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It is clear that change of posture can profoundly modify the diurnal excretory rhythm (Figs. 2 and 3). Standing up in the morning inhibits the matutinal increase in alkalinity, whereas standing in the afternoon enhances the increasing acidity. Conversely, continued recumbency in the morning augments the matutinal increase in sodium and alkali outputs, while lying down in the after- noon inhibits the usual decrease. The present experiments provide additional information on the pattern of diurnal rhythmic variations in urine excretion. In the control recumbent ex- periments, the sodium and potassium rhythms were usually in phase (Stan- bury & Thomson, 1951; Mills & Stanbury, 1954); this association is not obligatory, however (Mills & Stanbury, 1954; Mills, Thomas & Yates, 1954) and some dissociation was evident on prolonged standing, when potassium outputs sometimes showed a relative rise while sodium outputs fell. Further- more, even when the sodium and potassium rhythms were in phase, as in most of the continued recumbency experiments, the relative magnitude of the 502 S. THOMAS POSTURE AND DIURNAL RHYTHM change in outputs differed at various times of day. This is most clearly reflected in the spontaneous changes in the Na: K ratio (Figs. 3 and 7). Such sponta- neous rhythmic changes even under uniform experimental conditions point to the need for caution in using this ratio to assess activity of the adrenal cortex in short-term experiments. The relative contributions of changes in filtered sodium load and in tubular sodium reabsorption to the altered sodium excretion after change of posture are difficult to assess. Change in sodium excretion could be brought about in three ways; first by alteration in filtered load, secondly by an alteration in the tubular reabsorption of sodium with attendant anions, and thirdly by a change in tubular reabsorption of sodium by ion exchange for hydrion or potassium. The last possibility would be indicated in experiments where the change in sodium output was accompanied by inverse changes in hydrion or potassium outputs, or both; and where the ratio Na: B changed appreciably. The first and second mechanisms are more likely in experiments where inverse changes in sodium and either potassium or hydrion outputs did not occur, and where there was little change in Na: B; distinction between these two mechanisms is possible by the presence or absence of change in G.F.R., as indicated by creatinine excretion.