Relationship between renal prostaglandin E and renal sodium handling during water immersion in normal man.

Previous studies from this laboratory have demonstrated that the central hypervolemia induced by water immersion to the neck (NI) constitutes a suitable model for assessing the hormonal response to volume expansion without concomitant alterations in plasma composition.The NI model was used to assess in a kinetic fashion the relationship between renal prostaglandin E (PGE) and renal sodium handling.Nine normal subjects were studied twice in the sodium-replete state during NI: with indomethacin (Ind) pretreatment (50 mg q6h x 6)(NI + Ind) and without indomethacin (NI).Urinary sodium, potassium, and PGE excretion (UPGEV) were measured hourly.NI was associated with marked increases in U N .V [from 87 ± 20 (SE) to 219 ± 25 pEq/min (P < 0.06)] and UpG K V[from 6.4 ± 1.4 to 12.9 ± 2.5 ng/min (P < 0.05)].Although indomethacin administration lowered the basal rate of UPGBV prior to immersion, it neither prevented the subsequent augmentation of UPGEV during NI + Ind nor affected the magnitude of the natriuresis during NI + Ind. Subsequently, six of the subjects were restudied following dietary sodium restriction (10 mEq/day).The changes in UPGBV during NI and NI + Ind were qualitatively similar to those observed in the sodium-replete state.In contrast to the sodium-replete studies, however, the natriuresis of immersion was attenuated markedly by indomethacin pretreatment.In summary, the data demonstrate that immersion-induced central volume expansion is associated with a striking increase in renal PGE excretion which is attenuated but not prevented by indomethacin.In addition, indomethacin administration attenuates markedly the natriuretic response of immersion in sodium-depleted, but not in sodium-replete, normal subjects.These observations are consistent with the suggestion that renal PGE may constitute a determinant of the renal response to volume expansion in sodium-depleted man.Circ Res 45: 71-80, 1979