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KMID : 1155520110060040336
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Anesthesia and Pain Medicine
2011 Volume.6 No. 4 p.336 ~ p.341
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Mechanism of vasodilation by propofol in the rabbit renal artery
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Park Seung-Yong
Jung Il
Kwon Seong-Chun
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Abstract
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Background: Propofol directly inhibits vascular reactivity. However, available information regarding the underlying mechanisms of propofol is poor. Therefore, mechanisms of the underlying relaxant action of propofol were investigated using rabbit renal arteries.
Methods: Propofol-induced relaxation of rabbit renal arteries was studied in contracted preparations with 50 mM KCl or 10?M histamine. Vessel tension was recorded with a pen recorder. We were interested in determining whether propofol-induced vasodilation is affected by endothelium-denudation, L-NG-nitroarginine methyl ester (L-NAME), tetraethylammonium (TEA), iberiotoxin, glibenclamide, 4-aminopyridine, 7-ethoxyresorufin, caffeic acid, baiclalein, ryanodine, and thapsigargin.
Results: Propofol-induced concentration-dependent vasodilation was not affected either by endothelium denudation or by L-NAME during histamine-induced contraction. The relaxing effect of propofol on histamine-induced contraction was inhibited by either TEA, a K＋ channel inhibitor, or iberiotoxin (100 nM), a selective blocker of the large conductance Ca2＋-activated K＋ channel (BKCa channel). In contrast, the relaxing effect of propofol was unaffected by 10?M glibenclamide, an ATP-sensitive K＋ channel blocker, by 5 mM 4-aminopyridine, a blocker of delayed rectifier, by 7-ethoxyresorufin, a cytochrome P450 inhibitor, by 10?M caffeic acid and 10?M baiclalein, lipooxygenase inhibitors, or by 10?M ryanodine and thapsigargin, Ca2＋store inhibitors.
Conclusions: These results suggest that the relaxant effect of propofol may result from activation of BKCa channels by inhibiting voltage-gated Ca2＋ influx in a prolonged manner.
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KEYWORD
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Ca2＋-activated K＋ channel, Propofol, Renal artery, Vasodilation
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