6-ketoprostaglandin-f1-alpha and 3-((3-cholamidopropyl)dimethylammonium)-1-propanesulfonate

The effect of DL-propranolol on NO release in perfused rat hindquarters was studied by using oxyhemoglobin as a capture system to allow the quantitative assay of NO production. In some experiments the stable prostacyclin metabolite 6-keto-PGF1 alpha (6-keto) was simultaneously assayed. We observed that: (1) DL-propranolol induced an increase in NO and 6-keto release. The dextro isomer was inactive; (2) DL-propranolol-induced NO release was only slightly reduced by acetylsalicylic acid in a concentration that inhibits prostacyclin synthesis, and was abolished by the chemical removal of the endothelium with 3-3 cholamidopropyl dimethylammonium 1-propane sulphonate (CHAPS) applied before or during stimulation; (3) NG-nitro-L-arginine blocked DL-propranolol-induced NO production, an effect that was antagonized by L-arginine but not by its dextro isomer.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Arginine; Aspirin; Atropine; Carbachol; Cholic Acids; Endothelium, Vascular; Epoprostenol; Male; Nitric Oxide; Nitroarginine; Oxyhemoglobins; Propranolol; Rats; Rats, Inbred Strains