Answers are grounded in this paper and cite their sources.
The contractile responses of isolated uterine segments from 17 beta-estradiol-3-benzoate-treated ovariectomized rats to acetylcholine (ACh) and high KCl in Ca-depleted modified Locke-Ringer solution on addition of CaCl2 were used as indicators of Ca2+ influxes through ACh receptor- and voltage-operated Ca2+ channels, respectively. L-Methionine (L-Met) significantly enhanced these responses. The enhancement depended on the time of treatment with L-Met and concentration of L-Met. 3-Deazaadenosine (3-DAA) plus homocysteine thiolactone (HCTL), which inhibit S-adenosylmethionine-dependent methylation, caused dose-dependent inhibition of these contractile responses to ACh and high KCl. These inhibitory effects of 3-DAA plus HCTL were significantly attenuated in the presence of L-Met. Protein carboxylmethyltransferase and phospholipid methyltransferase activities were detected in the isolated uterine segment under conditions similar to those in which the contractile responses were observed. 3-DAA plus HCTL inhibited these enzyme activities. These findings suggest that S-adenosylmethionine-dependent methylations of protein and/or phospholipid in isolated uterine segment are involved in the contractile responses to ACh and high KCl in Ca-depleted modified Locke-Ringer solution on addition of CaCl2.
No takes yet. Share an insight, caveat, or question.
Ichida et al. (1987) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: