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Activation of the K+ channel BKCa is involved in the relaxing effect of propofol on coronary arteries

Published online by Cambridge University Press:  23 December 2004

A. P. Klockgether-Radke ,
H. Schulze ,
P. Neumann  and
G. Hellige
A. P. Klockgether-Radke
Affiliation:
Georg-August University of Göttingen, Centre of Anaesthesiology, Emergency and Intensive Care Medicine, Göttingen, Germany
H. Schulze
Affiliation:
Georg-August University of Göttingen, Centre of Anaesthesiology, Emergency and Intensive Care Medicine, Göttingen, Germany
P. Neumann
Affiliation:
Georg-August University of Göttingen, Centre of Anaesthesiology, Emergency and Intensive Care Medicine, Göttingen, Germany
G. Hellige
Affiliation:
Georg-August University of Göttingen, Centre of Anaesthesiology, Emergency and Intensive Care Medicine, Göttingen, Germany
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Abstract

Summary

Background and objective: Propofol may cause undesirable hypotension due to vasodilation. The underlying mechanisms are not completely understood. We investigated the mechanisms by which propofol relaxes vascular segments.

Methods: We studied the effect of propofol on isolated porcine coronary artery rings precontracted with potassium chloride or prostaglandin F2α.

Results: Propofol, in a concentration-dependent manner, relaxed all segments at concentrations of 5 μg mL−1 and above. This relaxation was unaltered in the presence of Nω-nitro-L-arginine, indomethacin, diltiazem and glibenclamide. Tetraethylammonium chloride, an inhibitor of the BKCa K+ channel (a high conductance Ca2+-sensitive K+ channel), dose-dependently attenuated the vasodilating effect of propofol (P < 0.001).

Conclusions: Our results suggests that the activation of the BKCa channel may contribute to the vasodilating effect of propofol, hereby causing hyperpolarization of the smooth muscle membrane and reduction of smooth muscle tone.

Keywords

ANAESTHETICS, INTRAVENOUS, propofolARTERIES, coronary vesselsION CHANNELS, K+ channel
Type
Original Article
Information
European Journal of Anaesthesiology , Volume 21 , Issue 3 , March 2004 , pp. 226 - 230
Copyright
2004 European Society of Anaesthesiology

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References

Kay B, Rolly G. ICI 35 868, a new intravenous induction agent. Acta Anaesth Belg 1977; 28: 303–316.Google Scholar
Goodchild CS, Serrao JM. Cardiovascular effects of propofol in the anaesthetized dog. Br J Anaesth 1989; 63: 87–92.Google Scholar
Nakamura K, Hatano Y, Hirakata H, Nishiwada M, Toda H, Mori K. Direct vasoconstrictor and vasodilator effects of propofol in isolated dog arteries. Br J Anaesth 1992; 68: 193–197.Google Scholar
Robinson BJ, Ebert TJ, O'Brien TJ, Colinco MD, Muzi M. Mechanisms whereby propofol mediates peripheral vasodilation in humans. Sympathoinhibition or direct vascular relaxation? Anesthesiology 1997; 86: 64–72.Google Scholar
Krassioukov AV, Gelb AW, Weaver LC. Action of propofol on central sympathetic mechanisms controlling blood pressure. Can J Anesth 1993; 40: 761–769.Google Scholar
Klockgether-Radke AP, Frerichs A, Kettler D, Hellige G. Propofol and thiopental attenuate the contractile response to vasoconstrictors in human and porcine coronary artery segments. Eur J Anaesthesiol 2000; 17: 485–490.Google Scholar
Kirkpatrick T, Cockshott ID, Douglas EJ, Nimmo WS. Pharmacokinetics of propofol (Diprivan) in elderly patients. Br J Anaesth 1988; 60: 146–150.Google Scholar
Servin F, Desmonts JM, Haberer JP, Cockshott ID, Plummer GF, Farinotti R. Pharmacokinetics and protein binding of propofol in patients with cirrhosis. Anesthesiology 1988; 69: 887–891.Google Scholar
Wallerstedt SM, Törnebrandt K, Bodelsson M. Relaxant effects of propofol on human omental arteries and veins. Br J Anaesth 1998; 80: 655–659.Google Scholar
Chang KSK, Davis R. Propofol produces endothelium-independent vasodilation and may act as a Ca2+ channel blocker. Anesth Analg 1993; 76: 24–32.Google Scholar
Park WK, Lynch C, Johns RA. Effects of propofol and thiopental in isolated rat aorta and pulmonary artery. Anesthesiology 1992; 77: 956–963.Google Scholar
Introna RPS, Pruett JK, Yodlowski EH, Grover E. Direct effects of propofol (2,6-diisopropylphenol) on canine coronary artery ring tension. Gen Pharmacol 1993; 24: 497–502.Google Scholar
Yamanoue T, Brum JM, Estafanous FG. Vasodilation and mechanisms of action of propofol in porcine coronary arteries. Anesthesiology 1994; 81: 443–451.Google Scholar
Gacar N, Gök S, Kalyoncu NI, Özen I, Soykan N, Aktürk G. The effect of endothelium on the response to propofol on bovine coronary artery rings. Acta Anaesth Scand 1995; 39: 1080–1083.Google Scholar
Park KW, Dai HB, Lowenstein E, Selke FW. Propofol-associated dilation of rat distal coronary arteries is mediated by multiple substances, including endothelium-derived nitric oxide. Anesth Analg 1995; 81: 1191–1196.Google Scholar
Petros AJ, Bogle RG, Pearson JD. Propofol stimulates nitric oxide release from cultured porcine aortic endothelial cells. Br J Pharmacol 1993; 109: 6–7.Google Scholar
Horibe M, Ogawa K, Sohn JT, Murray PA. Propofol attenuates acetylcholine-induced pulmonary vasorelaxation: role of nitric oxide and endothelium-derived hyperpolarizing factors. Anesthesiology 2000; 93: 447–455.Google Scholar
Yamashita A, Kajikuri J, Ohashi M, Kanmura Y, Itoh T. Inhibitory effects of propofol on acetylcholine-induced, endothelium-dependent relaxation and prostacyclin synthesis in rabbit mesenteric resistance arteries. Anesthesiology 1999; 91: 1080–1089.Google Scholar
Nagao T, Vanhoutte PM. Endothelium-derived hyperpolarizing factor and endothelium-dependent relaxation. Am J Resp Cell Mol Biol 1993; 8: 1–6.Google Scholar