Since suppression of arginine vasopressin (AVP) appears to be a determinant of the diuresis of water immersion (WI) in humans, a further understanding of its responsiveness has important implications for normal physiology, pathophysiology, and space physiology. In recent years, discrepant measurements of AVP in plasma during WI have led to conflicting conclusions. In studies in which the subjects ingested water before or during WI, plasma AVP was reported to be unchanged or even increased. In contrast, plasma AVP was suppressed in studies in which the subjects remained hydropenic. A critical review discloses that water intake before and/or during the experiments introduces several new stimuli for AVP release. Furthermore the lower base-line levels of AVP in hydrated subjects complicate detection of small changes in plasma AVP. Although the mechanisms of AVP suppression during WI are incompletely defined, it appears that not only cardiopulmonary mechanoreceptors but also arterial baroreceptors mediate the response. Additional studies are proposed to delineate further the mechanisms governing AVP release during WI.

Recent evidence indicates that stimulation of cardiopulmonary receptors in experimental animals results in a diminution of autonomic nervous system activity. Water immersion to the neck (NI) results in a preferential central hypervolemia (CV); thus it might be anticipated that NI would alter plasma catecholamine levels. Because two earlier studies have yielded divergent findings, we designed the present study utilizing more updated methodology to determine whether NI alters plasma catecholamines in normal humans. Eight normal subjects were studied on two occasions; during a seated control study (C) and during 4 h of NI. Norepinephrine (NE) and epinephrine (E) levels, determined by radioenzymatic assay, were measured hourly. Despite the induction of a marked natriuresis and diuresis indicating significant CV, NI failed to alter plasma NE or E levels compared with those of either C or the corresponding prestudy 1.5 h. Furthermore, the diuresis and natriuresis varied independently of NE. The current findings suggest that the response of the sympathetic nervous system to acute volume alteration may differ from the reported response to chronic volume expansion.

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Improvement in nocturia was associated with a decrease in both 24 h voided volume and NUV, but not MVV, suggesting that improved patients consumed less fluid. The increase in FUSP in the improved cohort demonstrates the potential for nocturia therapies to improve impaired sleep architecture.