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)

The effects of naturally occurring lysine and arginine vasopressins (LVP and AVP) were compared with those of 1-deamino-8-D-arginine-vasopressin (dDAVP) and 1-deamino-4-valine-D-arginine-vasopressin (dVDAVP). The changes of minute diuresis, urinary osmolarity and the duration of action were followed. dDAVP and dVDAVP in a single intravenous and intranasal dose decreased the diuresis more markedly (3.5-fold) and for a longer duration (3.3-fold) than did LVP in patients with central diabetes insipidus. The administration of dDAVP and dVDAVP in the form of sublingual tablets also proved to be effective, where dVDAVP acted more markedly and longer (16 hrs) than dDAVP (12 hrs) in a single dose of 30 micrograms. During one week of sublingual dDAVP administration, the accumulation of the drug was indicated by the gradual decrease of diuresis and the increase of urine osmolarity. The misuse of such highly active drugs may even result in iatrogenic inappropriate ADH syndrome (Schwartz-Bartter). The danger of this syndrome will be demonstrated in a case history. Some more recently synthesized vasopressin analogues with antagonistic action on the diuresis may have an important role in the therapy of Schwartz-Bartter syndrome. The authors present their results with one of these antagonists [1-(beta-mercapto-beta, beta-cyclopentamethylene-propionic acid), 2-O-ethyltyrosine, 4-valine] arginine vasopressin (d/CH2/5Tyr/Et/VAVP) both in Brattleboro and in R-Amsterdam rats. This analogue blocks the antidiuretic effect of both exogenous and endogenous vasopressin.
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PMID:[The effect of vasopressin analogs on water metabolism]. 666 81

A 24-year-old female with gastrointestinal disturbances, nausea and vomiting, had a convulsion with loss of urine and bitten lips on the 5th day of hospitalization. A significant decrease of sodium and potassium levels and lowered osmolality of the serum as well as urinary hyperosmolality permitted the diagnosis of the so-called syndrome of inappropriate antidiuretic hormone release (SIADH) of unknown aetiology, described by Schwartz-Bartter. Twice short tests for porphyria were negative; then the elevated porphyrin precursors collected in 24 h urine indicated the existence of an acute intermittent porphyria. A clinical follow-up and improvement were demonstrated by the EEG findings. Since animal experiments and pathohistological findings indicate that porphyrin metabolites such as delta-amino laevulinic acid and porphobilinogen may influence inhibitory and neurosecretory structures in central nervous tissue and interfere with GABA, cerebral hyperexcitability as well as disturbance of electrolytes may be explained. Finally, the question of whether the EEG changes are due to the significant electrolyte disturbances or are typical signs of acute intermittent porphyria is discussed.
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PMID:[EEG changes in a patient with acute intermittent porphyria and a Schwartz-Bartter syndrome (SIADH)]. 681 70

A sensitive and specific radioimmunoassay for the measurement of arg-vasopressin (AVP) in human plasma is described. Recovery of added AVP from plasma was about 65-70%. An acetone extraction step was necessary to prevent unspecific blank effects. Sensitivity of the assay is 0.5 pg AVP/ml plasma. In normally hydrated subjects AVP-concentration ranged from 0.7 pg/ml to 5.8 pg/ml and showed a good correlation with plasma osmolality. In patients with complete diabetes insipidus (D.i.) AVP-values were below the sensitivity limit of the method and they were subnormal when D.i. was incomplete. There was no increase of AVP-concentration during fluid restriction in patients with complete or incomplete D.i. In subjects with psychogenic polydipsia AVP-values were normal and dehydration produced adequate rises of plasma AVP. In patients with SIADH (Schwartz-Bartter-syndrome) AVP-values were greatly enhanced (greater than 10 pg/ml) when correlated to plasma osmolality (less than 170 mosmol/kg H2O).
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PMID:Radioimmunoassay of arginine-vasopressin in human plasma: development and clinical application. 684 47

In this article, we have discussed the localization of components of the renal renin-angiotensin system, as well as the existing information on the regulation of this axis and the effects of Ang II on renal function. All the components of the renin-angiotensin system are present in both fetal and adult kidney. In the adult kidney, renin is principally localized to jg cells of the distal afferent arteriole, where release is stimulated by increases in intracellular cAMP and inhibited by increases in cytosolic calcium. Four distinct stimuli mediating renin release are (1) NaCl sensed at the macula densa, (2) the sympathetic nervous system, (3) humoral factors, with Ang II, vasopressin, endothelin, and adenosine inhibiting renin release, and (4) changes in intrarenal blood pressure. Alterations in renal renin gene expression have been reported in pathophysiological states, such as salt depletion, diabetes mellitus, ureteral obstruction, Bartter's syndrome, and with high protein feeding. The highest renal concentrations of mRNA for the renin substrate angiotensinogen are found in the PT, where the protein is localized to subapical granules. Both salt depletion and androgens upregulate renal angiotensinogen mRNA. Of interest, renal angiotensinogen mRNA levels are lower in SHR than in normotensive WKY rats. As with angiotensinogen, renal ACE is mainly localized to the PT, with highest concentration on the brush border. The mechanisms of regulation of both renal angiotensinogen and ACE require further study. Using recently developed specific nonpeptide Ang II receptor antagonists, it appears that adult renal Ang II receptors are principally of the AT1 class, whereas fetal kidney Ang II receptors are of the AT2 subtype. By binding to AT1 receptors, Ang II exerts constrictive effects on both afferent and efferent arterioles, with increased effect reported on efferent arterioles. Glomerular Ang II receptors are localized to mesangial cells, mediating contractile responses resulting in changes in glomerular surface area and Kf, and potentially regulating mesangial sieving and phagocytosis. These receptors are reduced with salt restriction or in experimental diabetes. The highest concentrations of tubular Ang II receptors are found in PT, on both brush border and basolateral membranes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The intrarenal renin-angiotensin system. 843 83

Among the factors, which may influence on the uric acid metabolism, the excess or deficiency of some hormones apparently induces the abnormal serum uric acid level. We described hyperuricemia and hypouricemia associated with endocrine disorders. Hyperuricemia due to the increased production of uric acid is observed in myopathy associated with hypothyroidism, hyperthyroidism or hypoparathyroidism. Hyperuricemia due to the decreased renal uric acid clearance is associated with hypopituitarism, hypothyroidism, hyperparathyroidism, central diabetes insipidus, nephrogenic diabetes insipidus, Bartter syndrome, and diabetic ketoacidosis. Hypouricemia due to the increased renal uric acid clearance is associated with hypoparathyroidism, primary aldosteronism and inappropriate secretion of antidiuretic hormone (SIADH).
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PMID:[Abnormal serum uric acid level in endocrine disorders]. 897 20

Renal tubular function was studied in an 8-month-old male infant with Bartter's syndrome, which is characterized by hypokalemic metabolic alkalosis, normotensive hyperreninemic hyperaldosteronism, and reduced pressor response to angiotensin II. Chloride transport along the diluting segment (CH2O/CH2O + CCl) was impaired. Furthermore, furosemide did not elicit normal natriuresis, which suggested impaired chloride reabsorptive capacity at the furosemide-sensitive ascending limb of Henle's loop. Loss of antidiuretic hormone-mediated urinary concentration was in support of this. These findings pointed to the thick ascending limb of Henle's loop as the site of the primary defect in this child.
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PMID:Studies on the site of renal tubular defect in Bartter's syndrome. 924 1

A patient who developed syndrome of inappropriate secretion of antidiuretic hormone (SIADH) during progression of metastatic breast cancer is described. The classic criteria for SIADH as defined by Bartter and Schwartz were fulfilled and conditions other than malignant disease were excluded as causes of the syndrome. To the knowledge of the authors SIADH has never been reported to develop during the course of malignant disease in a patient with metastatic breast cancer. It should be borne in mind that SIADH may occur in patients with malignant disease and hyponatraemia, even in the absence of small-cell lung cancer, which is the classic tumour type to develop SIADH.
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PMID:Development of syndrome of inappropriate secretion of antidiuretic hormone during progression of metastatic breast cancer. 929 53

We have used homologous recombination to disrupt the mouse gene coding for the NaK2Cl cotransporter (NKCC2) expressed in kidney epithelial cells of the thick ascending limb and macula densa. This gene is one of several that when mutated causes Bartter's syndrome in humans, a syndrome characterized by severe polyuria and electrolyte imbalance. Homozygous NKCC2-/- pups were born in expected numbers and appeared normal. However, by day 1 they showed signs of extracellular volume depletion (hematocrit 51%; wild type 37%). They subsequently failed to thrive. By day 7, they were small and markedly dehydrated and exhibited renal insufficiency, high plasma potassium, metabolic acidosis, hydronephrosis of varying severity, and high plasma renin concentrations. None survived to weaning. Treatment of -/- pups with indomethacin from day 1 prevented growth retardation and 10% treated for 3 weeks survived, although as adults they exhibited severe polyuria (10 ml/day), extreme hydronephrosis, low plasma potassium, high blood pH, hypercalciuria, and proteinuria. Wild-type mice treated with furosemide, an inhibitor of NaK2Cl cotransporters, have a phenotype similar to the indomethacin-rescued -/- adults except that hydronephrosis was mild. The polyuria, hypercalciuria, and proteinuria of the -/- adults and furosemide-treated wild-type mice were unresponsive to inhibitors of the renin angiotensin system, vasopressin, and further indomethacin. Thus absence of NKCC2 in the mouse causes polyuria that is not compensated elsewhere in the nephron. The NKCC2 mutant animals should be valuable for uncovering new pathophysiologic and therapeutic aspects of genetic disturbances in water and electrolyte recovery by the kidney.
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PMID:Uncompensated polyuria in a mouse model of Bartter's syndrome. 1077 55

Nephrogenic diabetes insipidus which can be inherited or acquired, is characterized by an inability to concentrate urine despite normal or elevated plasma concentrations of the antidiuretic hormone, arginine-vasopressine (AVP). Polyuria, with hyposthenuria and polydipsia are the cardinal clinical manifestations of the disease. Hypercalcemia, hypokaliemia, lithium administration and chronic renal failure are the principal causes of acquired nephrogenic diabetes insipidus. About 90 percent of patients with congenital nephrogenic diabetes insipidus are males with X-linked recessive nephrogenic diabetes insipidus who have mutations in the arginine-vasopressin receptor 2 (AVPR2) gene that codes for the vasopressin V2 receptor. The gene is located in chromosome region Xq28. In about 10 percent of the families studied, congenital nephrogenic diabetes insipidus has an autosomal recessive or autosomal dominant mode of inheritance. In these cases, mutations have been identified in the aquaporin-2 gene (AQP2), which is located in chromosome region 12q13 and codes for the vasopressin-sensitive water channel. Other inherited disorders with mild, moderate or severe inability to concentrate urine include Bartter's syndrome and Cystinosis. Identification of the molecular defect underlying congenital nephrogenic diabetes insipidus is of immediate clinical significance because early diagnosis and treatment of affected infants can avert the physical and mental retardation associated with episodes of dehydration.
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PMID:[Nephrogenic diabetes insipidus]. 1708 61

Cl(-) channels play important roles in the regulation of a variety of functions, including electrical excitability, cell volume regulation, transepithelial transport and acidification of cellular organelles. They are expressed in plasma membranes or reside in intracellular organelles. A large number of Cl(-) channels with different functions have been identified. Some of them are highly expressed in the kidney. They include members of the CLC Cl(-) channel family: ClC-K1 (or ClC-Ka), ClC-K2 (or ClC-Kb) and ClC-5. The identification of mutations responsible for human inherited diseases (Bartter syndrome for ClC-Kb and Dent's disease for ClC-5) and studies on knockout mice models have evidenced the physiological importance of these CLC Cl(-) channels, permitting better understanding on their functions in renal tubule epithelial cells. The cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel, also expressed in renal tubule epithelial cells, is involved in the transepithelial transport of Cl(-) in the distal nephron. This short review focuses on intrarenal distribution, subcellular localization and function of the ClK(-1), ClC-K2 and ClC-5 Cl(-) channels in renal tubule epithelial cells, and the role of the CFTR Cl(-) channel in chloride fluxes elicited by vasopressin in the distal nephron.
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PMID:Expression and function of CLC and cystic fibrosis transmembrane conductance regulator chloride channels in renal epithelial tubule cells: pathophysiological implications. 1747 25


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