Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypernatremia has occasionally been observed in patients with myotonic muscular dystrophy (MyD). To elucidate the possibility of osmoregulatory dysfunction, we investigated hypothalamo-posterior pituitary function as well as serum electrolytes in eight patients with MyD. Blood samples were obtained early in the morning after overnight dehydration. Renal function was estimated by blood urea nitrogen, serum creatinine and creatinine clearance. Posterior pituitary function was evaluated by direct measurement of plasma vasopressin (AVP) during a 5% hypertonic saline infusion. Plasma AVP concentrations were determined by sensitive radioimmunoassay. In five patients, circulating blood volume (CBV), plasma renin activity (PRA) and serum aldosterone (S-Aldo.) were also measured. The mean serum sodium level (143.9 +/- 1.7mEq/1: Mean +/- SD) was significantly higher than in the controls (139.4 +/- 2.2mEq/1). A 5% hypertonic saline infusion showed a subnormal increase in AVP and diminished thirst, despite sufficient elevation of plasma osmolality, in all patients as compared with healthy adults. Renal function was intact. Biochemical evidence of dehydration, estimated by PRA, S-Aldo and CBV, was unremarkable in four of the five patients. These findings suggest that patients with MyD have neurogenic disorders of osmoregulation in addition to previously reported endocrine abnormalities. Impaired AVP secretion in response to osmotic stimuli and reduced thirst might be responsible for such failure.
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PMID:[Impaired vasopressin secretion in patients with myotonic dystrophy]. 328 99

Experiments were done in urethan-anesthetized rats to investigate the effect of plasma angiotensin II (ANG II) and hypernatremia on the excitability of subfornical organ (SFO) neurons projecting directly to paraventricular nucleus of the hypothalamus (PVH), supraoptic nucleus (SON), and nucleus medianus (NM). Extracellular recordings were made from 106 antidromically identified neurons in the SFO. The firing frequency of 53 (50%) was increased by the intracarotid infusion of ANG II and/or 0.5 M hypertonic NaCl. The intracarotid infusion of isotonic saline or the intravenous infusion of phenylephrine did not alter the discharge rate of these SFO neurons. Of 38 PVH projecting neurons, 21 (55%) responded to ANG II and/or hypertonic NaCl: 9 to ANG II only, 8 to hypertonic NaCl only, and 4 to both. Similarly, of 42 SON projecting neurons, 30 (71%) responded to ANG II and/or hypertonic NaCl: 10 to ANG II only, 15 to hypertonic NaCl only, and 5 to both. Finally, of 26 NM projecting neurons, one increased its firing frequency to ANG II and one other to 0.5 M NaCl. An additional eight SFO neurons were found to send collateral axons to both the PVH and SON (n = 6) and PVH and NM (n = 2): four responded in various combinations to intracarotid infusion of ANG II and 0.5 M NaCl. These data suggest that blood-borne ANG II and plasma hypernatremia can influence arterial pressure and the release of vasopressin from the neurohypophysis by altering the discharge rate of SFO neurons projecting to forebrain structures that contain magnocellular neurosecretory vasopressin neurons and neurons that are components of sympathoexcitatory pathways.
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PMID:Effects of plasma angiotensin II and hypernatremia on subfornical organ neurons. 336 4

The long-term results of surgical and specific drug therapy were compared in a group of 57 patients with primary aldosteronism (PA) (46 with aldosterone-producing adenoma (APA), 11 with idiopathic hyperaldosteronism (IHA) and bilateral adrenal hyperplasia). Unilateral adrenalectomy completely normalized blood pressure (BP) in 77.1% of surgically treated APA, evidently improving hypertension in remaining 22.9%. No recurrence of the adenoma in the remaining adrenal was seen in any of the surgical APA cases. In 19 of the non-surgical patients (11 with APA, 8 with IHA) monotherapy with spironolactone reduced blood pressure in 73%, though total BP normalization was an exception. The treatment normalized hypokalemia, low total exchangeable potassium, tendency to hypernatremia, and high total exchangeable sodium. Surgical as well as conservative therapy increased to normal or above-normal levels plasma renin activity suppressed prior to treatment. Pre-operatively high urine and plasma aldosterone levels normalized in all adrenalectomized patients, but remained above the normal range during spironolactone therapy in spite of a small decline in its absolute values. The disturbances of maximum renal concentrating capacity due to impaired nephron responsiveness to sufficiently high endogenous vasopressin concentrations were completely eliminated after kaliopenic nephropathy had been repaired. The other renal functions remained within normal values. Echocardiographically diagnosed left ventricular hypertrophy was seen less often than in the other types of arterial hypertension, tending to regress after APA management. Our longitudinal study (2-16 years) showed primary aldosteronism as a well curable, albeit rare, cause of hypertension. As regards BP and laboratory tests normalization, better results were achieved in surgical APA cases than in patients treated with spironolactone. Older age, longer history of hypertension and more frequent incidence of obesity, nephrosclerosis and pyelonephritis may be responsible for hypertension persisting after surgical treatment.
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PMID:Long-term results of surgical and conservative treatment of patients with primary aldosteronism. 345 May 33

We describe a patient with chronic hypernatraemia (plasma sodium 148-155 mmol/l) and partial nephrogenic diabetes insipidus who had received prolonged lithium treatment. Despite stopping the drug for one year the abnormalities remained. Infusion of hypertonic saline (NaCl 855 mmol/l) allowed the characterization of osmoregulation of thirst and vasopressin secretion. Linear regression analysis of plasma vasopressin and osmolality defined the function, pAVP = 0.27 (pOsm - 301), and analysis of thirst measured by a visual analogue scale and plasma osmolality, the function, thirst = 0.16 (pOsm - 302) where pAVP and pOsm represent plasma arginine vasopressin and osmolality respectively. The slopes of the regression lines which describe the sensitivity of the osmoreceptors were within the normal range, but both abscissal intercepts, which define the thresholds for vasopressin release and thirst, were markedly elevated in comparison to normal (upper limit less than 290 mOsm/kg). Other investigations of electrolytes, anterior pituitary function and high definition computed tomographic scanning of hypothalamo-pituitary region were all normal. We conclude that this patient's chronic hypernatraemia was due to resetting of the osmostats for both vasopressin release and thirst, a rarely described mechanism to account for hypernatraemia. Although it is probable that the partial nephrogenic diabetes insipidus was related to prolonged lithium therapy, the cause of the reset osmostats remains unclear.
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PMID:Hypernatraemia due to a reset osmostat for vasopressin release and thirst, complicated by nephrogenic diabetes insipidus. 345 Dec 25

A male, aged 16, with chronic hypernatremia, adipsia, polyphagia, and poikilothermia was studied regarding regulation and secretion of arginine vasopressin. During recumbency at night, low plasma arginine vasopressin levels and increased volumes of dilute urine were found; whereas plasma arginine vasopressin levels and urine osmolalities rose and urine volumes decreased during ambulation in the daytime. Neither a 25% reduction of mean arterial pressure nor hypertonic saline infusion increased plasma arginine vasopressin or urine osmolalities. Treatment with 1-desamino-D-arginine-vasopressin at 6 p.m. and a scheduled fluid intake according to actual body weight eradicated hypernatremia and hyperosmolality. These data demonstrate a complete loss of arginine vasopressin secretion to osmotic stimulation, a partial defect of arginine vasopressin secretion to non-osmotic stimulation, an abolished response to stimulation of high-pressure-baroreceptors, but an intact responsiveness to stimulation of low-pressure-baroreceptors.
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PMID:Recumbent cranial diabetes insipidus. Studies in a patient with adipsia, hypernatremia, poikilothermia and polyphagia. 347 Oct 44

We examined the release of vasopressin and the renal response to exogenous vasopressin before and during desoxycorticosterone acetate (DOCA) administration in the dog. As treatment with DOCA produced potassium loss, urine volume increased, urinary osmolality decreased, and urinary PGE2 tended to increase. The increase in urine volume was accompanied by increases in serum sodium, in plasma osmolality and in plasma arginine vasopressin. The threshold for vasopressin release measured during polyuria was higher than control but the rate of vasopressin release was unchanged. The DOCA-induced polyuria was not affected by treatment with vasopressin which further increased plasma vasopressin. Treatment with indomethacin which corrected the increase in urinary PGE2 excretion but not the hypokalemia, restored the renal responsiveness to vasopressin, decreased the secretion of vasopressin, and corrected the polyuria and the hypernatremia. These findings suggest that DOCA-induced polyuria is attributable to a decrease in renal responsiveness to vasopressin which may be mediated in part by an increase in the renal synthesis of prostaglandins.
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PMID:Diabetes insipidus with renal resistance to vasopressin in the desoxycorticosterone-treated dog: a possible role for prostaglandins. 347 17

A case of hypodipsic hypernatremia in a 16-month-old Japanese boy is reported. Partial antidiuretic hormone deficiency was present. Computed tomography of the brain revealed absence of septum lucidum. No ophthalmological abnormality could be found. He had hyposmia, which has not been reported previously in association with hypernatremia due to hypodipsia. Forced fluid administration and nasal 1-deamino-8-d-arginine vasopressin treatment could maintain serum electrolyte levels within normal ranges. However, episodes of hypernatremia could not be completely avoided while he was treated with 1-deamino-8-d-arginine vasopressin and ad libitum oral fluid.
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PMID:Hypodipsic hypernatremia associated with absence of septum lucidum and olfactory dysfunction. 356 67

1. Intake and output of water, Na+ and K+ were measured in Long Evans and Brattleboro rats (deficient in hypothalamic and pituitary vasopressin) before and after subcutaneous injection of polyethylene glycol (PEG) sufficient to cause a substantial hypovolaemia. 2. In the Long Evans rats an initial fluid retention (due to oliguria and polydipsia) was accompanied by Na+ retention and K+ loss. On the second day there was a diuresis but Na+ retention persisted until days 3 and 4 when there was a natriuresis. 3. Brattleboro rats initially also showed fluid retention but this was achieved by hypodipsia with a greater oliguria; there was an accompanying retention of Na+ and K+. On the second day, a reduced fluid balance was still accompanied by Na+ retention but associated with kaliuresis. Diuresis and natriuresis occurred on the third day after PEG injection. 4. Thus, rats deficient in vasopressin respond to hypovolaemia by retaining fluid. The renal actions of aldosterone do not explain fully the changes in renal electrolyte handling.
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PMID:Fluid and electrolyte handling in Long Evans and Brattleboro rats following injection of polyethylene glycol. 362 39

1. Intakes and urine outputs of fluid and electrolytes were measured before, during and after water deprivation in normal rats (Long-Evans strain) and in vasopressin-deficient rats (Brattleboro strain). 2. In a parallel experiment it was confirmed that the water-deprivation schedule used (Long-Evans rats 53 h, Brattleboro rats 14 h), and previously shown to cause similar percentage reductions in plasma volumes in the two strains, did produce more marked hypernatraemia and hyperosmolality and a greater percentage reduction in body weight in Brattleboro than in Long-Evans rats. 3. In Long-Evans rats, water deprivation caused a gradual reduction in urine output, a reduction in food intake and, during the first 24 h, increases in Na+ and K+ output. In Brattleboro rats, the reduction in urine output was more pronounced, but despite this total water losses were greater than from Long-Evans rats. Brattleboro rats showed a greater reduction in food intake. Their urinary Na+ and K+ losses were elevated during the first 9 h of water deprivation; thereafter these variables fell but remained above the level of intake. 4. The cumulative Na+ losses during water deprivation were similar in the two strains but the cumulative K+ losses in the Brattleboro rats were greater than in the Long-Evans rats. Thus the relative hypernatraemia and hyperkalaemia in water-deprived Brattleboro rats compared to water-deprived Long-Evans rats cannot be explained simply on the basis of differences in renal fluid and electrolyte handling. 5. There were significant increases in plasma angiotensin II and aldosterone levels at the end of the water deprivation periods in both strains of rat, and after the drinking water was returned there was a marked anti-natriuresis consistent with an expression of one of the renal actions of aldosterone.
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PMID:Water deprivation: effects on fluid and electrolyte handling and plasma biochemistry in Long-Evans and Brattleboro rats. 365 63

The infusion of isoosmolar glycerol (0.35 mol/dm-3) into the ventricles of laboratory rats for 120 minutes led to an increase in the serum osmolality by 11 mosm/kg and to hypernatremia. The brain water content of the cerebral hemispheres decreased by 0.9% (P less than 0.05). A corresponding intraventricular infusion of saline or d-glucose did not cause significant changes in these parameters. These findings support the view that glycerol, even in a dose incapable of creating a major osmotic gradient between plasma and brain, could have a beneficial effect in the control of intracranial volume-pressure perturbations. It is hypothesized that, besides acting as an osmotic dehydrating agent in certain concentrations, glycerol influences the central neuroendocrine system responsible for brain ion and volume homeostasis. By its presumed reduction of central and peripheral vasopressin release through lowering the cerebrospinal fluid sodium concentration, it may help in decreasing the brain water content.
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PMID:Effects of intraventricularly injected isoosmolar glycerol on brain water and electrolytes in the rat. 365 29


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