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)

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

Lithium (Li+) chloride, 2 to 3 mEq. per kilogram of body weight, was administered intraperitoneally to normal Wistar rats daily for 4 to 66 days. This resulted in a marked reduction in urine osmolality (Uosm.) and increase in the excretion of water, Na+, K+, uric acid, and phosphate. The excretion of uric acid and potassium was a direct function of UNaV. The magnitude of depression in urine osmolality was significantly related to the rate of excretion of lithium in the urine, suggesting that the change in water reabsorption is dependent on the presence of the ion in the luminal side of the tubule. During 2 per cent saline diuresis, Li+-treated rats achieved less fractional free water reabsorption (TcH2O/GFR times 100) at any level of fractional osmolar clearance (Cosm./GFR times 100) than normal rats. On the other hand, during 0.225 per cent saline diuresis, fractional free water clearance (CH2O/GFR times 100) was normal over a wide range of fractional urine flow (V/GFR times 100), indicating intact function of the ascending limb of the loop of Henle. The intravenous infusion of vasopressin (VP) or dibutyryl cyclic-adenosine monophosphate (dcAMP) to Li+-treated rats resulted in a modest rise in Uosm. and a reduction in V/GFR times 100 and CH2O/GFR times 100. Although the response to VP appeared earlier than that to dibutyryl cyclic-AMP, the magnitude of the changes in Uosm., V/GFR times 100, and CH2O/GFR times 100 was eventually the same with both substances. Comparison between normal and Li+-treated rats revealed that the response to both VP and dibutyryl cyclic-AMP was blunted, albeit to a greater extent in the former. Inhibition by Li+ of adenylate cyclase will only partially explain the present data. Impairment in the release of endogenous VP or a block distal to the formation of cyclic-AMP must have played a role. In view of a normal diluting capacity and the increase in the excretion of phosphate and uric acid, it is suggested that Li+, when administered chronically in the present doses, inhibits proximal tubular reabsorption.
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PMID:Renal effects of lithium administration in rats: alterations in water and electrolyte metabolism and the response to vasopressin and cyclic-adenosine monophosphate during prolonged administration. 16 79

1. The influence of partial hepatectomy on urinary concentrating ability and renal tissue sodium was determined in conscious rats deprived of water for 24 h. In comparison with a sham operation, partial hepatectomy resulted in: a) a 50% reduction in free-water reabsorption, urinary osmolality, and osmolal urine-to-plasma ratio; b) depression of free-water reabsorption at similar levels of osmolal clearance above 200 microliter/min per ml of GFR during the infusion of hypertonic NaCl and vasopressin; and c) a 30% reduction in sodium content of the renal papilla and outer medulla. 2. The renal response to an intravenous water load (2.5% glucose infused to 2.5% of body wt at 0.4 ml/min) was determined in sham-operated and partially hepatectomized, conscious rats. By 60 min after the water load, both groups had excreted practically all of the load. However, during and for 30 min after the infusion in the partially hepatectomized group, the percent of the water load excreted, urine flow, and free-water clearance were significantly reduced while urinary osmolality and osmolal urine-to-plasma ratio were significantly elevated. 3. These experiments demonstrate that shortly after partial removal of the liver the renal concentrating ability is defective and the excretion of a water load is not grossly impaired.
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PMID:Concentration and dilution of the urine in partially hepatectomized, conscious rats. 56 70

Thermoregulatory reactions evoked by selective preoptic-anterior hypothalamic (PO/AH) heating in conscious rabbits were associated with significant changes in renal function. Urine flow rate decreased from a control value of 0.92 +/- (S.E.) 0.08 to 0.47 +/- 0.07 ml/min after 10-20 min of heating, urine osmolality increased from 273 +/- 34 to 417 +/- 46 Osm/kg H2O, and free water clearance per 100 ml GFR decreased from 1.11 +/- 0.46 to -0.50 +/- 0.23 ml/min. These changes were followed by a gradual recovery despite continued heating. Clearances of exogenous creatinine and p-aminohippurate fell transiently during the first 10 min of heating and then returned to normal. Plasma antidiuretic activity (ADA) measured by rat bioassay increased regularly and markedly during PO/AH heating but was poorly correlated with changes in urine concentration. Moreover, a similar increase in plasma ADA observed with selective heating of a different brain area (supraoptic nucleus) never produced urine concentration or other renal changes. This suggests that a large and variable fraction of ADA appearing in rabbit blood in response to thermal stimuli was not identical with antidiuretic hormone. Therefore, the causal relationship of ADH release and antidiuresis associated with thermoregulatory reactions could not be clearly demonstrated. The physiological role of renal water conservation would be to compensate for extrarenal water loss related to thermal sweating or panting.
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PMID:Renal function changes during preoptic-anterior hypothalamic heating in the rabbit. 56 82

The effect of lowering the pressure of oxygen from 80 to 34 mm Hg was examined in anesthetized dogs that were undergoing a water diuresis. This degree of hypoxia was associated with an antidiuresis as urine osmolality (Uosm) increased from 107 to 316 mosmol/kg H(2)O (P < 0.001) and plasma arginine vasopressin increased from 0.06 to 7.5 muU/ml, (P < 0.05). However, hypoxia was not associated with significant changes in cardiac output (CO, from 4.2 to 4.7 liters/ min), mean arterial pressure (MAP, from 143 to 149 mm Hg), glomerular filtration rate (GFR, from 46 to 42 ml/min), solute excretion rate (SV, from 302 to 297 mosmol/min), or filtration fraction (from 0.26 to 0.27, NS). Hypoxia was associated with an increase in renal vascular resistance (from 0.49 to 0.58 mm Hg/ml per min, P < 0.01). The magnitude of hypoxia-induced antidiuresis was the same in innervated kidneys and denervated kidneys. To further examine the role of vasopressin in this antidiuresis, hypoxia was induced in hypophysectomized animals. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in hypophysectomized animals was the same as in intact animals. In contrast to intact animals, however, hypoxia did not induce a significant antidiuresis in hypophysectomized animals (Uosm from 72 to 82 mosmol/kg H(2)O). To delineate the afferent pathway for hypoxia-stimulated vasopressin release, hypoxia was induced in dogs with either chemo- or baroreceptor denervation. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in the denervated animals was the same as in nondenervated animals. Hypoxia resulted in an antidiuresis in chemoreceptor (Uosm from 113 to 357 mosmol/kg H(2)O, P < 0.001) but not in baroreceptor (Uosm from 116 to 138 mosmol/kg H(2)O, NS) denervated animals. To determine if hypoxia alters renal response to vasopressin, exogenous vasopressin was administered to normoxic and hypoxic groups of dogs. The antidiuretic effect of vasopressin was no different in these two groups. These results demonstrate that hypoxia induces an antidiuresis which is independent of alterations in CO, MAP, SV, filtration fraction, renal nerves, or renal response to vasopressin and occurs through baroreceptor-mediated vasopressin release. The nature of the baroreceptor stimulation remains to be elucidated.
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PMID:Mechanism of effect of hypoxia on renal water excretion. 70 76

The present investigation evaluated the renal and hemodynamic responses to head-out water immersion in dogs. Dogs were immersed in the vertical (seated) position in a 34 degrees C bath. Urine flow (V), osmolar clearance (Cosm), free water clearance (CH2O), sodium excretion (UNa+V), potassium excretion (UK+V), GFR, effective renal plasma flow (ERPF), central venous pressure (CVP), and cardiac output (CO) all increased significantly during immersion. This response was unchanged by bilateral cervical vagotomy or by deoxycorticosterone acetate and antidiuretic hormone administration. The control values of these dogs were low and indicated a state of peripheral vascular pooling which was readjusted to normal by the immersion maneuver. The renal and hemodynamic values during the period of immersion were similar to values of a group of dogs which were recumbent in air. Furthermore, when the latter group of dogs were tilted head down 19 degrees, there was no further increase in any of the measured parameters. These data are consistent with the view that water immersion in the upright dog simply redistributes blood volume back to that level seen in the recumbent dog, a position which is more natural for this species.
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PMID:Contribution of peripheral pooling to the renal response to immersion in the dog. 73 May 76

The diuretic effect of a three-day glibenclamide treatment was studied in 8 healthy subjects during maximal sustained water diuresis before and after administration of 0.04 mug l-deamino-8d-arginine vasopression (DDAVP). The antidiuretic response (decrease in free water clearance per 100 ml GFR and increase in urine osmolality) induced by DDAVP was significantly reduced by glibenclamide. In addition, changes in urine osmolality indicated a shorter duration of DDAVP -antidiuresis. These findings are consistent with the hypothesis that glibenclamide competitively inhibits the peripheral action of vasopressin.
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PMID:Inhibition of the antidiuretic effect of 1-deamino-8d-arginine vasopressin (DDAVP) by glibenclamide in water-loaded healthy subjects. 81 89

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

Various parameters of renal function were studied before, during, and after the infusion of physiological increments of angiotensin II directly into one renal artery of anesthetized dogs. During water diuresis and during antidiuresis induced with exogenous antidiuretic hormone (ADH), angiotensin II consistently reduced UNaV, UKV, and CPAH, and increased the filtration fraction in the infused kidney. Urinary osmolality was increased only in the presence of ADH, while during water diuresis angiotensin II had no apparent effect on urinary osmolality or flow rate. During saline diuresis, a mean increment of angiotensin II concentration of 14 pg/ml was sufficient to significantly reduce UNaV and urinary flow rate. Changes in CCr, CPAH, and filtration fraction did not correlate with changes in sodium excretion, and intracortical distribution of blood flow remained unaltered. These data support the hypothesis that normal circulating levels of angiogensin II play a direct renal role in the control of sodium, potassium, and water homeostasis, and that angiotensin II exerts a direct, stimulatory effect on tubular sodium reabsorption independent of changes in GFR, RPF, filtration fraction, or intracortical distribution of blood flow.
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PMID:Stimulation of renal sodium reabsorption by angiotensin II. 85 Nov 87

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


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