Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The carbon dioxide produced by toad urinary bladders bathed on their mucosal surfaces by sodium Ringer solution and on their serosal surfaces by modified Leibovitz tissue culture medium was analysed by multiple regression on both sodium transport and time. The fractions contributed by metabolism related to transport and by basal metabolism were assessed, and the extent to which these might vary with time was determined. This analytical method, which improves the accuracy with which suprabasal metabolism is estimated, was used to examine the effects on metabolism of vasopressin, aldosterone, and mucosa-positive voltage-clamping. Vasopressin (0.05 u./ml), which on average increased sodium transport 2.9 times and concurrently increased the rate of carbon dioxide production in these transporting tissues, also altered the carbon dioxide production of non-transporting, amiloride-treated control hemibladders. For each hemibladder the ratio of sodium transported to suprabasal carbon dioxide produced after vasopressin was compared with that observed before vasopressin. Differences between the ratios were much reduced when the carbon dioxide productions of the paired transporting hemibladders were corrected for the effects of vasopressin on basal carbon dioxide production. With such analysis, it was confirmed that vasopressin did not alter the stoichiometry of sodium transport. A 30 mV, mucosa-positive voltage clamp, applied near the peak of the response to vasopressin, further increased both sodium transport and carbon dioxide production. No alterations of the ratio of sodium to suprabasal carbon dioxide were seen under these conditions where the maximal rate of active sodium transport in this tissue must have been approached. Active sodium transport was more than doubled some 4 h after adding aldosterone (10(-7) M). However, the related increase in suprabasal carbon dioxide production was greater than threefold. Therefore, whereas the stimulation resulting from vasopressin and voltage clamping had no effect on the ratio of sodium transported to suprabasal carbon dioxide produced, this ratio was reduced significantly by aldosterone. When the sodium transport of aldosterone-treated bladders was increased further by voltage clamping, the ratio of sodium transported to suprabasal carbon dioxide production remained at the reduced value. Sodium transport was increased by approximately 35% more when aldosterone-treated hemibladders were voltage clamped after vasopressin, the control paired hemibladders being exposed to vasopressin and voltage clamping alone.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Effects of hormonal and electrical stimulation of sodium transport on metabolism of toad urinary bladder. 669 80

The role of the antidiuretic hormone-independent mechanisms underlying the impairment of water excretion in hypothyroidism remains controversial. We examined the excretion of an oral water load (50 ml/kg b.w.) over a 3-hour period before and after the administration of aldosterone, methylprednisolone, both aldosterone and methylprednisolone, and triiodothyronine in 12 hypothyroid and 7 age-matched control Wistar rats of the homozygous Brattleboro strain (DI). Conscious animals were studied to circumvent the adverse influence of anesthetics and to facilitate the re-examination of the same animals. At baseline, the hypothyroid DI rats exhibited a marked impairment in their response to water administration. In comparison to control DI rats they had a lower urine volume, CH2O, CH2O/V and creatinine clearance, and higher urine osmolality (p less than 0.005-less than 0.001). Because of the possibility of decreased delivery of filtrate due to dehydration in the DI animals, a separate group of DI rats received saline in place of the water load. Despite improvement in urine flow with saline, CH2O generation remained decreased in the hypothyroid DI rats. Methylprednisolone increased both urine volume (p less than 0.001) and CH2O (p less than 0.001) in the hypothyroid group, but CH2O formation remained below the values obtained in the control animals. While aldosterone and methylprednisolone alone and in combination improved utilization of distally-delivered filtrate for the formation of CH2O (p less than 0.02-0.005), neither hormone, either alone or in combination, fully corrected the dilution defect. In contrast, the administration of triiodothyronine fully normalized all the observed abnormalities in the hypothyroid rats, suggesting that thyroid hormone deficiency is directly responsible for the abnormal water-excretion in experimental hypothyroidism.
 ...
PMID:Effects of aldosterone, methylprednisolone and triiodothyronine on the response to water loading in the conscious hypothyroid rat with diabetes insipidus. 672 5

To determine the effects of acute blood gas derangements on renal water and solute excretion and vasopressin secretion, six unanesthetized mongrel dogs were studied during 1) combined acute hypoxemia and hypercapnic acidosis [arterial O2 partial pressure (PaO2) 36 +/- 1 Torr, arterial CO2 partial pressure (PaCO2) 54 +/- 2 Torr, pH 7.18 +/- 0.01], 2) acute hypoxemia (PaO2 33 +/- 2 Torr, PaCO2 33 +/- 1 Torr, pH 7.34 +/- 0.01), and 3) acute hypercapnic acidosis (PaO2 83 +/- 3 Torr, PaCO2 53 +/- 1 Torr, pH 7.19 +/- 0.02). Combined acute hypoxemia and hypercapnic acidosis increased (P less than 0.05) mean arterial pressure, but renal hemodynamic function deteriorated with decreased (P less than 0.05) glomerular filtration rate and increased (P less than 0.05) renal vascular resistance. Moreover free water clearance became more negative (P less than 0.05) and urine osmolality increased (P less than 0.05). During acute hypoxemia or acute hypercapnic acidosis alone, mean arterial pressure and renal hemodynamic function were unchanged but free water clearance became more negative (P less than 0.05). During acute hypoxemia, urine osmolality increased (P less than 0.05) comparably with values observed during combined acute hypoxemia and hypercapnic acidosis. Plasma vasopressin concentrations increased profoundly (P less than 0.05) during combined hypoxemia and hypercapnic acidosis and during acute hypoxemia alone and were significantly elevated (P less than 0.05) above the increased plasma vasopressin concentrations observed during acute hypercapnic acidosis. We conclude that acute hypoxemia and hypercapnic acidosis result in impairment of renal water excretion, probably mediated through vasopressin secretion.
 ...
PMID:Antidiuresis and vasopressin release with hypoxemia and hypercapnia in conscious dogs. 674 23

The aim of the present study was to determine the magnitude and direction of the shift of body fluids during water immersion of humans to the neck. Five healthy male subjects were studied lying in air for 1.5 h, sitting in 34 degrees C water to the neck for 1 h, and again lying in air for 1.5 h in two sets of experiments. For the first set, vasopressin (0.75 IU, sc) was injected before immersion. Blood and urine samples were drawn every 30 min in air and every 20 min in water. Urinary sodium, potassium, and osmolal clearances were significantly increased during immersion. When the mean maximum change during immersion was calculated for five subjects hematocrit fell by 1.1 U, plasma concentrations of sodium by 3.9 meq/l, chloride by 3.5 meq/l, potassium by 0.2 meq/l, osmolality by 7.9 mosmol/kg H2O, and proteins by 0.25 g/100 ml, whereas total plasma CO2 content increased by 1.33 mmol/l, threonine by 11.6%, proline by 9.0%, methionine by 14.0%, and alanine by 29%. Plasma volume increased 6.1%, and red blood cell volume calculated from hematocrit and hemoglobin increased 3.5%. In the second set of immersion experiments, without vasopressin injection, interstitial fluid pressures were measured with a cotton wick in PE-50 tubing inserted subcutaneously. A mean interstitial fluid pressure of -0.5 cmH2O was observed when the subjects were lying in air. Interstitial fluid pressure had started to decrease by 20 min of immersion, with a maximum decrease during immersion averaging 2.10 cmH2O. We conclude that hyposmotic fluid is mobilized into the blood from interstitial and other extravascular spaces during immersion.
 ...
PMID:Osmoregulation and interstitial fluid pressure changes in humans during water immersion. 679 64

Urinary excretion rate of antidiuretic hormone (UADHV) was studied in male volunteers in response to hypobaric hypoxia. The first series consisted of three groups. The chamber was decompressed to 465, 495, and 438 Torr during high-altitude (HA) exposure for groups I (n = 5), II (n = 5), and III (n = 4), respectively. In group I, the chamber air contained 3.77% CO2 to prevent alkalosis. The level of hypoxemia was similar in groups I and II. Mean 24-h UADHV was unchanged in group I, but increased 96% (P less than 0.05) and 180% (P less than 0.05) in groups II and III, respectively, on day 1 at HA and was normal during subsequent days at HA regardless of symptoms of acute mountain sickness. Shorter sampling intervals employed in a second series of experiments conducted at 495 Torr revealed a twofold increase in UADHV (P less than 0.05) 8-12 h after ascent in eight asymptomatic subjects; UADHV returned to base line within 9 h and remained low. The symptomatic subjects both had increased UADHV (3- and 8-fold from base line) between 2 and 4 h after ascent. Increased UADHV in asymptomatic subjects may be a result of the concomitant decrease in plasma volume, both of which appeared to be eliminated by CO2 supplementation.
 ...
PMID:Antidiuretic hormone responses to eucapnic and hypocapnic hypoxia in humans. 681 99

The effects on cerebral blood flow of alpha- or beta-adrenergic receptor stimulation of cerebral vessels were examined in 13 unanesthetized goats before and during hypercapnia produced by inhalation of 10% CO2 in air. This procedure increased the PCO2 from 34 to 52 and was accompanied by a fall in pH from 7.39 to 7.26. Electrical stimulation of the cervical sympathetic nerve and injections of norepinephrine and tyramine into the internal maxillary artery produced reductions in cerebral blood flow that were abolished or reduced in hypercapnia. The increase in cerebral blood flow in response to beta-adrenergic stimulation with isoproterenol was also reduced. Hypercapnia caused a similar depression of the constrictor and dilatory effects of the nonadrenergic drugs vasopressin and diazoxide. The results show a decreased response of cerebral vessels to adrenergic and nonadrenergic stimuli in hypercapnia. The findings do not suggest any difference between the refractoriness of cerebral vessels in hypercapnia and that described in other vascular beds.
 ...
PMID:Reduction of cerebrovascular reactivity during hypercapnia. 708 68

The effects of 75 ml ethanol ingested over 60 min on plasma osmolality (Posmol) and plasma vasopressin (PAVP) in four normal subjects were studied. In the 1st h of the investigation PAVP fell, then rose, even though plasma ethanol levels were still rising. The rise in PAVP was preceded by a rise in Posmol corrected for the influence of ethanol. The fall in PAVP was followed by an increase in free water clearance and a decrease in urine osmolality, while the later rise in PAVP was followed by a decrease in free water clearance (CH2O) and a rise in urine osmolality. The relationship between PAVP and Posmol was then studied during intravenous (iv) hypertonic saline infusion in five subjects. The results were compared with those from a second infusion in the same subjects after ingestion of ethanol (0.5 ml/kg). Ethanol reduced vasopressin release in response to iv hypertonic saline infusion, and this correlated with a reduced decrease in CH2O. We conclude that ethanol inhibits PAVP release by decreasing the response of the osmosodium receptors to changes in plasma tonicity.
 ...
PMID:Effect of ethanol ingestion on plasma vasopressin and water balance in humans. 708 77

1. In a preliminary study, a positive pressure of 25 mmHg applied to the lower body raised right atrial pressure by a mean of 7 mmHg. 2. Sustained application of lower-body positive pressure (LBPP) in six normal adult males increased sodium excretion ([Na]V) from a control level of 126.5 +/- 10 mumol/min to 213 +/- 21 mumol/min (P = 0.003) and fractional sodium excretion (EfNa) from 0.7 +/- 0.1 to 1.2 +/- 0.1 (P = 0.001). 3. Urine flow (UF) increased from 0.85 +/- 0.07 ml/min to 4.1 +/- 0.8 ml/min (P = 0.002), osmolar clearance (Cosm) from 2.6 +/- 0.13 ml/min to 4.2 +/- 0.4 ml/min (P = 0.003) and free water clearance (CH2O) from -1.75 +/- 0.1 ml/min to -0.1 +/- 0.01 ml/min (P = 0.001). Creatinine clearance (Ccr) showed no significant change. 4. After dopamine blockade with domperidone, LBPP did not cause a rise in [Na]V or EfNa. However, urine flow, Cosm. and CH2O remained significantly above control values, implying persistent suppression of antidiuretic hormone. 5. Dopamine blockade without positive pressure did not affect basal sodium excretion.
 ...
PMID:Abolition, by dopamine blockade, of the natriuretic response produced by lower-body positive pressure. 710 30

The effects of prostaglandin F2 alpha on renal function were studied in hydropenic dogs. Peak responses occurred in 45 to 60 min. PGF 2 alpha (0.3 microgram.kg-1.min-1) increased urine flow by 1.3 +/- 0.3 ml/min and increased sodium excretion by 27.1 +/- 4.6 microEq/min. Papillary nonurea solute concentration was decreased from 981 +/- 153 to 347 +/- 58 mOsm/kg of H2O and the corticomedullary urea gradient was abolished. Although renal blood flow, glomerular filtration rate, peritubule capillary hydrostatic pressure and renal venous pressure were not changed by PGF2 alpha, urine from the infused kidney became distinctly hypotonic. A "washout" of medullary solutes was not supported by the data since the volume of distribution of 125I-albumin, an index of papillary perfusion rate, was not changed by PGF2 alpha. The contribution of decreased salt reabsorption from Henle's loop was evaluated in dogs that received furosemide and produced essentially isotonic urine. Subsequent intrarenal PGF2 alpha, increased CH2O and produced hypotonic urine with no significant further change in UNaV. These studies suggest that inhibition by PGF2 alpha of salt reabsorption from the thick ascending limb of Henle's loop may account for the modest natriuretic effect and contribute to the dissipation of the nonurea solute gradient. Additionally, there is an inhibition of both vasopressin-mediated water and urea reabsorption which contributed to the diuretic and hyposthenuric effects of infused prostaglandins.
 ...
PMID:Mechanisms of the natriuretic and diuretic effects of prostaglandin F2 alpha. 722 97

Transcellular shifts of water and changes in the physiology of water excretion are common in diabetes mellitus and its treatment. Recent evidence indicates that hyperglycemia in diabetic patients, but not in normal subjects, is characterized by elevations of circulating levels of arginine vasopressin (AVP; antidiuretic hormone, ADH). The role and importance of these observations remain to be defined since elevations of plasma AVP levels do not decrease water excretion in diabetic patients. Certain oral sulfonylureas, notably chlorpropamide and tolbutamide, are known to decrease renal free water clearance (CH2O), whereas insulin increases CH2O; the insulin and tolbutamide effects may be clinically trivial, whereas that of chlorpropamide is important. The hyponatremic effect of chlorpropamide may be exaggerated in diabetic patients by concomitant diuretic therapy. Euglycemia during chlorpropamide therapy appears to allow full expression of the action of chlorpropamide on CH2O; hyperglycemia with attendant osmotic diuresis protects chlorpropamide-treated patients against hyponatremia. Inhibition of prostaglandin synthesis with nonsteroidal anti-inflammatory agents enhances expression of the ADH effect on the kidney, but it does not appear to potentiate chlorpropamide hyponatremia. Two other oral sulfonylurea agents, tolazamide and glyburide, increase CH2O. Diazoxide is an antihypertensive thiazide which is antidiuretic as well as hyperglycemic. Thus, abnormalities of water metabolism are common in diabetes mellitus. Whether certain of these abnormalities are clinically important depends upon the presence of the osmotic diuresis of hyperglycemia and the pharmacology of diabetic management.
 ...
PMID:Water metabolism in diabetes mellitus. 745 88


<< Previous 1 2 3 4 5 6 7 8 9 10