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) All Versions of this Article: 286/3/G377    most recent 00153.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science 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 Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Kovac, J. Articles by Vanner, S. Search for Related Content PubMed PubMed Citation Articles by Kovac, J. Articles by Vanner, S.

MUCOSAL BIOLOGY

Potassium currents regulating secretion from Brunner's glands in guinea pig duodenum

Gastrointestinal Diseases Research Unit, Queen's University, Kingston, Ontario, Canada KL7 5G2

Submitted 2 April 2003 ; accepted in final form 4 November 2003

This study examined the role of outward K⁺ currents in the acinar cells underlying secretion from Brunner's glands in guinea pig duodenum. Intracellular recordings were made from single acinar cells in intact acini in in vitro submucosal preparations, and videomicroscopy was employed in the same preparation to correlate these measures with secretion. Mean resting membrane potential was -74 mV and was depolarized by high external K⁺ (20 mM) and the K⁺ channel blockers 4-aminopyridine (4-AP), quinine, and clotrimazole. The cholinergic agonist carbachol (60–2,000 nM; EC₅₀ = 200 nM) caused a concentration-dependent initial hyperpolarization of the membrane and an associated decrease in input resistance. This hyperpolarization was significantly decreased by 20 mM external K⁺ or membrane hyperpolarization and increased by 1 mM external K⁺ or membrane depolarization. It was blocked by the K⁺ channel blockers tetraethylammonium (TEA), 4-AP, quinine, and clotrimazole but not iberiotoxin. When videomicroscopy was employed to measure dilation of acinar lumen in the same preparation, carbachol-evoked dilations were altered in a parallel fashion when external K⁺ was altered. The dilations were also blocked by the K⁺ channel blockers TEA, 4-AP, quinine, and clotrimazole but not iberiotoxin. These findings suggest that activation of outward K⁺ currents is fundamental to the initiation of secretion from these glands, consistent with the model of K⁺ efflux from the basolateral membrane providing the driving force for secretion. The pharmacological profile suggests that these K⁺ channels belong to the intermediate conductance group.

exocytosis; cholinergic; secretion

This article has been cited by other articles:

				D. Heitzmann and R. Warth Physiology and Pathophysiology of Potassium Channels in Gastrointestinal Epithelia Physiol Rev, July 1, 2008; 88(3): 1119 - 1182. [Abstract] [Full Text] [PDF]