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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Classical dehydration and vasopressin tests for estimation of renal concentrating capacity are inconvenient and sometimes hazardous. We attempted to use the new potent long-lasting synthetic vasopressin analogue (DDAVP) which has no side effects for testing renal concentrating capacity in adults. Four groups of persons were investigated: in Groups 1 and 3, 11 and another 11 healthy subjects; in Group 2, seven convalescent older patients; and in Group 4, 11 patients with pituitary diabetes insipidus (DI). Groups 1 and 2 were investigated during 15 hours' dehydration; DDAVP was given at the end of the 12th hour intravenously (4 microgram) or intransally (80 micron). DDAVP failed to influence strikingly the normal increase in renal concentration induced by lengthening the dehydration from 12 hours to 15 hours. On the other hand, in patients with DI under prolonged treatment as well as in healthy individuals (Group 3), a dose of 20 to 40 microgram of DDAVP administered intranasally induced (at least) as high peak urine osmolality during ad libitum fluid intake as was induced in normal subjects (Group 1) by 12 hours' dehydration alone. In patients with DI the maximal effect of DDAVP obtained during ad libitum fluid intake could be further enhanced by added dehydration. Urine sampling for osmolality three hours after a single intranasal dose of 40 microgram DDAVP during ad libitum fluid intake is a new safe, simple and convenient test for rapid estimation of concentrating ability.
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PMID:1-desamino-8-D-arginine vasopressin (DDAVP) concentration test. 66 11

A highly specific radioimmunoassay for arginine-vasopressin (AVP) in human urine has been developed, with a detection limit of 2.2 fmol/ml. The mean recovery of added AVP was 99.5 +/- 3.1 (S.D.)% when correction was made for the fact that an inverse relationship was observed between the recovery of AVP and the osmolality of the urine. The intra- and interassay coefficients of variation were 3.5--7 and 2.5--10% respectively. Arginine-vasopressin remains stable in urine after repeated freezing and thawing after storage at 4 or 20 degrees C for up to 7 days and at -20 degrees C for more than 3 months. During unrestricted fluid intake in normal people, the mean rate of renal excretion of AVP was 95 +/- 68 (S.D.) fmol/min. An isosmotic reduction of 9% in the plasma volume increased the excretion of AVP to 259 +/- 147 (S.D.) fmol/min. At the height of water-induced diuresis the rate of excretion fell to 70 +/- 28 (S.D.) fmol/min. Fluid deprivation for 18 h produced a moderate but significant increase in mean excretion of AVP, to a value of 116 +/- 67 (S.D.) fmol/min. Patients with compulsive water drinking showed a normal relationship between urine osmolality and the rate of excretion of AVP. In pituitary diabetes insipidus, AVP was undetectable, whereas in hereditary nephrogenic diabetes insipidus a progressive increase in the rate of excretion of AVP was observed in response to dehydration. There was a wide variation in the rate of excretion of AVP (range 126--8704 fmol/min) in patients with unexplained hyponatraemia, presumed to be due to an inappropriate secretion of antidiuretic hormone. Despite this variation, the relationship between urine osmolality and the rate of excretion of AVP clearly differed from that observed in normal people.
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PMID:Radioimmunoassay of arginine-vasopressin in human urine and its use in physiological and pathological states. 74 31

The antidiuretic effects of graded intravenous and intranasal doses of a new vasopressin analogue (DDAVP) were investigated in two groups of patients with pituitary diabetes insipidus. In the first group, three patients with a high requirement of maintenance doses of peroral anti-diuretic drugs were included; and in the second group, ten patients with a normal (usual) requirement were included. Comparing the antidiuretic responses during 24-hour collection periods, DDAVP, on a microgram basis, was less effective in the "high peroral-dose requirement" patients. The duration of action of single intravenous doses (0.04-24 micrograms) of DDAVP was significantly shortened in the "high peroral-dose requirement" group. However, comparing the peak responses induced by increasing doses of DDAVP in the two groups, there was no demonstrable diminution in the anti-diuretic ability of DDAVP in the "high peroral-dose requirement" patients. Although the possibility of a smaller remnant reserve of ADH was also considered, shortened duration of action ot DDAVP suggests more probably enhanced metabolic breakdown of vasopressin in "high peroral-dose requirement" patients.
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PMID:Shortened duration of action of 1-deamino-8-D-arginine vasopressin (DDAVP) in patients with diabetes insipidus requiring high doses of peroral antidiuretic drugs. 78 14

1. After administration of a new vasopressin analogue (DDAVP), a marked and prolonged antidiuresis occurred in 10 patients with pituitary diabetes insipidus. 2. The antidiuretic effects of single intravenous doses of 0.04--24 mug DDAVP and single intranasal doses of 5--320 mug DDAVP were investigated. Time curves of the antidiuretic responses expressed in changes of urine osmolality (Uosm) and free water clearance per 100 ml GFR (CH2O X 100/GFR) are described. 3. Maximal "peak" response was obtained after an intravenous dose of 1 mug within the first 12 hrs (Uosm was 7--800 mOsm/KgH2O). Further increase of dosage resulted only in prolongation of duration of action (up to 48 hrs) and peak ("plateau") effect (up to 24 hrs). 4. There was a linear relationship between the log dose and log osmolality of urine collected in the second 12 hours after administration of single intravenous and intranasal doses of DDAVP. 5. Comparison of the effects of 1 mug lysine-vasopressin and 1 mug DDAVP revealed only slight differences in peak effects, but extreme differences in duration of action. 6. It is concluded that in the evaluation of a synthetic vasopressin analogue the maximal antidiuretic ability and the prolongation of action have to be analysed separately.
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PMID:The antidiuretic action of 1-deamino-8-D-arginine vasopressin (DDAVP) in man. 95 Feb 63

Marked interindividual differences were found in the height and duration of the antidiuretic action induced by increasing single intravenous doses (0.5 mug and 8 mug) of DDAVP in patients with pituitary diabetes insipidus. It was assumed that differences in the duration of action reflected individual variations in the rate of removal of vasopressin.
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PMID:Individual differences in the antidiuretic response induced by single doses of 1-deamino-8-D-arginine-vasopressin (DDAVP) in patients with pituitary diabetes insipidus. 100 61

Cranial diabetes insipidus (DI) arises when release of arginine vasopressin (AVP, antidiuretic hormone) in response to osmotic stimuli is inadequate. The correct diagnosis and management of cranial DI is particularly important when it arises as an acute complication of surgery, trauma or in subjects who lack thirst sensation. Desmopressin (1-desamino-8-D-arginine-vasopressin, DDAVP) provides an effective and convenient replacement therapy when given by the intranasal route. However, nasal administration is difficult for some patients, and in the future oral or transcutaneous desmopressin formulations may prove to be satisfactory alternatives. By contrast, treatments for nephrogenic DI, where there is failure of the antidiuretic response to endogenous or exogenous vasopressin, have been disappointing and water replacement remains the mainstay of therapy. An understanding of the physiology and pathophysiology of water homeostasis and correct interpretation of water balance and electrolyte data are essential for correct diagnosis and management of all cases of DI.
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PMID:Diabetes insipidus. Current treatment recommendations. 138 16

Central diabetes insipidus was diagnosed in association with a dexamethasone-insuppressible adrenocorticotropin-secreting tumor in a dog. Over the 3 years before the dog's death, the combination of specific pituitary function tests, peptide hormone radioimmunoassays, and visualization of the tumor by use of x-ray computed tomography of the skull, allowed an etiologic diagnosis. Because initial signs of glucocorticoid excess were questionable and adrenolytic therapy was not allowed by the owners, treatment consisted only of administration of synthetic vasopressin, which was successful in the management of the diabetes insipidus.
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PMID:Diabetes insipidus and hyperadrenocorticism associated with high plasma adrenocorticotropin concentration and a hypothalamic/pituitary mass in a dog. 284 1

Angiotensin II has been implicated in the regulation of adrenocorticotropin and vasopressin secretion. Angiotensin II may influence the secretion of these hormones either directly at the pituitary gland or by increasing corticotropin-releasing hormone or vasopressin release from cells that are located in the paraventricular hypothalamic nucleus. Pituitary hormone release may also be influenced by circulating angiotensin II through receptors outside the blood-brain barrier in the subfornical organ. We have used alterations in angiotensin II receptors in hypophysectomized, adrenalectomized, and vasopressin-deficient Brattleboro rats as indicators of the activity of angiotensin II in the regulation of adrenocorticotropin and vasopressin secretion. Angiotensin receptor number in the paraventricular nucleus and the subfornical organ, but not in the anterior pituitary gland, was significantly decreased by adrenalectomy, and this effect was reversed by corticoids. Vasopressin deficiency decreased angiotensin receptors in the subfornical organ and increased them in the anterior pituitary gland but did not affect angiotensin II binding in either magnocellular or parvocellular subnucleus of the paraventricular nucleus. Our results suggest that angiotensin II may have a corticoid-dependent role in the regulation of corticotropin-releasing hormone secretion, which could be important in the adaptation to elevated corticosterone secretion in stress.
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PMID:Angiotensin II receptors in paraventricular nucleus, subfornical organ, and pituitary gland of hypophysectomized, adrenalectomized, and vasopressin-deficient rats. 291 2

A 7-month-old Suffolk-cross ram was examined because of polydipsia and polyuria of 2 months" duration. Neurogenic diabetes insipidus was diagnosed on the basis of failure to concentrate urine of low specific gravity in response to water deprivation and a positive response to antidiuretic hormone administration. Post-mortem examination of the brain revealed degeneration in the cerebral peduncles, an absence of pituitary neural tissue and evidence suggesting external pressure as the cause.
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PMID:Neurogenic diabetes insipidus in a sheep. 394 84


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