PubMed Citation Articles by Jiang, Z.-G. Articles by Yang, Y.-Q.

¹ Oregon Hearing Research Center, Oregon Health and Science University, Portland, OR 97239, USA
² Department of Otolaryngology, Eye Ear Nose and Throat Hospital, Fudan University, Shanghai, PR China
³ Department of Physiology, Shihezi University Medical College, Xinjiang, PR China

The physiological basis of ACh-elicited hyperpolarization in guinea-pig in vitro cochlear spiral modiolar artery (SMA) was investigated by intracellular recording combined with dye labelling of recorded cells and immunocytochemistry. We found the following. (1) The ACh-hyperpolarization was prominent only in cells that had a low resting potential (less negative than –60 mV). ACh-hyperpolarization was reversibly blocked by 4-DAMP, charybdotoxin or BAPTA-AM, but not by N-nitro-L-arginine methyl ester, glipizide, indomethacin or 17-octadecynoic acid. (2) Ba²⁺ (100 µM) and ouabain (1 µM) each attenuated ACh-hyperpolarization by 30% in smooth muscle cells (SMCs) but had only slight or no inhibition in endothelial cells (ECs). A combination of Ba²⁺ and 18ß-glycyrrhetinic acid near completely blocked the ACh-hyperpolarization in SMCs. (3) High K⁺ (10 mM) induced a smaller hyperpolarization in ECs than in SMCs, with an amplitude ratio of 0.49 : 1. Ba²⁺ blocked the K⁺-induced hyperpolarization by 85% in both cell types, whereas ouabain inhibited K⁺-hyperpolarization differently in SMCs (19%) and ECs (35%) and increased input resistance. 18ß-Glycyrrhetinic acid blocked the high K⁺-hyperpolarization in ECs only. (4) Weak myoendothelial dye coupling was detected by confocal microscopy in cells recorded with a propidium iodide-containing electrode for longer than 30 min. A sparse plexus of choline acetyltransferase-immunoreactive (ChAT) fibres was observed around the SMA and its up-stream arteries. (5) Evoked excitatory junction potentials (EJP) were partially blocked by 4-DAMP in half of the cells tested. We conclude that ACh-induced hyperpolarization originates from ECs via activation of Ca²⁺-activated potassium channels, and is independent of the release of NO, cyclo-oxygenase or cytochrome P450 products. ACh-induced hyperpolarization in smooth muscle cells involves two mechanisms: (a) electrical spread of the hyperpolarization from the endothelium, and (b) activation of inward rectifier K⁺ channels (K_ir) and Na⁺–K⁺ pump current by elevated interstitial K⁺ released from the endothelial cells, these being responsible for about 60% and 40% of the hyperpolarization, respectively. The role ratio of K_ir and pump current activation is at 8 : 1 or less.

(Received 9 December 2004; accepted after revision 21 February 2005; first published online 24 February 2005)
Corresponding author Z.-G. Jiang: Oregon Hearing Research Center, NRC04, Oregon Health & Science University, Portland, OR 97239, USA. Email: jiangz{at}ohsu.edu

This article has been cited by other articles:

				Z.-G. Jiang, X.-R. Shi, B.-C. Guan, H. Zhao, and Y.-Q. Yang Dihydropyridines Inhibit Acetylcholine-Induced Hyperpolarization in Cochlear Artery via Blockade of Intermediate-Conductance Calcium-Activated Potassium Channels J. Pharmacol. Exp. Ther., February 1, 2007; 320(2): 544 - 551. [Abstract] [Full Text] [PDF]