Key result
Antidiuresis in rats reduces renal cortex phosphomonoesterase activity by ~50% versus controls.
Water deprivation in rats leads to a reduction in non-specific phosphomonoesterase activity, suggesting activation of a pathway for GPC formation from L-alpha-glycerylphosphate.
Hypothesis-generating for phosphomonoesterase regulation of renal GPC metabolism; human studies required before any clinical relevance.
Glycerylphosphorylcholine (GPC) concentration was reported to be elevated in renal medulla of experimental animals deprived of water. The activities of GPC phosphodiesterases were similar in homogenates and membrane subfractions of renal cortex prepared from control, diuresis and antidiuresis rats. There were no differences in these preparations' ability to hydrolyze phosphorylcholine. In contrast, there was a nearly 50% reduction of non-specific phosphomonoesterase activity, using p-nitrophenylphosphate as substrate and membrane subfractions prepared from the antidiuresis animals. It is suggested that as a consequence, a pathway for the formation from L-alpha-glycerylphosphate is activated.
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Kanfer et al. (1989) studied Water deprivation (antidiuresis) and diuresis. Antidiuresis (water deprivation) vs. Control and diuresis rats was evaluated on GPC phosphodiesterase and phosphomonoesterase activities (nearly 50% reduction). Antidiuresis in rats resulted in a nearly 50% reduction of non-specific phosphomonoesterase activity in renal cortex membrane subfractions compared to controls.
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