The aim of this study was to investigate whether, in the short term, physiological blood pressure changes are coupled with changes in urinary sodium excretion in normotensive subjects, maintained at fixed sodium intake and under controlled postural and behavioural conditions. Twelve normotensive subjects were recruited. For each subject, seven urine samples were collected at fixed time intervals during an overall 26 h period: late afternoon (16.00–20.00 hours), evening (20.00–24.00 hours), night (24.00–06.00 hours), quiet wakefulness (06.00–09.00 hours), morning (09.00–12.00 hours), post-prandial (12.00–15.00 hours) and afternoon (15.00–18.00 hours). Blood pressure was monitored by an ambulatory blood pressure device during the whole 26 h period. Each urine sample was used to measure urinary sodium excretion and glomerular filtration rate (creatinine clearance). Blood pressure, heart rate, urinary sodium excretion and glomerular filtration rate recorded in the daytime were higher than those measured during the night-time. A significant positive correlation between mean blood pressure and urinary sodium excretion was found during the night, over the whole 26 h period, and during two subperiods of the daytime: quiet wakefulness and the post-prandial period. The coefficient of the pressure–natriuresis curve was significantly decreased by postural changes. We conclude that, in normotensive subjects, blood pressure and urinary sodium excretion are coupled in the short term. The assumption of an upright posture can mask this relationship, presumably by activating neurohumoral factors.

1. In order to examine the potential role of endogenous atrial natriuretic peptide (ANP) in modulating the increased sodium excretion per nephron in chronic renal failure, we studied healthy subjects with normal renal function (group I) and patients with moderate (group II) or severe chronic renal failure (group III) before, during and after administration of an intravenous sodium load. All subjects had been on a controlled diet containing 120 mmol of sodium per day for 5 days before the study. 2. Under basal conditions, plasma ANP and fractional excretion of sodium (FE Na ) were highest in group III. Both parameters increased in response to the sodium load in the three groups studied ( P < 0.001). Changes with time differed from group to group ( P < 0.05), the more marked response for both parameters being observed in group III. After adjustment with respect to plasma ANP (analysis of covariance), FE Na was no longer modified in response to the sodium load, whereas adjustment of FE Na with respect to mean blood pressure was without consequence on the significance of its change with time. This demonstrates that plasma ANP, but not mean blood pressure, represents the main factor producing variation in FE Na during and after the sodium load. 3. These results suggest an important role for plasma ANP in promoting adaptation of short-term sodium excretion in response to an acute sodium load in patients with chronic renal failure who ingest a normal sodium intake.

1. Eight normotensive subjects were studied in a randomized crossover trial of a high calcium diet (1800 mg of calcium/day) for a week against a low calcium diet (200 mg of calcium/day) for a further week. 2. The subjects were placed on a diet containing 200 mg of calcium/day throughout the study and the high calcium diet was achieved by supplementing the low calcium diet with calcium glubionate and galactogluconate. Sodium and potassium intake were kept constant throughout the study. 3. Twenty-four hour urinary sodium, potassium, calcium and phosphate were measured daily. 4. In spite of a highly significant increase in calcium excretion from the low to the high calcium diet ( P < 0.0001), there was no increase in sodium or change in potassium excretion with the increased calcium intake. A transient but significant fall in urinary sodium excretion was observed up to the fourth day of the high calcium diet ( P = 0.021). Twenty-four hour urinary phosphate excretion fell significantly on the high calcium diet ( P < 0.0001). Body weight, blood pressure, plasma renin activity, aldosterone, plasma creatinine and serum ionized calcium did not change. 5. These results suggest that a short-term increase in calcium intake in normotensive subjects does not increase urinary sodium and potassium excretion.

1. The role of the plasma sodium concentration in the regulation of aldosterone secretion and sodium excretion was investigated by comparing in 13 conscious sodium-depleted dogs the effects of the same sodium load (2.5 mmol/kg) given as either a hypertonic or hypotonic infusion. 2. The plasma sodium concentration was significantly higher and the plasma aldosterone concentration and urinary aldosterone excretion were significantly lower after the hypertonic infusion as compared with the hypotonic infusion. 3. The cumulative urinary sodium excretion during the 22 h after beginning the infusion was significantly greater after the hypertonic infusion, but this difference was not observed in five sodium-depleted dogs who were treated with deoxycorticosterone acetate before the infusions were given. 4. These data suggest that elevations in plasma sodium concentration are effective in decreasing aldosterone secretion and, hence, in increasing sodium excretion in conscious sodium-depleted dogs.

1. Extracts were prepared from bovine hypothalamus and cerebral cortex by gel filtration on Sephadex G-25 and G-50. 2. The vasopressin in the hypothalamic extracts was inactivated with thioglycollate and the effectiveness of inactivation was tested in the alcohol-anaesthetized rat. 3. The inactivated hypothalamic extracts caused a significant rise, and the cortical extracts an insignificant fall, in the urinary sodium excretion of the conscious rat. 4. Incubation of tubule fragments in hypothalamic extracts caused a significant rise in intracellular sodium concentration of the tubules when compared with incubation in Ringer, whereas incubation in cortical extracts caused a rise which was not significant. Nevertheless the rise in intracellular sodium concentration produced by incubating the tubules in hypothalamic extracts was not significantly different from the rise produced by incubation in cortical extracts.