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: 287/1/R161    most recent 00609.2003v1 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 ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Akiyama, T. Articles by Sunagawa, K. Search for Related Content PubMed PubMed Citation Articles by Akiyama, T. Articles by Sunagawa, K.

NEUROHUMORAL CONTROL OF CIRCULATION AND HYPERTENSION

Effects of Ca²⁺ channel antagonists on acetylcholine and catecholamine releases in the in vivo rat adrenal medulla

¹Department of Cardiac Physiology and ²Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Suita, Osaka 565–8565, Japan

Submitted 20 October 2003 ; accepted in final form 13 March 2004

To elucidate the types of voltage-dependent Ca²⁺ channels controlling ACh and catecholamine releases in the in vivo adrenal medulla, we implanted microdialysis probes in the left adrenal medulla of anesthetized rats and investigated the effects of Ca²⁺ channel antagonists on ACh, norepinephrine, and epinephrine releases induced by nerve stimulation. The dialysis probes were perfused with Ringer solution containing a cholinesterase inhibitor, neostigmine. The left splanchnic nerves were electrically stimulated at 2 and 4 Hz before and after intravenous administration of Ca²⁺ channel antagonists. -Conotoxin GVIA (an N-type Ca²⁺ channel antagonist, 10 µg/kg) inhibited ACh release at 2 and 4 Hz by 40%, norepinephrine release at 4 Hz by 50%, and epinephrine release at 2 and 4 Hz by 45%. A fivefold higher dose of -conotoxin GVIA (50 µg/kg) did not further inhibit these releases. -Conotoxin MVIIC (a P/Q-type Ca²⁺ channel antagonist, 50 µg/kg) inhibited ACh and epinephrine releases at 4 Hz by 30%. Combined -conotoxin GVIA (50 µg/kg) and MVIIC (250 µg/kg) inhibited ACh release at 2 and 4 Hz by 70% and norepinephrine and epinephrine releases at 2 and 4 Hz by 80%. Nifedipine (an L-type Ca²⁺ channel antagonist, 300 and 900 µg/kg) did not change ACh release at 2 and 4 Hz; however, nifedipine (300 µg/kg) inhibited epinephrine release at 4 Hz by 20%, and nifedipine (900 µg/kg) inhibited norepinephrine and epinephrine releases at 4 Hz by 30%. In conclusion, both N- and P/Q-type Ca²⁺ channels control ACh release on preganglionic splanchnic nerve endings while L-type Ca²⁺ channels do not. L-type Ca²⁺ channels are involved in norepinephrine and epinephrine releases on chromaffin cells.

anesthetized rats; microdialysis; norepinephrine; epinephrine; preganglionic autonomic nerve endings