Mechanism of vasodilation by propofol in the rabbit renal artery

Park, Seung Yong; Jung, Il; Kwon, Seong Chun

Clinical Research

Anesthetic Pharmacology

Anesthesia and Pain Medicine 2011;6(4):336-341.
Published online October 31, 2011.

Mechanism of vasodilation by propofol in the rabbit renal artery

Seung Yong Park, Il Jung, Seong Chun Kwon

¹Department of Anesthesiology and Pain Medicine, Gangneung Asan Hospital, University of Ulsan College of Medicine, Gangneung, Korea. tourji@naver.com
²Department of Physiology, Kwandong University College of Medicine, Gangneung, Korea.

Abstract

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 10microM 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 Ca(2+)-activated K+ channel (BKCa channel). In contrast, the relaxing effect of propofol was unaffected by 10microM 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 10microM caffeic acid and 10microM baiclalein, lipooxygenase inhibitors, or by 10microM 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.

Key Words: Ca(2+)-activated K+ channel, Propofol, Renal artery, Vasodilation