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It has been postulated that alterations in the intravascular distribution of blood affect antidiuretic hormone (ADH) secretion in man. The studies reported here were designed to alter blood distribution by thermal and by positional change to test this thesis.HUMAN BLOOD ADH LEVELS HAVE BEEN SHOWN TO VARY WITH POSITION: a mean value of 0.4 +/- 0.6 (SD) muU/ml was obtained while the subject was supine, a value of 1.4 +/- 0.7 muU/ml while sitting, and 3.1 +/- 1.5 muU/ml while standing. In 79 control subjects, sitting comfortably for 30 min in a normal environment, a blood ADH level of 1.65 +/- 0.63 muU/ml was found. It is suggested that subjects assume this position during experiments in which blood is drawn for measurement of ADH levels.In eight seated subjects the ADH level rose from 1.6 +/- 0.4 to 5.2 +/- 0.8 muU/ml after a 2 hr exposure at 50 degrees C and fell to 1.0 +/- 0.26 muU/ml within 15 min at 26 degrees C.Six subjects with a mean ADH level of 2.2 +/- 0.58 muU/ml sat quietly in the cold (13 degrees C) for 1 hr, and the ADH level fell to 1.2 +/- 0.36 muU/ml. After 15 min at 26 degrees C, the level rose to 3.1 +/- 0.78 muU/ml. The serum sodium and osmolal concentrations remained constant during all studies.Water, sodium, and total solute excretion decreased during exposure to the heat, whereas the urine to plasma (U/P) osmolal ratio increased. During cold exposure, water, sodium, and total solute excretion increased, and there was a decrease in the U/P osmolal ratio.These data are interpreted as indicating that changes in activity of intrathoracic stretch receptors, in response to redistribution of blood, alter ADH secretion independently of changes in serum osmolality. The rapidity of change of blood ADH concentration indicates a great sensitivity and a prime functional role for the "volume receptors" in the regulation of ADH secretion.

Renal tubular lesions during the early phases of progressive potassium depletion in rats were found in nephrons isolated by microdissection in two locations, the collecting tubules and the proximal convolutions. All other portions of the nephron, in particular the "distal tubule," i.e. ascending limbs of Henle's loop and distal convolutions, showed no structural alterations except the passive effects of dilatation and cellular compression which developed as a result of primary disturbances lower in the tubular system. The alterations affected all the collecting tubules uniformly and took two forms; the more severe, a swelling and hyperplasia of the tubular epithelium and the lesser, an intracellular accumulation of granule droplets. The former was limited to the outer zone of the medulla, the latter to its inner zone. In the proximal convolution the structural alteration began in its middle third and extended downward towards the medulla; only occasional nephrons were affected. The essential nature of the more severe epithelial lesion was similar in both collecting tubule and proximal convolution, beginning as a swelling of cell bodies, increasing to protoplasmic disturbances with disintegration of the mitochondrial pattern, followed by rupture of cells and nuclear disappearance. These retrogressive alterations were followed by prolific regenerative hyperplasia. In the collecting tubules of the outer zone these epithelial alterations were present in both the clear and the intercalcated cells; in the latter the swelling of the cells was not prominent, but the hyperplastic proliferative increase in their number was the predominating feature of the lesion when the dissected tubules were viewed intact in the continuity of their topographical relations. The cellular alterations in the tubules are associated with an inability to concentrate the urine; reasons are given for considering this functional disturbance a correlate of the structural lesion in the collecting tubules.