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

The purpose of this review is to provide an update on the use of the urine electrolyte and osmolality measurements in patients with disorders of fluid, electrolytes, and/or acid-base metabolism. It is critical to appreciate that there are no 'normal values' for these parameters, only 'expected values' relative to clinical situations. Pitfalls in the interpretation of each electrolyte in the urine are also provided. To detect a mild to moderate degree of reduction of the 'effective' intravascular volume, both urine sodium (Na) and chloride (Cl) concentrations should be measured. Pitfalls in this assessment are abnormal renal and adrenal function and the use of diuretics. Insights into the etiology of the low 'effective' intravascular volume can be deduced by comparing the urine Na, potassium (K), and Cl concentrations. The urine net charge (Cl vs. Na + K) is the most reliable way to estimate the urine ammonium concentration short of its direct measurement, an assay that is not provided by most laboratories. This measurement is important in the differential diagnosis of hyperchloremic metabolic acidosis. To examine the renal response to hypokalemia or hyperkalemia, the two components of K excretion (K secretion and urine flow rate) should be examined separately. The former is evaluated using the transtubular K, concentration gradient. The urine osmolality is used to assess antidiuretic hormone action and the osmolality of the renal medulla and to determine the etiology of polyuria and/or hypernatremia. The urine osmolality can also be used to assess the ammonium concentration, using the urine osmolal gap, and to detect unusual urine osmoles.
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PMID:Urine electrolytes and osmolality: when and how to use them. 219 Apr 69

Renal function was evaluated in six patients with fetal alcohol syndrome (FAS) and eight control subjects before and after fluid restriction and acute acid loading. Baseline serum electrolytes, creatinine clearance, fractional sodium excretion, tubular reabsorption of phosphate, urine and blood pH and osmolalities, plasma renin activity, and plasma aldosterone level were normal in all subjects, but fractional potassium excretion (FEK) was lower in FAS patients than in control subjects (P less than 0.001). Despite equivalent plasma osmolalities (295 +/- 3 vs 293 +/- 2 mosmol/kg, P = 0.2), the maximum urinary osmolality after 12 h of water deprivation in patients with FAS was significantly lower compared with controls (560 +/- 107 vs 965 +/- 77 mosmol/kg; P less than 0.001) and increased to only 578 +/- 101 mosmol/kg after vasopressin administration. After ammonium chloride loading, minimum urine pH was significantly higher in patients than in controls (5.7 +/- 0.17 vs 4.81 +/- 0.19; P less than 0.001). Net acid excretion and FEK were also lower in patients than in controls (102 +/- 11 vs 139.6 +/- 11.3 microEq/min per 1.73 m2 and 23.5 +/- 1.3 vs 29 +/- 1.6%, respectively; P less than 0.001). The data indicate a subclinical renal tubular defect in urine concentration and acidification in patients with FAS.
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PMID:Renal tubular dysfunction in fetal alcohol syndrome. 220 81

The isolated perfused tubule technique was used to study net acid transport in rat terminal inner medullary collecting duct (IMCD) segments. The stop-flow luminal pH [measured fluorometrically with the acidic form of the pH-sensitive dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein in the lumen] fell 0.35 units below the bath pH in tubules from control rats and 0.53 units below the bath in tubules from deoxycorticosterone-treated rats. Tubules from control rats absorbed bicarbonate and secreted ammonium against concentration gradients, although at low rates. In control rats, 10(-8) M vasopressin added to the bath increased bicarbonate absorption almost threefold. Treatment of rats in vivo with deoxycorticosterone significantly increased the rate of bicarbonate absorption in vitro. In vivo NH4Cl loading also significantly increased bicarbonate absorption. Staining microdissected tubules with acridine orange confirmed that the perfused segments lacked intercalated cells. We conclude that the terminal IMCD spontaneously acidifies the lumen despite an absence of intercalated cells. Bicarbonate absorption appears to be regulated by the same factors that affect net acidification in other collecting duct segments.
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PMID:Net acid transport by isolated perfused inner medullary collecting ducts. 230 97

In vitro microperfusion experiments were performed to examine the effects of peptide hormones on bicarbonate and ammonium transport by the medullary thick ascending limb (MTAL) of the rat. Arginine vasopressin (AVP; 2.8 X 10(-10) M in the bath) reduced bicarbonate absorption by 50% (from 7.8 to 3.7 pmol/min per mm). AVP caused a similar reduction in bicarbonate absorption in tubules perfused with 10(-4) M furosemide to inhibit net NaCl absorption. Glucagon (2 X 10(-9) M in the bath) also reduced bicarbonate absorption (from 11.7 to 7.6 pmol/min per mm). The inhibition of bicarbonate absorption could be reproduced with either exogenous 8-bromo-cAMP or forskolin. With 8-bromo-cAMP (10(-3) M) in the bath, addition of vasopressin to the bath did not significantly affect bicarbonate absorption. PTH significantly inhibited bicarbonate absorption, but the extent of inhibition was less than that observed with either AVP or glucagon. Vasopressin had no effect on net ammonium absorption in MTAL perfused and bathed with 4 mM NH4Cl. These findings indicate that: (a) vasopressin, glucagon, and PTH directly inhibit bicarbonate absorption in the MTAL of the rat; (b) this inhibition occurs independent of effects on net NaCl absorption and appears to be mediated in part by cAMP; and (c) HCO3- and NH4+ absorption can be regulated independently in the MTAL.
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PMID:Inhibition of bicarbonate absorption by peptide hormones and cyclic adenosine monophosphate in rat medullary thick ascending limb. 231 60

Cytotoxic ether lipid analogues have been studied for their ability to inhibit growth factor-dependent [Ca2+]i signaling in Swiss 3T3 fibroblasts. 1-Octadecyl-2-methyl-rac-glycero-3-phosphocholine (ET-18-OCH3) inhibited 45Ca2+ uptake and inositol(1,4,5)trisphosphate-induced 45Ca2+ release in saponin permeabilized cells with concentration producing 50% inhibition values of 55 and 360 microM, respectively. When cells were exposed to ET-18-OCH3 for 18 h before permeabilization there was selective inhibition of inositol(1,4,5)trisphosphate-induced 45Ca2+ release with a concentration producing 50% inhibition value of 20 microM, but no effect on 45Ca2+ uptake, or on 45Ca2+ release by arachidonic acid. The concentration of ET-18-OCH3 with continuous exposure to inhibit cell growth 50% was 19 microM. The ether lipid analogues 1-hexadecylthio-2-ethyl-rac-glycero-3- phosphocholine and 1-S-octadecyl-2-O-methylthiopropyl-3-N,N-dimethyl-gamma-hydroxy pro pyl ammonium iodide had effects similar to those of ET-18-OCH3 but the noncytotoxic analogue 1-alkyl-2-hydroxy-sn-glycero-3- phosphocholine was without effect. Exposure of cells to 10 microM ET-18-OCH3 produced 81% inhibition of platelet-derived growth factor-stimulated inositol phosphate formation and 66% inhibition of fluoroaluminate anion-stimulated inositol phosphate formation. Addition of ET-18-OCH3 to cells in medium with 10% fetal calf serum gave a transient increase in [Ca2+]i without causing an increase in resting [Ca2+]i, while the addition of ET-18-OCH3 to cells in medium without serum gave a sustained increase in resting [Ca2+]i. Cells exposed to 5 microM ET-18-OCH3 for 18 h showed no increase in resting [Ca2+]i but there was 95% inhibition of the [Ca2+]i response to platelet-derived growth factor, 63% inhibition of the response to bradykinin, and 55% inhibition of the response to vasopressin. The block by ether lipid analogues of inositol phosphate-mediated [Ca2+]i signaling suggests a mechanism for preventing the action of growth factors that could contribute to the inhibition of cell proliferation by the agents.
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PMID:Inhibition of growth factor-dependent inositol phosphate Ca2+ signaling by antitumor ether lipid analogues. 236 23

Since the first paravertebral blockade was carried out by Sellheim in 1905, this method has proved effective for the isolated blockade of spinal nerves. The efficacy of preoperative intercostal blockade (ICB) in combination with neuroleptanalgesia (NLA) or Pentothal-pentazocine-N2O anesthesia (Pe-Pz) was studied (unilateral analgesia for cholecystectomy). Group 1: NLA; group 2: NLA with ICB; group 3: Pe-Pz; group 4: Pe-Pz with ICB. The analgesic requirement differed significantly between groups 1 (0.33 mg fentanyl) and 2 (0.15 mg fentanyl) and groups 3 (63.5 mg pentazocine) and 4 (31.5 mg pentazocine). There were also significant differences in circulatory responses. The maximum deviation from the initial value at the beginning of the operation in group 1 compared to group 2 was pulse rate + 28.7% vs + 2.4%, mean arterial pressure (Part) + 24.6% vs + 3.1%, and systolic pressure (Psyst) + 33% vs +/- 0%; group 3 compared to group 4: pulse rate + 16.4% vs + 3.2%, Part + 24.5% vs 0.0%, and Psyst + 26.5% vs + 196. The times of action of ICB extended from 7.54 h to 11.33 h for partial analgeisa, time to the first dose of analgesic from 12.3 h to 16.9 h (etidocaine 0.5% and 1% respectively without and with epinephrine). The mean blood levels after 100 mg bupivacaine-CO2 rose to 1.16 micrograms/ml after 5 min and reached a maximum after 15 min (1.29 micrograms/ml) as compared to 0.98 micrograms/ml after addition of ornithine-vasopressin. These values are very much higher than those after the use of bupivacaine-HCl solution. Etidocaine and bupivacaine-HCl have comparable durations of analgesia. Toxicologically, both substances can be applied safely with consideration of all pharmacological data for ICB. Of a total of 3,485 intercostal blockades, 2,775 were applied perioperatively (pre- and postoperatively); 265 were carried out for trauma patients (rib fractures) and 445 for therapeutic indications (herpes zoster neuralgia, tumor pain, costovertebral pain). In 8 blocks 10% ammonium sulfate, in 4 blocks absolute alcohol, and in 19 blocks 5% phenol were used for neurolysis. In 2 cases a marginal pneumothorax was seen, which was resorbed spontaneously (0.06%). Altogether 16,270 single intercostal nerves were blocked. Single-session intercostal blockade can be combined as unilateral analgesia with general anesthesia. This combination is characterized by stable circulatory conditions with avoidance of hypertensive reactions. The long-lasting analgesia allows early mobilization and physiotherapy both postoperatively and posttraumatically in patients with unilateral thoracic and abdominal pain.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The single intercostal block--surgical and therapeutic indications]. 264 21

The thick ascending limb of the rat influences urinary net acid excretion by reabsorbing both bicarbonate and ammonium. The bicarbonate absorption is mediated predominantly by apical membrane Na+-H+ exchange and occurs at rates that are comparable to or greater than rates measured in cortical and medullary collecting ducts. The ammonium absorption is mediated predominantly by apical membrane Na+-NH4+-2Cl- cotransport and enhances urinary ammonium excretion by promoting countercurrent multiplication of ammonium, which facilitates ammonium secretion into medullary collecting ducts. Studies with medullary thick ascending limbs (MTAL) in vitro have shown that the regulation of these transport processes involves both acute responses to changes in the luminal and peritubular environment and adaptive changes in tubule transport capacity in response to chronic systemic acid-base perturbations. In particular, an increase in potassium concentration inhibits ammonium absorption with no effect on net bicarbonate absorption whereas vasopressin inhibits bicarbonate absorption with no effect on net ammonium absorption. Chronic metabolic acidosis causes an adaptive increase in the ability of the MTAL to reabsorb both bicarbonate and ammonium. These results demonstrate that the MTAL is a site of regulation of renal acid-base transport and that ammonium and bicarbonate transport rates can vary independently in this nephron segment.
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PMID:Regulation of acid-base transport in the rat thick ascending limb. 267 55

Isolated rat neurohypophyses were fixed by their stalks to a platinum wire electrode and superfused with Krebs-HEPES solution. Vasopressin and oxytocin released into the medium were determined by specific radioimmunoassays. Hormone secretion was increased by electrical stimulation of the pituitary stalk at different frequencies. The effects of several potassium channel blockers, tetraethyl-ammonium (TEA) ions, 4-aminopyridine (4-AP) and 3,4-diaminopyridine (3,4-DAP) were tested. The release of vasopressin and oxytocin evoked by electrical stimulation with 900 pulses at 15 Hz (about 900 and 1,000 microU, respectively) was about 10 times higher than that evoked by 900 pulses at 3 Hz. Both 10 and 30 mmol/l TEA enhanced the release of vasopressin evoked by stimulation at 3 and 15 Hz, by 25- and 2-fold, respectively, to attain a maximum release of about 1,800 microU per stimulation. The stimulated release of oxytocin attained a maximum of about 9,000 microU at 15 Hz in the presence of 10 mmol/l TEA or at 3 Hz with 30 mmol/l TEA. Thus, in the presence of maximally effective concentrations of TEA both stimulation frequencies (3 and 15 Hz) were equieffective in evoking release of vasopressin and oxytocin. 4-AP or 3,4-DAP enhanced the release of vasopressin evoked by 15 Hz stimulation maximally to about 1,600 microU. In the presence of 4-AP or 3,4-DAP the release of oxytocin evoked by stimulation at 15 Hz increased maximally to about 8,000 microU and that evoked by stimulation at 3 Hz to about 1,500 microU.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of potassium channel blockers on neurohypophysial release of oxytocin and vasopressin. Evidence for frequency-dependent interaction with the endogenous opioid inhibition of oxytocin release. 285 13

The rat mesenteric vasculature contains high affinity binding sites specific for [3H]Arg8-vasopressin which mediate its vasoconstrictor action. We have investigated the in vitro effect of monovalent and divalent cations and guanine nucleotides on the interactions between [3H]Arg8-vasopressin and its receptor in this preparation. Binding was increased by divalent cations from fourfold in the presence of Mg2+ at 5 mM to ninefold in the presence of Mn2+ at 5 mM. The potency order of divalent cations to increase binding was Mn2+ greater than Co2+ greater than Ni2+ greater than Mg2+ greater than Ca2+ approximately equal to control without cations. Addition of Na2+ or other monovalent cations (K+, Li+, and NH4+) in the presence or absence of divalent cations reduced binding significantly. Analysis of saturation binding curves showed a single high affinity site. In the presence of 5 mM Mn2+, binding capacity (Bmax) increased to 139 +/- 23 fmol/mg protein. Receptor affinity was enhanced (KD decreased to 0.33 +/- 0.07 nM). In presence of 5 mM Mg2+ or 150 mM Na+, Bmax and affinity were reduced. The addition of 100 microM GTP or its nonhydrolyzable analogue, Gpp(NH)p, reduced receptor affinity in the presence of Mn2+ + Na+, Mg2+, and Mg2+ + Na+, but not in the presence of Mn2+ alone. Computer modeling of competition binding curves demonstrated that in contrast with saturation studies, the data were best explained by a two-site model with high affinity, low capacity sites and low affinity, high capacity sites. Mn2+ or Mn2+ + Na+ with or without guanine nucleotides resulted in a predominance of high affinity sites. GTP or Gpp(NH)p in the presence of Mg2+ or Mg2+ + Na+ induced a reduction of affinity of the high affinity binding sites and the number of these sites. In the presence of Mg2+ + Na+ and guanine nucleotides, high affinity sites were maximally decreased. An association kinetic study indicated that the association rate constant (K+1) was increased by divalent cations and reduced by guanine nucleotides, without change in the dissociation rate constant (K-1). The equilibrium dissociation constant (KD) calculated with these rate constants (K-1/K+1) was similar to that obtained in saturation experiments at steady state. Dissociation kinetics were biphasic, indicating the presence of two receptor states, one of high and one of low affinity, associated with a slow and a rapid dissociation rate. Cations and guanine nucleotides interact with one or more sites closely associated with vasopressin receptors, including possibly with a GTP-sensitive regulatory protein, to modulate receptor affinity for vasopressin.
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PMID:Effects of monovalent and divalent cations and of guanine nucleotides on binding of vasopressin to the rat mesenteric vasculature. 295 41

To determine the nature, extent, and severity of renal involvement in Laurence-Moon-Biedl syndrome (obesity, mental retardation, polydactyly, hypogonadism, and pigmented retinal dystrophy), we evaluated 20 of 30 patients with the disorder identified from ophthalmologic records in Newfoundland. The mean age was 31 years, and seven were male. All 20 patients had structural or functional abnormalities of the kidneys or both. Three had end-stage renal disease, with two requiring maintenance hemodialysis. The remaining 17 patients had normal serum creatinine values and estimated creatinine clearances. Half the subjects had hypertension. Fourteen of 17 patients could not concentrate urine above 750 mOsm per kilogram of body weight even after vasopressin, whereas all 10 normal controls could. Urinary pH decreased below 5.3 after ammonium chloride administration in all 15 normal controls, but in only 13 of 18 patients. Calyceal clubbing or blunting was evident in 18 of 19 patients studied by intravenous pyelography; 13 patients had calyceal cysts or diverticula. Seventeen of 19 patients had lobulated renal outlines of the fetal type. Four patients had diffuse renal cortical loss, but only two of these had renal insufficiency. We conclude that Laurence-Moon-Biedl syndrome includes the presence of renal abnormalities.
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PMID:The spectrum of renal disease in Laurence-Moon-Biedl syndrome. 341 78


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