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 rat hypothalamo-neurohypophyseal system (HNS) in organ culture has been used as an in vitro system for studying the osmotic control of vasopressin (VP) release. The HNS retains osmotically sensitive components as demonstrated by changes in the rate of VP release following alterations in the osmolality of the culture medium. Increasing the osmolality from 295 to 305 mosmol/kg H2O by the addition of NaCl resulted in a 2.5-fold increase in VP release. VP release was significantly decreased subsequent to reducing the osmolality from 295 to 280 mosmol/kg H2O by the addition of distilled water. Also, VP release was stimulated when the osmolality was increased to 300 mosmol/kg H2O by the addition of mannitol, but not by additions of urea or glucose which resulted in comparable increases in the tonicity of the culture medium. These studies demonstrate that the HNS in organ culture responds appropriately to osmotic challenges within the physiological range, and support Verney's concept of an osmoreceptor inasmuch as both NaCl and mannitol were effective osmotic agents.
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PMID:Osmotic control of vasopressin release by rat hypothalamo-neurohypophyseal explants in organ culture. 59 Jan 95

Seven chronically prepared dogs (electromagnetic flow transducers around the pulmonary and left renal artery, left atrial catheter) maintained on a controlled sodium and water intake were studied. About 20 h after the last intake of food and water, the effects of i.v. methohexitone (initial dose: 6.10 +/- 0.84 mg/kg bw; sustaining infusion: 0.34 +/- 0.10 mg/min.kg bw) on renal excretion of sodium, potassium, urea and water as well as on several haemodynamic values were investigated over a period of 60 min (MP) after a control period (CP) of 60 min in the unanaesthetized state. In 18 of 19 experiments water diuresis (U/Posm less than 1) was observed between 20 and 40 min after starting the administration of methohexitone. Urine volume increased from 44 +/- 21 microliter/min.kg bw (CP) to 104 +/- 62 microliter/min.kg bw (MP).I.v. administration of arginine-vasopressin (ADH) completely abolished water diuresis. During MP, there was a decrease in cardiac output (-11%), stroke volume (-36%) and left atrial pressure (-27%), heart rate increased (+ 43%). Mean arterial blood pressure and renal blood flow did not change. It is assumed-as plasma osmolality did not change-that the central release of antidiuretic hormone is suppressed by methohexitone.
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PMID:[Water diuresis during methohexitone anaesthesia. Studies in chronically instrumented dogs (author's transl)]. 65 67

In awake rats the entire urine output was continuously reinfused i.v. Urine-reinfusion (UR) consistently led to the appearance, within one to two hours, of massive, sustained natriuresis and diuresis, suggesting the existence of potent natriuretic factors in the urine. At the time of maximal natriuresis, mean sodium excretion rate and urine flow rate were 25 and 15 times their respective values in control rats. Ths "urine-reinfusion natriuresis" could be demonstrated despite treatment with desoxycorticosterone acetate, blockage of prostaglandin synthesis by indomethacin or meclofenamate, reduction of plasma urea by pretreatment with a protein-free diet, or heating the urine to 100 degrees C. The natriuresis was not prevented by the absence of vasopressin (in Brattleboro rats) and was augmented by vasopressin infusion. In the Brattleboro rats, a marked increase in (CH2O + CNa)/GFR with only a slight rise in CH2O/GFR during UR suggests inhibition of both proximal and distal tubular reabsorption. Renal blood flow and plasma flow increased markedly during UR with a lesser rise in GFR, consistent with post-glomerular vasodilatation. Thus, the phenomenon of urine-reinfusion natriuresis suggests the presence in rat urine of potent, heat stable natriuretic factors, whose action is largely independent of changes in mineralocorticoids, prostaglandins, urea, or vasopressin. Renal vasodilatation with decreased sodium reabsorption at both proximal and distal nephron sites, appears to play an important role in the natriuresis.
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PMID:Urine-reinfusion natriuresis: evidence for potent natriuretic factors in rat urine. 84 67

There is increasing evidence that urea movement across many epithelia involves more than passive diffusion. Of particular interest is the observation that urea transport across the erythrocyte membrane and across the vasopressin-stimulated urinary bladder of the toad occurs by facilitated diffusion, and can be selectively inhibited by phloretin and chromate. These inhibitory agents have been employed in studies of renal urea reabsorption by the spiny dogfish Squalus acanthias. Both agents inhibit urea reabsorption; the effect of chromate is of particular interest, since it blocks urea reabsorption to a proportionately greater extent than sodium reabsorption, and does so irreversibly.
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PMID:Urea transport in the dogfish kidney. 85 Jan 13

The effect of bradykinin on the renal medullary osmotic gradient was evaluated in anesthetized dogs which were undergoing water diuresis and which received a unilateral renal arterial infusion of bradykinin. The effect of the peptide on the medullary osmotic gradient was determined by analysis of medullary tissue electrolyte and urea concentrations and by analysis of changes in urine osmolality induced by vasopressin. Bradykinin decreased the total osmolality per kg H2O in tissue from inner medulla and papilla (-18.7 +/- 6% and -19.3 +/- 8%) and increased fractional water excretion (3.8 +/- 1.3%). Furthermore, a direct relationship between changes in free water clearance and changes in papillary tissue, osmolality was found. Finally, the increase in urine osmolality after ADH was significantly less in vasodilated than in control kidneys. These results indicate that bradykinin can diminish the medullary osmotic gradient during water diuresis in the dog. Thus, a bradykinin-induced increase in free water clearance may be accounted for by other than an inhibition of proximal tubular sodium reabsorption.
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PMID:Effect of bradykinin on the renal medullary osmotic gradient in water diuresis. 90 88

Recent examinations of the inner medullary collecting tubule membrane in vitro have demonstrated that its reflection coefficient to urea (sigma urea) is significantly less than unity and less than sigma NaClhe presence of antidiuretic hormone. Fluid entering the inner medullary collecting tubule has a higher urea concentration and lower NaCl concentration than does the medullary interstitium, although total osmolarity is nearly equal on either side of the membrane. The transtubular difference in solute composition, together with the difference between sigma urea and sigma NaCl, should result in a driving force for extraction of water from the tubule. This hypothesis was examined in a differential analysis of water and solute fluxes across the collecting tubule epitheliu. The results indicate that this driving force contributes significantly to water extraction from the inner medullary collecting tubule.
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PMID:Water extraction from the inner medullary collecting tubule system: a role for urea. 96 51

The concentrating ability of the kidney was studied by clearance and micropuncture techniques and tissue slice analyses in normal rats with two intact kidneys (intact controls), normal rats with a solitary kidney (uninephrectomized controls), and uremic rats with a single pyelonephritic kidney. Urinary osmolality after water deprivation for 24 h and administration of antidiuretic hormone was 2,501+/-217 and 2,874+/-392 mosmol/kg H2O in intact and uninephrectomized control rats, respectively, and 929+/-130 mosmol/kg H2O in pyelonephritic rats (P less than 0.001 compared to each control group). Fractional water reabsorption and concentrating ability were significantly decreased in the pyelonephritic group, and, to achieve an equivalent fractional excretion of urea, a greater fractional excretion of water was required in the pyelonephritic rats than in the control rats. Whole animal glomerular filtration rate was 1.57+/-0.19 ml/min and 1.39+/-0.18 ml/min in intact and in uninephrectomized controls, respectively, and 0.30+/-0.07 ml/min in pyelonephritic rats (P less than 0.001 compared to each control group). Single nephron glomerular filtration rate was 35.6+/-3.8 nl/min in intact control rats and was significantly increased (P less than 0.05) in both uninephrectomized (88.0+/-10.8 nl/min) and pyelonephritic rats (71.5+/-14.4 nl/min). In all groups fractional water delivery and fractional sodium delivery were closely comparable at the end of the proximal convoluted tubule and at the beginning of the distal convoluted tubule. In contrast, fractional urea delivery out of the proximal tubule was greater in the intact control group (73+/-8%) than in either the uninephrectomized (52+/-2%) or the pyelonephritic group (53+/-3%) (P less than 0.005). Fractional urea delivery at the early part of the distal tubule increased significantly to 137+/-11% and 93+/-6% of the filtered load in intact control and uninephrectomized control rats, respectively (P less than 0.001 compared to the late proximal values of each group), but failed to increase significantly in pyelonephritic rats (65+/-13%), indicating interruption of the normal recycling of urea in the latter group. Analysis of tissue slices demonstrated a rising corticopapillary gradient for total tissue water solute concentration as well as for tissue water urea concentration in both groups of control rats. In contrast, the pyelonephritic animals exhibited no similar gradients from cortex to papilla. These data indicate that the pyelonephritic kidney fails to recycle urea and accumulate interstitial solute. The latter must inevitably lead to a concentrating defect.
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PMID:A study of the intrarenal recycling of urea in the rat with chronic experimental pyelonephritis. 99 48

Twenty-six patients with the syndrome of inappropriate secretion of antidiuretic hormone were reviewed. The underlying diseases were bronchogenic carcinoma (12 cases); myxoedema (five cases); diseases of the nervous system (five cases); bronchopneumonia, carcinoma of the oesophagus, acute intermittent porphria and chlorpropamide therapy (each one case). Serum sodium levels ranged between 104 and 125 mEq per litre. Eighteen patients presented neurological manifestations, which in 14 were considered to be due to hyponatraemia. Neurological signs included disorders of consciousness (stage I and II coma), extrapyramidal signs, asterixis and epileptic seizures. An hyponatraemic coma was the first manifestation of the syndrome in five cases. In all cases where the EEG was recorded it showed non-specific signs of metabolic coma. The fundi never showed signs of intracranial hypertension. Blood urea and creatinine levels were invariably low in the euthyroid patients; these values were normal or elevated in patients with myxoedema and hyponatraemia. Hypokalaemia was frequent, and hypocalcaemia constant. In eleven cases an excess of water intake revealed the clinical syndrome: six patients were excessive beer drinkers and five had received extensive intravenous infusions. In one case the deleterious effect of diuretics was evident, and in another, the syndrome became evident during radiotherapy of an oesophageal tumour. Treatment of the syndrome was successful in all cases. A review of the literature concerning the various pathogenic mechanisms corresponding to the different underlying diseases is presented. The concept of aberrant hormonal production by a tumour is illustrated by an electron microscopic study.
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PMID:Clinical, biological and pathogenic features of the syndrome of inappropriate secretion of antidiuretic hormone. A review of 26 cases with marked hyponatraemia. 100 53

Increases in transepithelial solute permeability were elicited in the frog skin with external hypertonic urea, theophylline, and vasopressin (ADH). In external hypertonic urea, which is known to increase the permeability of the extracellular (paracellular) pathway, the unidirectional transepithelial fluxes of Na (passive), K, Cl, and urea increased substantially while preserving a linear relationship to each other. The same linear relationship was also observed for the passive Na and urea fluxes in regular Ringer and under stimulation with ADH or 10 mM theophylline, indicating that their permeation pathway was extracellular. A linear relationship between Cl and urea fluxes could be demonstrated if the skins were separated according to their open circuit potentials; parallel lines were obtained with increasing intercepts on the Cl axis as the open circuit potential decreased. The slopes of the Cl vs. urea lines were not different from that obtained in external hypertonic urea, indicating that this relationship described the extracellular movement of Cl. The intercept on the ordinate was interpreted as the contribution from the transcellular Cl movement. In the presence of 0.5 mM theophylline or 10 mU/ml of ADH, mainly the transcellular movement of Cl increased, whereas 10 mM theophylline caused increases in both transcellular and extracellular Cl fluxes. These and other data were interpreted in terms of a possible intracellular control of the theophylline-induced increase in extracellular fluxes. The changes in passive solute permeability were shown to be independent of active transport. The responses of the active transport system, the transcellular and paracellular pathways to theophylline and ADH could be explained in terms of the different resulting concentrations of cyclic 3'-5'-AMP produced by each of these substances in the tissue.
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PMID:Actions of external hypertonic urea, ADH, and theophylline on transcellular and extracellular solute permeabilities in frog skin. 108 Jul 96

Ethanol (3%) decreases the potential difference and short-circuit current across the isolated frog skin in chloride Ringer's solution. Unidirectional fluxes of Na and Cl indicate that the drop in short-circuit current is due to an inhibition of the sodium influx. However, ethanol had no effect on the electrical parameters or sodium fluxes, when the frog skin was bathed in chloride-free solutions on both sides or the outside alone. The ethanol response is anion-dependent. In addition, chloride-free media in the inside bathing solution reduced the short-circuit current, indicating a sodium transport pathway which is dependent on chloride and confirming previous data in the literature. Other anions such as sulfate and nitrate could not substitute for chloride. The vasopressin-induced natriferic response and the ethanol effect were found to work independently of each other and different pathways of action are suggested for these agents. The intracellular sodium content of the isolated frog skin epithelium increased and potassium decreased in the presence of the Na-K adenosine triphosphatase inhibitor, ouabain, whereas ethanol or amiloride had no effect. The oxygen consumption of the isolated frog skin was unaffected by up to 10% ethanol. A general metabolic action is probably thus not mediating the response. Urea, in iso-osmotic concentrations to the ethanol, did not mimic its effect. Tritiated water fluxes (in the absence of an osmotic gradient) were reduced by 30% in the presence of 3% ethanol. It is suggested that ethanol may impede the flow of water across frog skin by a physicochemical interaction with membrane pores and the water molecules. The permeability coefficient (Ktrans) for ethanol was found to be 10 times smaller than the Ktrans for water.
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PMID:Effects of ethanol on the permeability of frog skin. 108 5


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