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) A corrigendum has been published All Versions of this Article: 285/3/R682    most recent 00123.2003v1 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 (5) Citing Articles via Google Scholar Google Scholar Articles by Jelson, G. S. Articles by Hardwick, J. C. Search for Related Content PubMed PubMed Citation Articles by Jelson, G. S. Articles by Hardwick, J. C.

CARDIAC, RENAL, AND RESPIRATORY INTEGRATION

Modulation of guinea pig intrinsic cardiac neurons by prostaglandins

Department of Biology, Ithaca College, Ithaca, New York 14850

Submitted 7 March 2003 ; accepted in final form 29 May 2003

Activation of cardiac mast cells has been shown to alter parasympathetic neuronal function via the activation of histamine receptors. The present study examined the ability of prostaglandins to alter the activity of guinea pig intracardiac neurons. Intracellular voltage recordings from whole mounts of the cardiac plexus showed that antigen-mediated mast cell degranulation produces an attenuation of the afterhyperpolarization (AHP), which was prevented by the phospholipase A₂ inhibitor 5,8,11,14-eicosatetraynoic acid. Exogenous application of either PGD₂ or PGE₂ produced a biphasic change in the membrane potential and an inhibition of both AHP amplitude and duration. Examination of prostanoid receptors using bath perfusions (1 µM PGE₂ and PGD₂), specific agonists (BW245C, sulprostone, and butaprost), and antagonists (AH6809 and SC19220) found evidence for both the PGE₂-specific EP2 and EP3 receptors, but not for EP1 or the PGD₂-specific prostanoid (DP) receptors. Sulprostone was able to mimic the PGE₂ responses in some cells, but not in all PGE₂-sensitive cells. Butaprost was able to mimic the PG-induced hyperpolarization in some cells, but did not alter the AHP. Inhibition of specific potassium channels with either TEA, charybdotoxin, or apamin showed that neither TEA nor charybdotoxin could prevent the PGE₂-induced AHP attenuation. Apamin alone inhibited AHP duration, with PGs having no further effect in these cells. These results demonstrate that guinea pig intracardiac neurons can be modulated by PG, most likely through either EP2, EP3, or potentially EP4 receptors, and this response is due, at least in part, to a reduction in small-conductance K_Ca currents.

parasympathetic; prostaglandin E₂; prostaglandin D₂; prostanoid receptor; K channels

This article has been cited by other articles:

				J. C. Hardwick, C. N. Baran, E. M. Southerland, and J. L. Ardell Remodeling of the guinea pig intrinsic cardiac plexus with chronic pressure overload Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2009; 297(3): R859 - R866. [Abstract] [Full Text] [PDF]

				J. C. Hardwick, E. M. Southerland, and J. L. Ardell Chronic myocardial infarction induces phenotypic and functional remodeling in the guinea pig cardiac plexus Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2008; 295(6): R1926 - R1933. [Abstract] [Full Text] [PDF]

				J. C. Hardwick, A. F. Kotarski, and M. J. Powers Ionic mechanisms of histamine-induced responses in guinea pig intracardiac neurons Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2006; 290(1): R241 - R250. [Abstract] [Full Text] [PDF]