TITLE

Vasorelaxant mechanisms of ketamine in rabbit renal artery

AUTHOR(S)
Il Jung; Sung Hwan Jung
PUB. DATE
December 2012
SOURCE
Korean Journal of Anesthesiology;Dec2012, Vol. 63 Issue 6, p533
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Background: Ketamine is a non-barbiturate anesthetic agent which has various effects on the cardiovascular system. Among them, ketamine is known for its hypotensive properties. The hypotension is thought to be mediated by a direct effect on vascular smooth muscles. This study is designed to examine the effects of ketamine on KCl- and histamine-induced contraction in isolated rabbit renal arteries. Methods: Endothelium-intact or -denuded smooth muscle rings were prepared and mounted in myographs for isometric tension measurements. The inhibitory effect of ketamine were investigated in smooth muscle rings precontracted with either 50 mM KCl- or 10 µM histamine. Results: Ketamine (0.1-100 µg/ml) produced similar concentration-dependent inhibition of contractile responses induced by either 50 mM KCl or 10 µM histamine. The respective IC50 values measured for ketamine following precontractions by 50 mM KCl and 10 µM histamine were 28.9 µg/ml (105.5 µM) and 26.7 µg/ml (97.5 µM). The inhibitory effect of 30 µg/ml ketamine were similarly observed after removal of endothelium or pretreatment with NG-Nitroarginine Methyl Ester (0.1 mM). The inhibitory effect of 30 µg/ml ketamine on histamine-evoked contraction was reduced by either tetraethylammonium (10 mM) or iberiotoxin, a large conductance Ca2+-activated K+ channel blocker. However, depletion of intracellular Ca2+ stores by ryanodine (10 µM) or thapsigargin (10 µM) showed no significant effect on 30 µg/ml ketamine-induced relaxation. Pre-incubation with 30 µg/ml ketamine significantly inhibited CaCl2-induced contraction at almost all ranges of concentration. Conclusions: Ketamine-induced relaxation of rabbit renal arteries is mediated by both the activation of large conductance Ca2+-activated K+ channel and the inhibition of Ca2+ influx.
ACCESSION #
88001180

 

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