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)

Brain serotonin depletion induced by peripheral parachlorophenylalanine (pCPA) is frequently used to evaluate the role of the central serotoninergic system in the regulation of a number of physiological functions, including the secretion of renin by the kidney. We found that due to the treatments applied in the protocol used for the investigation of pCPA effect on renin and vasopressin secretion in rats (300 mg/kg i.p. 64 and 40 h before sacrifice) renal injury was induced as well. Typical changes indicating acute renal failure were observed--an initial polyuria, natriuresis and body mass loss, succeeded by oliguria, decreased glomerular filtration rate, and salt and creatinine retention. Morphological changes in the glomeruli included a thickening of the basal membranes, a confluence and a reduced number of podocyte pedicles. A slight to moderate granular degeneration was observed in epithelial cells of the proximal convoluted tubule, combined with mitochondrial changes--an increase in number, matrix disorganization, and myelin degeneration. In conclusion, the renal function changes after i.p. pCPA may be due not to brain serotonin depletion-alone, but also to nephrotoxic effect.
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PMID:Nephrotoxic effect of the specific brain serotonin depletor para-chlorophenylalanine. 215 5

A fullterm infant had fetal distress and stained amnion. He underwent an exchange blood transfusion at 12 hours after birth because of hyperbilirubinemia. He developed oliguria combined with high urine osmolality during the first 27 hours of life despite normal creatinine clearance. The diagnosis of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) was made on the basis of high urine osmolality, low plasma osmolality and elevated plasma arginine vasopressin (AVP) concentration. We determined the plasma atrial natriuretic peptide (ANP) concentration for the first 4 days of life. After 27 hours after birth, urine volume increased while plasma AVP concentration remained high. On the other hand, plasma ANP concentration gradually increased after 27 hours of life. We speculate that ANP may play an important role in producing the spontaneous diuresis in the newborn infant with SIADH.
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PMID:Role of atrial natriuretic peptide in the diuresis of a newborn infant with the syndrome of inappropriate antidiuretic hormone secretion. 253 65

Acute cerebral compression by a supra- and infratentorial balloon produced a triphasic pattern of diuresis. The 1st phase was characterized by polyuria associated with five fold increase of plasma (p) antidiuretic hormone (ADH) concentration, decreased urine osmolality in spite of natriuresis and blood pressure elevation. The 2nd phase was characterized by oliguria, a decrease of pADH and reduced urine Na+ concentration, whereas urine osmolality transiently increased. At this stage there was respiratory arrest and fall of blood pressure. The final stage was diabetes insipidus (DI), when EEG activity had disappeared. An increase of serum osmolality mainly occurred during the last DI phase. Serum Na+ concentration fluctuated slightly during the whole period of diuresis. These results present evidence, that the diuresis pattern reflects the hypothalamo-hypophyseal antidiuretic system (HHAS) reaction to acute intracranial pressure (ICP) increase with the vegetative symptoms of cerebral shock.
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PMID:Dissociation between activation of the hypothalamo-hypophyseal antidiuretic system and the type of diuresis during acute intracranial hypertension. Experimental observation. 292 92

Injection of a synthetic progesterone, medroxyprogesterone acetate (MPA or Depo-ProveraR), a widely used contraceptive, into Chinese hamsters (Cricetulus griseus) induced a profound polyuria with daily output of dilute urine equal to about 50% body weight of the hamster. However, relatively normal ability for renal urine concentration was demonstrated by administration of exogenous vasopressin. Body weight did not increase during onset of MPA-induced polyuria or during interval of vasopressin-induced oliguria, suggesting that primary polydipsia was not etiologic. Administration of this steroid to Chinese hamsters was nontoxic, although these polyuric animals were unusually sensitive to water deprivation. This polyuria was not observed when progesterone alone was injected into Chinese hamsters or when MPA was given to other related hamster species (Armenian, Syrian, Turkish or Djzungarian). The MPA-injected Chinese hamster represents a unique model of vasopressin sensitive diabetes insipidus induced by a steroid in a species-specific fashion.
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PMID:Medroxyprogesterone acetate induces diabetes insipidus in Chinese hamsters. 293 35

Babies with chronic bronchopulmonary dysplasia (BPD) can sometimes develop pallor, systemic and pulmonary edema, oliguria, and hyponatremia not attributable to cardiopulmonary or renal impairment. These signs and symptoms might, however, be explained by inappropriate control of vasopressin secretion. To test this hypothesis, we measured plasma vasopressin and osmolality, serum sodium and potassium concentrations, urine output and osmolality, and free water clearance in 26 normoxic infants with BPD aged 1-4 months. All of these infants required supplemental oxygen (FiO2 0.41 +/- 0.03, mean +/- 1 SE) to maintain O2 saturation of greater than 88%, and six infants also required mechanical ventilation. As controls, 10 infants of similar age but without BPD were also studied. None of the infants had been discharged from the nursery and was receiving any medications, and all were clinically stable when studied. Compared to control infants, infants with BPD had significantly elevated plasma vasopressin concentrations (control 5.2 +/- 0.9 pg/ml; BPD 42.4 +/- 5.1; mean +/- SE, p less than 0.05). Moreover, infants with BPD had hyponatremia and hypotonic plasma, and both urine output and free water clearance were significantly reduced. These data suggest that some infants with chronic BPD have elevated vasopressin levels that are functionally significant. We speculate that excessive stimulation of vasopressin secretion may explain some of the pulmonary and nonpulmonary signs and symptoms in infants with chronic BPD.
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PMID:Control of water balance in infants with bronchopulmonary dysplasia: role of endogenous vasopressin. 334 Apr 51

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

The role of blood volume regulatory mechanisms located in the low pressure system in the control of urinary excretion was studied using hypobaric pressure breathing in normal and diabetes insipidus (Brattleboro strain with a congenital lack of vasopressin) rats. Rats were placed in an altitude simulator chamber for 4 h. A pump maintained pressure reduced to 701, 577 and 472 mbar simulating respectively altitude of 3,000, 4,500 and 6,000 m. In normal rats, hypobaric breathing induced an increase in urine flow, urinary urea and K+ excretion and urinary pH but did not significantly modify creatinine and Na+ excretion. In diabetes insipidus rats, hypobaric breathing produced oliguria and an decrease in urea, creatinine, Na+, K+, Cl- urinary excretions. Since acute hypobaric pressure breathing induced opposed effects in normal and Brattleboro rats, it is suggested that this kind of experimental procedure which increases intrathoracic blood volume elicits a diuretic response through an inhibition of vasopressin release. These experiments confirm the main role of vasopressin in the control of central blood volume.
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PMID:Renal effect of acute hypobaric pressure breathing in normal and diabetes insipidus rats. 376 Dec 5

Perioperative plasma antidiuretic hormone (vasopressin) levels were determined in 8 patients undergoing radical cystectomy. Marked elevations of antidiuretic hormone were noted immediately postoperatively in all patients and these levels persisted for 48 hours. Plasma antidiuretic hormone was elevated beyond the physiological levels needed for maintenance of intravascular volume and osmolarity. Excessive antidiuretic hormone secretion is common after radical cystectomy and should be considered in the differential diagnosis of postoperative oliguria in these patients.
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PMID:Excessive antidiuretic hormone secretion after radical cystectomy. 398 18

Mental confusion with hyponatremia and oliguria was recorded during each of three successive episodes of acute bronchitis. Antibiotics proved sufficient therapy and led to recovery. Thus, as in pneumonia, inappropriate secretion of antidiuretic hormone (ADH) may be seen in acute bronchitis.
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PMID:[Recurrent water intoxication during successive episodes of acute bronchitis: Schwartz-Bartter syndrome? (author's transl)]. 628

The renal effects of clonidine (100 and 500 micrograms/kg s.c.) during acute hypobaric pressure breathing (i.e. a protocol which induces an increase in intrathoracic blood volume) were studied in normal and diabetes insipidus rats. In normal rats, clonidine enhanced the increase in urine flow and urea concentration elicited by hypobaric breathing without change in urinary creatinine level. By contrast, in Brattleboro diabetes insipidus rats, clonidine reinforced the hypoxia-induced mechanisms: oliguria, decrease in both urinary urea and creatinine excretions. During normobaric and hypobaric conditions in normal rats administration of clonidine induced an increase in electrolytes (Na+, K+, Cl-) excretion. In Brattleboro rats, clonidine potentiated the decrease in electrolytes excretion elicited by the hypobaric pressure breathing. Since the diuretic reflex elicited by the hypobaric pressure breathing is due to an inhibition of vasopressin release, the present data show that clonidine induces an inhibition of vasopressin release. However, it is suggested that beside this property clonidine also possesses direct vasoconstrictor actions during hypobaric pressure breathing.
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PMID:Renal effect of clonidine during acute hypobaric pressure breathing in normal and diabetes insipidus rats. 649 1


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