Abstract
Dikstein and Sulman (1) reported that the treatment of the rectus abdominis muscle of Bufo viridis toad with 3.4 M (25%) acetone for 2 minutes eliminated the response of the muscle to acetylcholine (ACh), but 5 to 20 μg/ml of phospholipids such as phosphatidylserine could restore the response of the treated muscle to ACh. They also observed similar effects of phospholipids on the rabbit uterus treated with acetone and restoration of the response of the ileum to norepinephrine after the treatment with phospholipids, and postulated that the phospholipids of receptors were extracted by acetone and could be replaced by those from an exogenous source.
In a recent report, however, Ehrenpreis, Hazra and Bigo-Gullino (2) presented evidence that smooth muscles of various organs treated with 3.4 M (25%) acetone were not restored in their responses to agonists by application of phospholipids, and the effect of acetone was concerned with the denaturation of the receptor protein by acetone, but not with lipid extraction from the receptor.
We have found in this paper that the mode of action of acetone is very similar to that of papaverine. The aims of this paper are to study the mechanism of antiacetylcholine action of acetone and papaverine, and to test the restoration of the response of the papaverine or acetone-treated ileum to ACh by phospholipids.
Also in our experiments, as described by Ehrenpreis, Hazra and Bigo-Gullino (2), 3.4 M (25%) acetone applied for 2 minutes at 32°C abolished the response of ileum to ACh, and even large doses of phospholipids could not restore the responsiveness of the ileum after the acetone treatment. In an ileum maintaining a moderate response to ACh after the acetone treatment under milder conditions, however, various phospholipids could restore distinctly the responsiveness of the ileum.
