Abstract
Acetylcholine, which stimulates NaCl secretion in the avian salt gland, causes the rapid formation of a fraction of phosphatidic acid, as measured by (32)P incorporation, which amounts maximally to about 0.18 micromoles per g of fresh tissue. This does not appear to involve synthesis of the diglyceride moiety of phosphatidic acid, as measured by glycerol-1-(14)C incorporation. It presumably involves formation of phosphatidic acid by the diglyceride kinase pathway from preformed diglyceride and ATP. The specific activity of the AT(32)P of the tissue is not increased in the presence of acetylcholine. At time intervals after addition of acetylcholine during which a full response, measured as increased O(2) uptake, may be observed, phosphatidic acid appears to be the only phosphatide which shows any increase either in total (32)P radioactivity or in net specific acitvity. This responsive fraction of phosphatidic acid undergoes continuous turnover of its phosphate moiety. There is no evidence that this turnover is due to the phosphatidic acid acting as a pool of intermediate for the synthesis of other phospholipids or glycerides. The responsive fraction amounts to not more than 20% of the total phosphatidic acid of the tissue; it does not mix with the other (non-responsive) phosphatidic acid of the tissue. The observations suggest that this phosphatidic acid plays some role in the over-all secretory process.
MeSH Terms
Acetylcholine/pharmacology
Adenine Nucleotides/metabolism
Adenosine Triphosphate/metabolism
Animals
Birds
Carbon Isotopes
Glycerides/metabolism
Oxygen Consumption
Phospholipids/metabolism
Phosphorus Isotopes
Salt Gland/drug effects
Sodium Chloride/physiology
Chemicals
Adenine Nucleotides
Carbon Isotopes
Glycerides
Phospholipids
Phosphorus Isotopes
Sodium Chloride
Adenosine Triphosphate
Acetylcholine
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Hokin M R
Hokin L E
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25 references, click to expand
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