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)

Intranasal administration of DDAVP (1-deamino-8-D-arginine vasopressin), a synthetic analogue of vasopressin, followed by measurement of urine osmolaity 6 h afterwards, represents a convenient, reliable and simple method for the estimation of renal concentrating capacity in children. The DDAVP-test is as accurate and reproducible as the water deprivation test, irrespective of the degree of concentrating capacity. Mean urine osmolality after DDAVP in children without renal disease was found to be 984 +/- 218 mosmol/kg water (m +/- 2 SD). In children with recurrent pyelonephritis, urine osmolality after DDAVP was decreased. The values were significantly lower with bilateral changes than with unilateral changes of chronic pyelonephritis in the i.v. urograms. In chronic pyelonephritis the concentrating capacity appears to be earlier impaired than other parameters of renal function.
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PMID:Intranasal DDAVP-test in the study of renal concentrating capacity in children with recurrent urinary tract infections. 42 96

The renal reabsorption of water independent of solute is the result of the coordinated function of the collecting duct and the ascending limb of the loop of Henle. The unique juxtaposition of the ascending and descending portions of the loop of Henle and of the vasa recta permits the function of a counter-current multiplier system in which water is removed from the tubular lumen and reabsorbed into the circulation. The driving force for reabsorption is the osmotic gradient in the renal medulla which is dependent, in part, on chloride (followed by sodium) pumping from the thick ascending loop of Henle. Urea trapping is also thought to play an important role in the generation of a hypertonic medullary interstitium. Arginine vasopressin (AVP) acts by binding to receptors on the cell membrane and activating adenylate cyclase. This, inturn, results in the intracellular accumulation of cyclic adenosine monophosphate (AMP) which in some fashion abruptly increases the water permeability of the luminal membrane of cells in the collecting duct. As a consequence, water flows along an osmotic gradient out of the tubular lumen into the medullary interstitium. Diabetes insipidus is the clinical condition associated with either a deficiency of or a resistance to AVP. Central diabetes insipidus is due to diminished release of AVP following damage to either the neurosecretory nuclei or the pituitary stalk. Possible causes include idiopathic, familial, trauma, tumor, infection or vascular lesions. Patients present with polyuria, usually beginning over a period of a few days. The diagnosis is made by showing that urinary concentration is impaired after water restriction but that there is a good response to exogenous vasopressin therapy. Nephrogenic diabetes insipidus can be identified by a patient's lack of response to AVP. Nephrogenic diabetes insipidus is caused by a familial defect, although milder forms can be acquired as a result of various forms of renal disease. Central diabetes insipidus is eminently responsive to replacement therapy, particularly with dDAVP, a long lasting analogue of AVP. Nephrogenic diabetes insipidus is best treated with a combination of thiazide diuretics as well as a diet low in sodium and protein.
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PMID:The clinical physiology of water metabolism. Part II: Renal mechanisms for urinary concentration; diabetes insipidus. 54 67

Two patients with sodium-losing renal disease were studied in detail. Both presented with shock and hypotension which was attributed at first to other causes, as was the recurrent hyponatraemia in one of them. In both patients the cause of the sodium loss was probably unrelieved urinary obstruction which has been reported previously to cause water loss but not sodium loss. Both patients had severe hyponatraemia when they were sodium depleted, which has previously been attributed to water retention from excessive secretion of antidiuretic hormone. Plasma arginine vasopressin concentrations were raised in one patient but not in the other. The cause of the water retention in the other patient is not known. One of the patients, like others described in the literature, was only able to vary his sodium excretion within narrow limits. He became sodium depleted on a normal intake and oedematous when he was given saline intravenously. We suggest that the term sodium-losing renal disease should be replaced by the term 'fixed sodium' excretion renal disease.
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PMID:Sodium losing renal disease: Two cases and a review of the literature. 67 48

We observed idiopathic light-chain proteinuria in a patient with multiple abnormalities of proximal-tubule transport mechanisms (Fanconi syndrome), nephrogenic diabetes insipidus, and distal renal tubular acidosis. Seventeen of the 19 urinary amino acid levels measured were elevated. Uric acid and phosphate clearances were greater than 60 per cent and 50 per cent, respectively, of the simultaneous inulin clearance. When water deprivation was coupled with vasopressin administration, the maximum urinary concentration observed was 384 mOsm per kilogram of water. During ammonium-chloride loading, the level of hydrogen-ion concentration in the urine remained less than 100 times that in the blood. Kappa light-chain excretion was 149 mg per 24 hours. It appears that the concurrence of proximal tubular dysfunction, distal tubular dysfunction and light-chain proteinuria represents a distinct syndrome, which we call "combined light-chain nephropathy." Available evidence indicates that excessive light-chain production with subsequent filtration, reabsorption and catabolism, causes the complex tubular dysfunctions observed.
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PMID:Light-chain nephropathy. Renal tubular dysfunction associated with light-chain proteinuria. 81 85

The influence of antidiuretic hormone (ADH) and papaverine on hydroxyquinoline-induced nephropathy in rats was tested, using histotopochemistry, enzyme activity measurement and morphometric investigation. Hydroxyquinoline causes a marked increase in renal weight, the development of wedge-shaped foci with severely dilated tubule segments, and a simultaneous reduction in dehydrogenases, alkaline phosphatase, and alpha-naphthyl esterase. Both ADH and papaverine produced a significant inhibition of renal damage. The subjective findings were quantitatively confirmed by measurement of enzyme activity, using the microscope photometer, and by morphometric studies with the Leitz-Classimat (determination on the basis of the alkaline phosphatase reaction) of the surface percentage of brush border in the proximal tubules. A disturbance of the hairpin counter-current system is to be considered as the cause of the renal lesion. This disturbance is caused by hydroxyquinoline-induced impairment of Na+/K+ transport, especially in the thick ascending limb of Henle's loop. Our results show that the hydroxyquinoline nephropathy can be favourably influenced both by stimulation of water re-absorption and possibly also transepithelial Na+ transport (ADH), and by increasing the blood flow of the arteriolae rectae with a resultant lowering of the intratubular urine concentration (papaverine). The dependency of hydroxyquinoline nephropathy on the phylogenetically determined concentration capacity of the kidney, and the effective influencing of the condition by ADH and papaverine indicate the importance of the degree of efficiency of the medullary countercurrent system in the pathogenesis of this renal lesion.
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PMID:The significance of the hairpin counter-current principle in the pathogenesis of toxic kidney lesions. An investigation of the influence of antidiuretic hormone and papaverine on hydroxyquinoline nephropathy of the rat. 88 59

Basic physiology and pathophysiological mechanisms of renal concentrating ability and its defects are discussed. Normal urinary concentration depends on the concerted action of a variety of factors. Consequently, many different causes may underly the symptom of polyuria. Clinical tests of concentrating ability (water deprivation, pitressin test) are of diagnostic importance in diabetes insipidus and polydipsia, but have little practical value in the work-up for chronic renal disease. A critical analysis of maximal concentrating capacity (TcH2O) during induced osmotic diuresis is conducted. It is inferred that the height and shape of the normal TcH2O curve results basically from two physiological processes: It is raised by increasing NaCL transport out of the medullary parts of the ascending limbs of Henle's loops and lowered by influx of hypotonic tubular urine into the collecting ducts. Preponderance of hypotonic influx may result in hypotonic final urine in the absence of tubular functional abnormalitiy. It is not appropriate, therefore, to classify renal concentrating defects according to the shape and height of the TcH2O curve. A synopsis and short description of the known renal concentrating defects is given. They are classified into hereditary, metabolic, diuretic-induced, and toxic disturbances, as well as those seen in renal disease of various etiology. Each defect is discussed in terms of the underlying pathophysiological mechanism as far as currently understood. The most important mechanisms are either disturbed NaCL transport in the ascending limb of Henle's loop, or antidiuretic hormone (ADH) dependent or ADH independent decrease in water permeability of the enddistal convolutions and collecting ducts, or osmotic diuresis.
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PMID:[Diagnosis and pathophysiology of renal concentration disorders]. 100 42

1. Healthy subjects, given a long-acting preparation of vasopressin intramuscularly, excreted a significantly less concentrated urine than when subjected to fluid deprivation for 28 h. 2. When fludrocortisone, a potent mineralocorticoid, was given in addition to vasopressin the urine was not significantly less concentrated than after fluid deprivation. 3. Oral urea-loading also enhanced the urine-concentrating power of vasopressin but its effect was less marked than that of fludrocortisone. Oral urea did not increase further the urine concentration achieved by combined fludrocortisone and vasopressin. 4. Renal concentrating power was assessed in fourteen patients with renal disease and impaired concentrating ability. Fludrocortisone significantly enhanced the urine concentration achieved by vasopressin alone and the resultant urine was not significantly less concentrated than that achieved by fluid deprivation. 5. The action of fludrocortisone in enhancing the urine-concentrating effect of vasopressin is similar to that of aldosterone and is probably due to the increased sequestration of solute in the renal medulla, caused by increased reabsorption of sodium chloride in the ascending limb of the loop of Henle. 6. In the clinical assessment of renal concentrating power, the combined use of fludrocortisone and vasopressin has potential advantages over established methods.
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PMID:Assessment of urine-concentrating ability in man: effect of fludrocortisone and urea in enhancing response to vasopressin. 112 20

The metabolism and renal effects of enflurane were studied during and after anesthesia in ten surgical patients without renal disease; ten control patients received halothane. Enflurane was metabolized to inorganic fluoride with a mean peak serum level of 22.2 +/- 2.8 muM four hours after anesthesia. Urinary inorganic and organic fluoride excretions were increased but oxalic acid excretion was not, suggesting that the latter is not an enflurane metabolite. Postanesthetic renal function, including the response to vasopressin, was normal in both groups. During enflurane anesthesia renal blood flow, glomerular filtration rate, and urinary flow rate were 77, 79, and 67 per cent of control values, respectively. In this study of patients without renal disease, metabolism of enflurane to inorganic fluoride was insufficient to cause clinically significant renal dysfunction.
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PMID:Metabolism and renal effects of enflurane in man. 124 74

Studies of renal afferent fibers and their functions have continued since the work of Pines in 1959 (Fiziol. Zh. SSSR Im. I M Sechenova 45: 1339-1347, 1959). The kidney contains mechanoreceptors and chemoreceptors that appear to have two major functions. First, renal mechano- and chemoreceptors evoke a variety of renorenal reflexes, while more global cardiovascular reflexes are primarily evoked by renal mechanoreceptors. A second function of renal afferent fibers is to cause the pain of renal disease. Recent studies suggest that renal afferent fibers may also regulate secretion of vasopressin from the pituitary gland. Substantial evidence indicates that, although most renal afferent fibers enter the spinal cord, their functions depend to a large extent on supraspinal circuitry. Thus our research has focused on defining characteristics of spinal neurons that relay renal information to the brain. In the cat, neurons in the L2-T11 segments with excitatory responses to renal A delta and C fiber input project to the medial medullary reticular formation and to the caudal and rostral ventrolateral medulla. Renal afferent information reaches these cells by way of the least splanchnic nerve and by way of more than one dorsal root. In the monkey spinothalamic neurons in the L3-T10 segments respond to renal nerve stimulation. Excitatory responses predominate, but inhibitory responses occur in L2 and L3. These cells also respond to renal A delta and C fibers. Stimulation of renal mechanoreceptors by occlusion of the ureteropelvic junction or renal vein excites feline spinoreticular neurons. Graded increases in renal vein pressure produce graded increases in cell responses. Activation of renal chemoreceptors increases activity of spinal interneurons. Within the L2-T11 segments, cells responding to ureteral occlusion are located caudally, cells with responses to renal artery occlusion are located rostrally, and cells responding to renal vein occlusion are located in between. The differential locations of cells with these inputs suggests the existence of a coding mechanism for different renal receptor populations. Distention of the renal pelvis is a potent stimulator of primate spinothalamic neurons. These neurons encode renal pelvic pressures in the noxious range and appear to be important in mechanisms of renal pain.
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PMID:Bowditch Lecture. Renal afferent inputs to ascending spinal pathways. 131 32

This review summarizes various aspects of the inherited kidney disorder nephrogenic diabetes insipidus (NDI). The clinical manifestations of the disease are presented. The important role of the genetic localization of the NDI gene to the X-chromosome long arm, in region Xq28, for carrier detection and early (prenatal) diagnosis of the disorder is emphasized. Following an overview of the cellular physiology involved in the antidiuretic action of vasopressin, possible mechanisms in the pathogenesis of NDI are discussed. We hypothesize that NDI is most probably due to the absence or abnormality of the renal V2 receptor. This assumption is strengthened by recent findings in receptor studies, which indicate a general V2 receptor defect in NDI, and in experiments with somatic cell hybrid cell lines, which are consistent with a co-localization of the genes for NDI and for the V2 receptor in the Xq28 region. Finally, the efficacy of the combination amiloride-hydrochlorothiazide, compared with the indomethacin-hydrochlorothiazide regimen, in the treatment of NDI is presented and the advantages of the former combination are discussed.
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PMID:Nephrogenic diabetes insipidus: clinical symptoms, pathogenesis, genetics and treatment. 145 33


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