Effect of Propofol on Norepinephrine-induced Increases in [Ca2+](i) and Force in Smooth Muscle of the Rabbit Mesenteric Resistance Artery 

Abstract

In smooth muscle of the rabbit mesenteric resistance artery, propofol attenuates norepinephrine-induced contractions due to an inhibition both of Ca2+ release and of Ca2+ influx through L-type Ca2+ channels. Propofol also increased resting [Ca2+]i, possibly as a result of an inhibition of [Ca2+]i removal mechanisms. These results may explain in part the variety of actions seen with propofol in various types of vascular smooth muscle.

The pressure fl ow relationship of the internal mammary artery after offpump anastomosis to the left anterior descending coronary artery

“…Propofol has been shown to increase basal vascular tone at clinical and low concentrations, but decrease basal tone in arteries at high concentrations. (24,25) This increase in basal tone seems to be endothelium independent, and is thought to be via activation of voltage dependant calcium channels. (26) Propofol has also been shown to directly inhibit calcium release from the sarcoplasmic reticulum, as well as decreasing inositol phosphate production.…”

Effect of propofol on human fetal placental circulation

“…Vasoconstriction induced by increases in intracellular calcium is triggered by one of two mechanisms: influx of calcium through the sarcolemma and mobilization of calcium from intracellular stores. 22 Propofol has been demonstrated to induce vasodilatation by inhibition of calcium mobilization induced by phenylephrine and norepinephrine, which has been studied in the rat aorta 23 and rabbit mesenteric resistance vessels; 24 and propofol to inhibits calcium influx through L-type Ca 2+ channels induced by endothelin-1 in rat aortic smooth muscle. 25 This effect of propofol has also been shown and to inhibit calcium influx induced by norepinephrine in rabbit mesenteric resistance vessels, 24 rat aorta, 23 and porcine coronary arteries.…”

Propofol and thiopental attenuate adenosine triphosphate-sensitive potassium channel relaxation in pulmonary veins

“…However, the underlying mechanism for this effect has not been previously investigated. Because propofol and thiopental have been shown to inhibit L-type VGCCs in vascular smooth muscle (12,37), tracheal smooth muscle cells (38), and myocardial cells (3), we hypothesized that propofol and thiopental could attenuate levcromakalim-induced PV relaxation via an inhibitory effect on L-type VGCCs. To test this hypothesis, we assessed the effects of the anesthetics on changes in [Ca 2ϩ ] i induced by levcromakalim.…”

“…Moreover, underlying mechanisms responsible for the anesthesia-induced attenuation of the smooth muscle component of K ATP ϩ channel-induced relaxation have not been elucidated. Because propofol and thiopental have been shown to inhibit L-type VGCCs in vascular smooth muscle (12,37), tracheal smooth muscle cells (38), and myocardial cells (3), it is reasonable to hypothesize that these anesthetics could attenuate the vascular smooth muscle component of K ATP ϩ channelmediated relaxation via an inhibitory effect on L-type VGCCs. Because PV constriction can increase pulmonary capillary pressure and transvascular fluid flux to cause pulmonary edema, an anesthesia-induced attenuation of a PV vasodilator mechanism could result in an increase in pulmonary capillary pressure, pulmonary edema formation, and congestive heart failure.…”