Normal Plasma Osmolality Research Articles

A syndrome of periodic ACTH and ADH discharge

A girl aged 8 yrs had suffered from periodic attacks of vomiting, psychotic depression and hypertension lasting for 5 to 6 days at monthly intervals since 16 months before admission. At the initiation of the attack, serum corticotropin (ACTH) and vaso-pressin (ADH) levels were prominently increased (610 pg/ml and 41 uU/ml respectively) despite normal plasma osmolality, which consequently produced hypertension (160/110 mmHg), hypercortisolemia and hyponatremia. Serum prolactin was also increased (91 ng/ml). During the attack, urinary excretion of epinephrine (E) and nor-epinephrine (NE) was elevated while that of dopamine (D) was reduced, resulting in marked rise in E+NE/D ratio (0.8 − 4.5), which decreased to normal level when symptoms disappeared (0.08 − 0.17). Provocation of the attack by hypertonic saline infusion or by metyrapone administration was not successful. Infusion of somatostatin at early stage of the attack suppressed the symptoms and chronic administration of methyl-DOPA with reserpine effectively inhibited the recurrence of the episodes. Her symptoms appear to be induced by periodic discharge of ACTH and ADH. Although the exact cause of this syndrome is unknown, disturbance in catechol-aminergic mechanism in hypothalamus is postulated.

Antidiuretic hormone in end-stage renal disease.

Quantative data on plasma levels of antidiuretic hormone (ADH) in renal failure are limited. We measured predialysis plasma ADH levels using a double antibody radioimmunoassay in 14 patients with end-stage renal failure. Plasma ADH was inappropriately elevated in the majority of tested patients despite normal plasma osmolality, moderately elevated blood pressure, and hypervolemia. The etiology of increased plasma ADH in our population is unclear.

Primary dysmenorrhoea and vasopressin.

SummaryThe circulating concentrations of arginine vasopressin on day 1 and on day 5 to 7 of the menstrual cycle were measured by radioimmunoassay in six women with primary dysmenorrhoea and five controls. All women had ovulated in the previous cycle, as indicated by the mid‐luteal phase plasma progesterone levels and had normal plasma osmolality and sodium concentrations. The plasma concentrations of progesterone and oestradiol on day 1 of the cycle were also measured, and no significant difference between the two groups was seen. In women with dysmenorrhoea the vasopressin concentration on day 1 was 0.400.038 (SE) μU/ml which was significantly higher than the concentration in normal women on the same day of the cycle 0.20±0.063 (SE) μU/ml (p <0.01). The plasma concentration of vasopressin in normal women on day 5 to 7 was 0.68 0.119 (SE) μU/ml which was significantly higher than on day 1 (p <0.01). A significant difference between day 1 and day 5 to 7 was not seen in dysmenorrheic women, possibly because the values were already elevated on day 1. The results suggest that vasopressin could be a factor of aetiological importance in primary dysmenorrhoea, and also indicate that the vasopressin concentration in plasma can vary according to the day of the menstrual cycle.

Plasma arginine vasopressin in the syndrome of antidiuretic hormone excess associated with bronchogenic carcinoma

A study of plasma arginine vasopressin in 17 patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) associated with bronchogenic carcinoma, revealed that the arginine vasopressin levels were distinctly elevated in most. In 14 patients with bronchogenic carcinoma, but without overt SIADH, plasma levels of arginine vasopressin were significantly higher than in normal subjects (p < 0.001). This, together with the finding of a lower than normal plasma osmolality in this group, suggests that inappropriate ADH excess might be much more common in patients with bronchogenic carcinoma than previously thought. The normal positive correlation between plasma osmolality and plasma arginine vasopressin was found to be reversed in SIADH. Seven of nine patients with overt SIADH, studied after fluid deprivation, showed an increase in plasma arginine vasopressin coincident with an increase in plasma osmolality (r = + 0.8, p < 0.01); in one patient, plasma arginine vasopressin returned to the original level following rehydration. The possibility that this might imply a degree of physiologic control to what is generally considered an autonomous secretion is discussed. It is, however, considered more likely that other factors, including changes in plasma volume and glomerular filtration, might explain the increase in plasma levels of arginine vasopressin.

Postconcussive hyperosmolality and deficient thirst

Following head trauma, a young man had chronic serum hyperosmolality and grossly diminished thirst perception. The urine ordinarily was concentrated with respect to serum, and fasting serum and urine osmolalities showed a linear correlation. Renal function was normal. Plasma and other extracellular fluid volumes were normal or expanded, and total body water was normal. Saline solution or water loads induced diuresis and a return to baseline body weight, suggesting regulation of extracellular volume. During standard water load studies, urine hypotonic to plasma was excreted despite continued serum hyperosmolality, but water excretion was less than normal. Extreme hydration produced normal plasma osmolality and a very dilute urine. During marked hydration, nicotine administration and exogenous vasopressin elicited an appropriate renal concentrating response, whereas administration of hypertonic saline solution produced only a slight increase in urinary concentration. These data are consistent with an extremely wide setting of osmoreceptors whose effect is modulated by oppositely acting volume stimuli. Hypernatremia probably resulted from a combination of deficient thirst, a habitually small water intake and a diet containing ordinary amounts of salt. The capacity of the patient's system to excrete a dilute urine despite continued hyperosmolality both stabilized extracellular volume and perpetuated the hypernatremia.