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

Intramembranous particle aggregates in the luminal membrane of toad bladder granular cells after vasopressin stimulation have been found to correlate closely and specifically with induced alterations of water permeability. Roles for microtubules and microfilaments in mediating the latter response have been proposed on the basis of studies involving colchicine and cytochalasin B, respectively. In the present investigation the effects of these agents on both initiating and sustaining vasopressin-induced osmotic water flow and the particle aggregation phenomenon were studied. The results indicate that during initiation the aggregation and water flow responses to vasopressin are each colchicine- and cytochalasin B-sensitive and that these sensitivities can be wholly additive. However, after full vasopressin stimulation is established, the same responses demonstrate sensitivity only to cytochalasin B, not to colchicine. The findings, therefore, suggest that microtubules and microfilaments may be independently necessary for the initiation of the aggregation and water flow responses to vasopressin, and that microfilaments, but not microtubules, are required for their maintenance.
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PMID:Possible roles for microtubules and microfilaments in ADH action on toad urinary bladder. 10 10

Concentrations of the antidiuretic hormone, arginine vasopressin, were measured in 28 patients with severe hyperglycemia to determine if abnormalities in hormonal regulation of water excretion could contribute to the extreme dehydration of uncontrolled diabetes mellitus. Vasopressin levels were markedly elevated in both nonketotic and ketotic patients, indicating that vasopressin deficiency plays no role in the polyuria that accompanies hyperglycemia. Instead, the observed increases in vasopressin represent an ineffective effort to conserve water in the face of an overwhelming solute diuresis caused by the glucosuria. The reasons for such marked elevations in plasma vasopressin in these diabetic patients are multifactorial. Both groups of diabetic patients had evidence of hypovolemia, which was sufficient in magnitude to stimulate vasopressin release. Furthermore, nausea provided an independent stimulus to vasopressin secretion in many patients. Osmotic stimulation might have resulted from the large fraction of unidentified plasma solutes, but this factor alone was not sufficient to explain the markedly increased concentrations of vasopressin. Whether such elevations in vasopressin could have metabolic and/or hemodynamic effects in uncrontrolled diabetes remains to be established.
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PMID:Plasma vasopressin in uncontrolled diabetes mellitus. 10 67

The hypothalamic-neurohypophyseal system functions to maintain plasma osmolality within narrow limits. It also is an important mechanism in maintaining normal body fluid volume. The system exerts its influence via release or inhibition of vasopressin (antidiuretic hormone, ADH) which acts on the kidney to decrease water excretion. Deficiency of ADH is usually due to hypothalamic-neurohypophyseal lesions (central diabetes insipidus) or insensitivity of the kidney to ADH (nephrogenic diabetes insipidus). These patients, if untreated, have the predictable result of dehydration, hyperosmolality, hypovolemia, and eventual death in severe cases. On the other hand, ADH excess of the syndrome of inappropriate ADH secretion due to a variety of causes promotes water retention, hypoosmolality and hyponatremia which, if untreated, may progress to convulsions, coma, and death. It is obviously important to diagnose accurately these pathologic states of hydration. Not only is initiation of treatment in general dependent upon recognition of the disease, but each type of pathologic hydration state has specific treatment which rewards both patient and physician with effective correction of the problem.
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PMID:Vasopressin: deficiency, excess and the syndrome of inappropriate antiduretic hormone secretion. 10 6

The ability of somatostatin to modify the water premeability of the toad bladder was examined. Somatostatin had a small effect on basal water flow and antagonized the hydrosmotic effect of vasopressin. Water flow induced by cyclic AMP was enhanced. These results may explain the diuretic and hyposthenuric effects of somatostatin in vivo.
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PMID:Antagonism of vasopressin-induced water flow by somatostatin. 10 4

The effects of intracerebral injection of angiotensin II (AII) on both water intake and arginine-vasopressin (AVP) release were tested on unanesthetized rhesus monkeys (Macaca mulatta). Injection of 10(-10) mol of peptide was administered with a cannula microinjection system stereotaxically implanted into different diencephalic structures. The preoptic area, anterior part of third ventricle, caudate nucleus, and septum appeared to be the injection sites most effective in eliciting both drinking behavior and AVP release when the animal did not have access to water. On the contrary, when water was presented, AVP release was blocked after AII microinjections in the preoptic area and the third ventricle. No drinking was observed after microinjection in the supraopticus nucleus although AVP release was stimulated. These data suggest that AII might be effective in the regulation of water balance by centrally controlling both the input (drinking) and the output (ADH secretion) of water.
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PMID:Vasopressin release and drinking induced by intracranial injection of angiotensin II in monkey. 11 63

A patient with a syndrome of inappropriate antidiuretic hormone secretion secondary to an undifferentiated bronchogenic carcinoma with distant metastases was treated with demethylchlortetracycline. Up until recently, treatment of this syndrome was based on water restriction and when the plasma sodium concentration became extremely low, hypertonic saline solution administration. Recently it has been demonstrated that the antibiotic demethylchlortetracycline inhibits the action of the antidiuretic hormone on the renal tubules. The drug has been used successfully in five patients with the syndrome of inappropriate antidiuretic hormone secretion. The administration of 900 mg of demethylchlortetracycline per day for 7 days in our patient produced an increase of free water clearance, diuresis, plasma sodium concentration, and plasma osmolarity. Urinary excretion of sodium and urinary osmolarity declined. Furthermore, the neurological symptoms attributed to hyponatremia improved markedly. The patient lost 6 kg during treatment, probably because of negative water balance induced by demethylchlortetracycline. Even though the administration of demethylchlortetracycline did not produce significant decreases in the glomerular filtration rate or renal blood flow in our patient, it is advisable to control the renal function in individuals treated with this drug since it may on occasion determine renal insufficiency.
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PMID:[Treatment of the syndrome of inappropriate antidiuretic hormone secretion with demethylchlortetracycline (author's transl)]. 11 37

A 72-year-old woman with the syndrome of inappropriate secretion of antidiuretic hormone of unknown cause during more than one year of observation is reported. Plasma vasopressin levels were excessively elevated, even during a water load test. Her serum electrolyte abnormalities and general state were ameliorated after fluid restriction. During treatment with demeclocycline the patient was able to increase fluid without deterioration.
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PMID:The syndrome of inappropriate secretion of antidiuretic hormone. A case report. 11 86

In the urinary bladder of amphibia, hypertonicity of the serosal bath (SH) evokes an increase in transepithelial water permeability, the characteristics of which resemble the response to antidiuretic hormone (ADH). The ionic dependency, in particular for Ca2+, appears very similar for SH- and ADH-induced water fluxes. In the present experiments La3+ was used as a probe to study the Ca2+-dependency of the hydrosmotic response to SH in isolated urinary bladder of the toad Bufo marinus. Addition of La3+ (5 mM) on the serosal side of the membrane produced a significant and reversible increase in basal transepithelial water flux. The hydrosmotic response elicited by adding 250 mM mannitol to the serosal Ringer's solution was inhibited by 30% in the absence of serosal Ca2+. Similarly, the hydrosmotic response to SH was inhibited by 37%, 30% and 40% when 5 mM La3+ was added to the serosal medium 30 min before, concommitantly with, or 60 min after induction of SH. The inhibition of transepithelial water flux observed in the absence of serosal Ca2+ or in the presence of serosal La3+ was reversible. The results support a critical role for Ca2+ in the modulation of transepithelial water permeability in the urinary bladder of amphibia. Ca2+ presumably exerts its effects at a post-cyclic AMP step.
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PMID:Reversible inhibition by lanthanum of the hydrosmotic response to serosal hypertonicity in toad urinary bladder. 11 63

1. Large concentrations (in mM) of ethacrynic acid (0.1), furosemide (1.0), theophylline (5.0) and osmotic diuretics (100.0) sharply increased the flux of water along an osmotic gradient through the frog urinary bladder wall. Spironolactone (0.1), and hydrochlorothiazide (5.0) showed only a weak action on osmotic permeability. MercusalR, clopamide and triamterene did not affect water transport. 2. The presence of 0.2--1.0 mU/ml vasopressin (ADH) after pretreatment with a diuretic did not result in summation of the effects of both drugs used. 0.01--0.1 mM ethacrynic acid and 0.01 mM MercusalR significantly decreased the reaction to ADH. 1.0 mM furosemide, 0.1 mM spironolactone, 0.01 mM clopamide and 0.8 mM acetazolamide did not change the reaction to ADH. A reduction in the cellular response to ADH and a decrease in the osmotic permeability of the tubular wall may be responsible in part for the diuretic action of ethacrynic acid and MercusalR.
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PMID:The effect of diuretics and vasopressin on the osmotic permeability of the frog urinary bladder. 13 27

Using micropuncture techniques, the author studied the effect of vasopressin on renal function in young rats at three stages of development -- in the middle of the weaning period (22 days), after weaning was over (30 days) and at the beginning of the sexual maturation period (42 days). In the presence of a hypotonic load, a small dose of vasopressin (12 muU/100 g b.w., i.v.) was most effective in the youngest age group, where it reduced the urine flow by 82% both by increasing water reabsorption and by reducing the GFR. In this group, vasopressin lowered the TF/P Na+ ratio and raised the TF/P K+ ratio in the initial part of the distal tubules of the superficial nephrons, but raised water absorption only beyond the initial part of the distal tubules. Vasopressin reduced the urine flow by 72% in 30-day-old rats by raising water reabsorption beyond the initial part of the distal tubules. The only ion to be affected was K+, whose concentration rose in the final urine. In 42-day-old rats the effect of vasopressin was manifested in only mild depression of the GFR. In this age group, as distinct from younger animals, anaesthesia and surgery evidently led to endogenous vasopressin release, so that the small dose of exogenous vasopressin did not significantly influence the test parameters. This is also underlined by the significant difference between the control urine flow of the 42-day-old and the younger rats.
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PMID:The effect of vasopressin on renal function in young rats a clearance and micropuncture study. 13 28


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