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The Regulation of Antidiuretic Hormone Release in Man: I

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The Regulation of Antidiuretic Hormone Release in Man: I The regulation of antidiuretic hormone release in man: I. Effects of change in position and ambient temperature on blood ADH levels William E. Segar, Ward W. Moore J Clin Invest. 1968;47(9):2143-2151. https://doi.org/10.1172/JCI105900. 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) μU/ml was obtained while the subject was supine, a value of 1.4 ± 0.7 μU/ml while sitting, and 3.1 ± 1.5 μU/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 μU/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 μU/ml after a 2 hr exposure at 50°C and fell to 1.0 ± 0.26 μU/ml within 15 min at 26°C. Six subjects with a mean ADH level of 2.2 ± 0.58 μU/ml sat quietly in the cold (13°C) for 1 hr, and the ADH level fell to 1.2 ± 0.36 μU/ml. After 15 min at 26°C, the level rose to 3.1 ± 0.78 μU/ml. The serum sodium and osmolal concentrations remained constant during all studies. Water, sodium, and […] Find the latest version: https://jci.me/105900/pdf The Regulation of Antidiuretic Hormone Release in Man I. EFFECTS OF CHANGE IN POSITION AND AMBIENT TEMPERATURE ON BLOOD ADH LEVELS WILLAm E. SEGAR and WARD W. MooRE From the Departments of Pediatrics and Physiology, Indiana University School of Medicine, Indianapolis, Indiana 46202 A B S T R A C T It has been postulated that altera- ,uU/ml. The serum sodium and osmolal concentra- tions in the intravascular distribution of blood tions remained constant during all studies. affect antidiuretic hormone (ADH) secretion in Water, sodium, and total solute excretion de- man. The studies reported here were designed to creased during exposure to the heat, whereas the alter blood distribution by thermal and by posi- urine to plasma (U/P) osmolal ratio increased. tional change to test this thesis. During cold exposure, water, sodium, and total Human blood ADH levels have been shown to solute excretion increased, and there was a de- vary -with position: a mean value of 0.4 ±0.6 crease in the U/P osmolal ratio. (SD) uU/ml was obtained while the subject was These data are interpreted as indicating that supine, a value of 1.4 + 0.7 buU/ml while sitting, changes in activity of intrathoracic stretch recep- and 3.1 ± 1.5 uU/ml while standing. In 79 control tors, in response to redistribution of blood, alter subjects, sitting comfortably for 30 min in a nor- ADH secretion independently of changes in serum mal environment, a blood ADH level of 1.65 ± osmolality. The rapidity of change of blood ADH 0.63 pU/ml was found. It is suggested that sub- concentration indicates a great sensitivity and a jects assume this position during experiments in prime functional role for the "volume receptors" in which blood is drawn for measurement of ADH the regulation of ADH secretion. levels. In eight seated subjects the ADH level rose from 1.6 ± 0.4 to 5.2 ± 0.8 AU/ml after a 2 hr INTRODUCTION exposure at 50'C and fell to 1.0 ± 0.26 uU/ml There is evidence that at least two mechanisms within 15 min at 260C. regulate the release of antidiuretic hormone Six subjects with a mean ADH level of 2.2 ± (ADH) and thereby control the tonicity and 0.58 MAU/ml sat quietly in the cold (13'C) for volume of the body fluids. The first of these has 1 hr, and the ADH level fell to 1.2 + 0.36 MU/ml. been elucidated by the investigations of Verney After 15 min at 260C, the level rose to 3.1 + 0.78 (1) and many subsequent workers (2-4) who Dr. Segar's present address is Section of Pediatrics, have demonstrated the existence of receptors, Mayo Clinic and Mayo Graduate School of Medicine, probably located in the hypothalamus (5), which Rochester, Minn. 55901. Dr. Moore's present address is are sensitive to changes in the effective solute con- c/o The Rockefeller Foundation, G.P.O. Box 2453, centration of the extracellular fluid. These recep- Bangkok, Thailand. Received for publication 5 February 1968 and in re- tors stimulate the release of ADH in response to vised form 4 April 1968. increased extracellular solute concentration and The Journal of Clinical Investigation Volume 47 1968 2143 inhibit ADH secretion when the extracellular fluid gradient elution of the eluate from carboxymethyl cellu- becomes dilute. lose and demonstrated that the antidiuretic activity emerged as a single peak in a position similar to that The second mechanism was originally predicted found with highly purified arginine vasopressin. by Peters (6). His suggestion that the fullness of The material is assayed by injection of 0.14.5 ml of the intravascular compartment could be "sensed" the acidified saline solution containing the vasopressin by the organism directed attention toward a search originally present in 1.0-5.0 ml of blood into water-loaded for receptors sensitive to changes in intravascular (5 ml/100 g) ethanol-anesthetized Holtzman rats weigh- ing 150-200 g. During the assay the rats are maintained volume which, in turn, might influence the release at a constant ambient temperature (350C) in an Arm- of ADH. Henry, Gauer, and Reeves (7, 8) have strong incubator. The high ambient temperature is used demonstrated the presence of such receptors in the to prevent a fall in the rectal temperature of the ethanol- thoracic vessels of dogs. They observed that disten- anesthetized bioassay animal, to maintain a constant cen- tral blood volume and constant renal hemodynamics, to tion of the left atrium was associated with an in- insure that all solutions are administered at a temperature crease in urine flow, whereas diuresis was not ob- of 350C, and to maintain a constant temperature on the served during distention of other segments of the conductivity cell. The assay animals are maintained on a intrathoracic vascular system. Subsequent studies constant fluid load by the continuous intravenous replace- have demonstrated that this response can be ment of urine losses with an equal volume of a solution containing 0.3% NaCl, 1.6% glucose, and 2% ethanol. blocked by vagotomy (9). Thus, although this All samples and solutions are administered intravenously. mechanism is well established in the experimental Urine conductivity is recorded continuously via a con- animal, its presence has not been demonstrated ductivity cell and recording device described by Rothe, convincingly in man. Johnson, and Moore (17). The area under the conduc- tivity curve is taken as an index of response and is mea- The studies to be reported support the concept sured by planimetry beginning with the initial upward that intravascular stretch receptors, presumably deflection of the recording pen above a stable base line intrathoracic, in response to alteration in left and continuing for 10 min. A 2 X 2 factorial design is atrial filling, alter ADH release independently of used to estimate the potency of the unknown solutions, and a complete assay consists of at least two injections changes in serum osmolality in man. Furthermore, of standard synthetic arginine vasopressin (Sandoz, Inc., the rapidity of change of blood ADH concentration Hanover, N. J.) and at least two injections of unknown, indicates a great sensitivity and a prime functional each at two dose levels. The procedure detects 1 AU/ml role for the "volume receptors" in the regulation (95% confidence limits) of arginine vasopressin (14). When kept in a frozen state until use, the synthetic argi- of ADH secretion. nine vasopressin has seemed to be a reliable reference standard as indicated by the linearity and reproducibility METHODS of the dose response curve (14). Since this standard was Vasopressin assay. The procedure of extraction, ab- not checked against USP Reference Standard a signifi- sorption, concentration, and bioassay of ADH were modi- cant error in absolute values may have been introduced. fied from methods described by Weinstein, Berne, and Since the aliquot of the acidified saline solution injected Sachs (10), Share (11), Yoshida, Motohashi, and Oki- into the assay animal may contain the amount of vaso- naka (12), and Moran, Miltenberger, Shu'Ayb, and pressin present in as much as 5 ml of blood, the assay will Zimmerman (13). These modifications and the dose- detect concentrations of blood ADH as low as 0.20 response relationship are described by Rogge, Moore, AU/ml. Recovery of arginine vasopressin (2.5-5.0 AU/ Segar, and Fasola (14). The method involves extraction ml) added to whole blood in 18 trials is 92 ± 5% (SEM). of ADH from blood with trichloroacetic acid (TCA), The specificity and limitations of such bioassay proce- removal of the TCA with ether, absorption on a column dures for ADH have been reviewed recently by Share of resin, Amberlite CG-50 (Rohm & Haas, Philadelphia, (18). Pa.), and elution with 50% acetic acid. The eluent is 10 ml of whole blood was withdrawn from the ante- lyophilized and taken up in 1.0 ml of a solution contain- cubital vein and transferred directly to 4 volumes of cold ing 0.85% NaCl and 0.03% acetic acid.
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