Effect of L-Methionine on Contractile Response, Calcium Influx and Calcium Channel Blocking Agents in the Rat Aorta

Abstract

L-Methionine incubated with aorta strips and S-adenosyl-L-methionine incubated with aorta membranes methylate membrane phospholipids. L-Methionine enhances the contractile response of helical strips of rat aorta to KC1. L-Methionine also enhances the slow component of the contractile response of rat aorta to norepinephrine associated with influx of exogenous calcium. L-Homocysteinethiolactone inhibits methylation of membrane phospholipids and depresses the contractile response to KC1 and to norepinephrine. L-Methionine enhances and L-homocysteinethiolactone depresses KCl-stimulated influx of calcium into rat aorta strips. L-Methionine has no effect on calcium efflux. Tested against calcium channel blocking agents, L-methionine reduces the inhibition caused by diltiazem and chlorpromazine but not that caused by TMB 8 or verapamil. It is postulated that methylated intermediates of phospholipid methylation enhance the function of membrane calcium channels.

Enhancement by L-Methionine of Contractile Responses to Acetylcholine and High KCl in Uterine Segment

“…Recently, Landon et al (25) also reported that the contractile response of rat aorta to high KCI was enhanced by L methionine.…”

Homocysteine as a Risk Factor for Atherosclerosis: Is Its Conversion toS-Adenosyl-L-Homocysteine the Key to Deregulated Lipid Metabolism?

“…In contrast, phospholipid methylation is inhibited by quinidine, an antiarrhythmic drug that causes repression of myocardial contractility [41]. Phospholipid methylation was also observed in microsome preparations from aorta [42, 43] and was suggested to affect membrane fluidity and function of membrane calcium channels in aorta [42, 43] as well as in heart [40]. Moreover, phospholipid methylation appears to be coupled to Ca 2+ influx and von Willebrand factor release in endothelial cells [35].…”

Enhancement by L-methionine on the contractile response of uterine segments to acetylcholine and high KCl is mainly due to enhancement of Ca uptake.

“…In the present experiment, it is uncertain whether the enhancing effect of L-methionine is due to the increase of Ca influx and/or the decrease of Ca efflux. However, Landon et al (14) reported that the contractile response of rat aorta to high KCI was enhanced by L-methionine and suggested that L-methionine enhanced and HCTL depressed the KCI-stimulated influx of calcium into rat aorta strips. They also showed that L-methionine had no effect on Ca efflux.…”