Abstract

Pharmacological experiments indicate that prostaglandins (PGs) have a role in the control of sodium regulation in freshwater mussels and the mechanism may be linked to cyclic AMP and serotonin. To test this hypothesis we used radioimmunoassay to investigate the ability of freshwater mussels to synthesize PGs. The levels of precursor fatty acids were determined in a gas-liquid chromatograph. Arachidonic acid (precursor to the diene PGs) was the major fatty acid component of total lipids in the gill and accounted for 14% of the total. In addition, gill homogenates synthesize PG-like material from [3H]arachidonic acid. Material corresponding to PGE2 and PGF2 alpha were identified on thin-layer radiochromatograms. These data indicate that gills (the primary site of Na transport) can produce PGs. The presence of PGs in freshwater mussels was verified by radioimmunoassay of blood. Both PGE2 and PGF2 alpha were identified using highly specific antisera. The concentrations of both PGs was significantly reduced when the mussels were injected with inhibitors of phospholipase A2 or cyclooxygenase before sampling blood. Stimulation of Na transport by serotonin and cyclic AMP results in a depression of blood PGE2 with no effect on circulating PGF2 alpha. PGE2 levels are inversely correlated with net Na flux. These data indicate endogenous PGE2 negatively modulated Na transport and PGE2 levels are regulated by a serotonin-cyclic AMP mediated system.