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      Role of Plasma Vasopressin in Changes of Water Balance Accompanying Acute Alcohol Intoxication

      , , , ,
      Alcoholism: Clinical and Experimental Research
      Wiley

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          Abstract

          Acute alcohol intoxication causes diuresis presumably resulting from inhibition of vasopressin (also called antidiuretic hormone) release from the posterior pituitary gland. In contrast, in alcoholics during withdrawal from alcohol, vasopressin release is stimulated, resulting in water retention (antidiuresis) and dilutional hyponatremia. The purpose of this study was to evaluate the role of this biphasic response of vasopressin secretion to alcohol in normal persons. We studied eight healthy men who took part in two study sessions: one involving the ingestion of ethanol (1.2 g/kg of body weight) and the other the ingestion of the same volume of fruit juice during 3 hr from 6 to 9 PM. Starting at 6 AM the following morning, subjects were loaded with water (20 ml/kg of body weight within 15 min). During the first 3 hr of the study, ethanol intake increased diuresis, whereas from midnight to 6 AM, a phase of antidiuresis was obtained. Antidiuresis continued during water loading when the retention of water was 44 +/- 6% during the alcohol experiment and 12 +/- 4% during the control session (p < 0.05). During the alcohol-induced diuresis, the plasma arginine vasopressin levels did not differ from the control experiment, but were higher during the phase of antidiuresis from 10 PM to 6 AM (p < 0.05- < 0.01). Also, after water loading at 8 and 9 AM, they were higher in the alcohol study than in the control experiment (p < 0.05). After alcohol ingestion, serum osmolality was higher than the corresponding control values from 8 PM to 2 AM (p < 0.01- < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

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          Development and clinical application of a new method for the radioimmunoassay of arginine vasopressin in human plasma.

          A radioimmunoassay has been developed that permits reliable measurements of plasma arginine vasopressin (AVP) at concentrations as low as 0.5 pg/ml in sample volumes of 1 ml or less. Nonhormonal immunoreactivity associated with the plasma proteins is eliminated by acetone precipitation before assay, leaving unaltered a component that is immunologically and chromatographically indistinguishable from standard AVP. Storage of plasma results in a decline in AVP concentration and, thus, must be carefully regulated. The plasma AVP values obtained by our method approximate the anticipated levels and vary in accordance with physiologic expections. In recumbent normal subjects, plasma AVP ranged from (mean +/-SD) 5.4+/-3.4 pg/ml after fluid deprivation to 1.4+/-0.8 pg/ml after water loading, and correlated significantly with both plasma osmolality (r=0.52; P<0.001) and urine osmolality (r=0.77; P<0.001). After fluid restriction, plasma AVP was uniformly normal relative to plasma osmolality in patients with nephrogenic diabetes insipidus and primary polydipsia but was distinctly subnormal in all patients with pituitary diabetes insipidus. The infusion of physiologic amounts of posterior pituitary extract caused a dose-related rise in plasma vasopressin that afterwards declined at the expected rate (t(1/2)=22.5+/-4 min). We conclude that, when used appropriately, our radioimmunoassay method provides a useful way of assessing AVP function in man.
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            The role of blood osmolality and volume in regulating vasopressin secretion in the rat.

            A sensitive and specific radioimmunoassay for plasma arginine vasopressin (AVP) has been used to study the effects of blood osmolality and volume in regulating AVP secretion in unanesthetized rats. Under basal conditions, plasma AVP and osmolality were relatively constant, averaging 2.3+/-0.9 (SD) pg/ml and 294+/-1.4 mosmol/kg, respectively. Fluid restriction, which increased osmolality and decreased volume, resulted in a progressive rise in plasma AVP to about 10 times basal levels after 96 h. A 2-3-fold increase in plasma AVP occurred as early as 12 h, when osmolality and volume had each changed by less than 2%. Intraperitoneal injections of hypertonic saline, which had no effect on blood volume, also produced a rise in plasma AVP that was linearly correlated with the rise in osmolality (r > 0.9) and quantitatively similar to that found during fluid restriction (plasma AVP increased 2-4-fold with each 1% increase in osmolality). Intraperitoneal injection of polyethylene glycol, which decreased blood volume without altering osmolality, also increased plasma AVP but this response followed an exponential pattern and did not become significant until volume had decreased by 8% or more. At these levels of hypovolemia, the osmoregulatory system continued to function but showed a lower threshold and increase sensitivity to osmotic stimulation. We conclude that AVP secretion is regulated principally by blood osmolality but that the responsiveness of this mechanism may be significantly altered by modest changes in blood volume.
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              Renal tubular dysfunction in chronic alcohol abuse--effects of abstinence.

              Alcohol abuse may be accompanied by a variety of disorders of electrolyte and acid-base metabolism. The role of the kidney in the pathogenesis of these disturbances is obscure. We sought to evaluate the alcohol-induced abnormalities of renal function and improvement during abstinence and to assess the relation between renal dysfunction and electrolyte and acid-base disorders. We measured biochemical constituents of blood and renal function before and after four weeks of abstinence in 61 patients with chronic alcoholism who had little or no liver disease. On admission, 18 patients (30 percent) had hypophosphatemia and hypomagnesemia, 13 patients (21 percent) had hypocalcemia, and 8 patients (13 percent) had hypokalemia. Twenty-two patients (36 percent) had a variety of simple and mixed acid-base disorders. Twenty of these patients had metabolic acidosis, and among them, 80 percent had alcoholic acidosis. A wide range of defects in renal tubular function, with normal glomerular filtration rate, were detected in these patients. The defects included decreases in the threshold and maximal reabsorptive ability for glucose (38 percent of patients) and in the renal threshold for phosphate excretion (36 percent); increases in the fractional excretion of beta 2-microglobulin (38 percent), uric acid (12 percent), calcium (23 percent), and magnesium (21 percent); and aminoaciduria (38 percent). Seventeen patients (28 percent) had a defect in tubular acidification, and five an impairment in urinary concentrating ability. Urinary excretion of N-acetyl-beta-D-glucosaminidase and alanine aminopeptidase were increased in 41 and 34 percent of patients, respectively. The abnormalities of blood chemistry and renal tubular function disappeared after four weeks of abstinence. Transient defects in renal tubular function are common in patients with chronic alcoholism and may contribute to their abnormalities of serum electrolyte and blood acid-base profiles.
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                Author and article information

                Journal
                Alcoholism: Clinical and Experimental Research
                Alcoholism Clin Exp Res
                Wiley
                0145-6008
                1530-0277
                June 1995
                June 1995
                : 19
                : 3
                : 759-762
                Article
                10.1111/j.1530-0277.1995.tb01579.x
                7573805
                dc75c8b6-25bb-4f75-bacc-2bb8ca9ae965
                © 1995

                http://doi.wiley.com/10.1002/tdm_license_1.1

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