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)

Isoprenaline, a beta adrenergic agonist, strongly increases both transepithelial fluxes across the urinary bladder of Bufo bufo; this effect is dose dependent, 10(-6)M being necessary for the maximal action. This effect is less selective than that of vasopressin: the ratio J urea/J thiourea is 3.8 under isoprenaline and 30.4 under vasopressin treatment. Both hormones differently affect the permeability of a mainly liposoluble molecule, i.e. antipyrine: vasopressin increases antipyrine permeability, while isoprenaline decreases it. Moreover diethylpyrocarbonate treatment of the luminal membrane strongly inhibits vasopressin effect on urea permeability leaving unmodified that of isoprenaline. However, the actions of both hormones are not additive. These results allows to assume that the tissue has a feedback mechanism which inhibits other hormonal action while the bladder is stimulated by a particular hormone.
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PMID:Permeability properties of the Bufo bufo bladder as affected by isoprenaline and vasopressin. 248 13

Pos and Pd, osmotic and diffusive water permeability coefficients of isolated rabbit proximal tubule (PT) cells (expressed per cm2 of real cell membrane area, in microns/sec) are: Pos 396; Pd, 22; Pos/Pd, 18 (control), and after exposure to parachloromercuribenzenesulfonate (pCMBS): Pos, 32; Pd, 10; Pos/Pd, 3. The sulfhydryl reagent dithiothreitol (DTT) reverts pCMBS action. The activation energies (kcal/mol) are Pos, 3.2 (control); 9.2 (pCMBS); Pd, 5.2 (control) and 9.1 (pCMBS). Thus water channels pierce the control plasma membrane and are reversibly closed by pCMBS. High control PT permeabilities are comparable with those of amphibian urinary bladder and collecting tubules (CT) stimulated with antidiuretic hormone (ADH), and low PT (pCMBS) values with those of CT in the resting state, respectively. Transcellular permeability is regulated in PT by the state of sulfhydryl groups and in CT by ADH induced insertion (or, no ADH, suppression) of water channels. In PT (a) large extracellular markers are dragged by water flow indicating extracellular solute-water interaction, (b) transepithelial Pos is much higher than transcellular Pos. Therefore water also flows paracellularly, in addition to the transcellular flow. In PT paracellular permeability is increased if urea in lumen is higher than in blood. It is reduced in the reverse situation. In CT paracellular permeability is virtually zero (resting condition). It may be increased by high lumen urea. Thus, paracellular permeability (which is significant in control PT and zero in CT) can be regulated by changes in the transepithelial urea concentrations. Transcellular permeability depends on the number of channels/cm2 epithelium, their probability of being opened and their individual permeability.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Channels for water flow in epithelia: characteristics and regulation. 248

Vasopressin (ADH) acts in humans mainly upon renal collecting tubules. By changing their water permeability it plays a key role in regulation of renal water excretion. Acting upon vascular smooth muscle cells, it causes vasoconstriction and raised arterial blood pressure. This hormone was also proven to cause constriction of cultured mesangial cels, it causes vasoconstriction and raised arterial blood pressure. This urea (Seldin, Giebisch 1985), to release the natriuretic hormone as well as to stimulate hepatic glycogenolysis (Abramov et al. 1987). The influence of vasopressin upon peritoneal transport of solutes was studied, too. ADH influenced the passage of phosphate and rubidium through the isolated rabbit mesentery (Berndt, Gosselin 1961) as well as sodium flux through isolated rabbit omentum (Shear et al. 1966). It caused the drop in urea dialysance in dogs subjected to peritoneal dialysis (Henderson et al. 1971). The subject of our study was the assessment of the action of the antidiuretic hormone under "in vitro" conditions upon the peritoneal transfer of urea, the solute present in human body fluids and removable by peritoneal dialysis.
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PMID:Vasopressin-induced changes in permeability of peritoneal mesothelium for urea "in vitro". 248 58

Arginine vasopressin (AVP) increases the urea permeability of the rat terminal inner medullary collecting duct (IMCD) to levels much greater than can be explained by lipid-phase permeation or paracellular diffusion, suggesting the presence of an AVP-stimulated facilitated transport pathway. We tested whether inhibitors of facilitated urea transport in erythrocytes and toad bladder also inhibit urea transport in the isolated perfused IMCD. Apparent urea permeability (Purea) was determined by measuring the flux due to an imposed 5 mM concentration gradient. Phloretin (0.25 mM in lumen or bath) reversibly inhibited Purea. Phloretin, however, did not alter the osmotic water permeability. Urea analogues (200 mM) in the bath inhibited Purea (thiourea, 74% inhibition; methylurea 65%; acetamide 35%). Urea analogues in the lumen decreased Purea with the same order of potency. The inhibitory K1/2 for thiourea in the lumen was 27 +/- 2 mM and did not change with 10(-10) M AVP (28 +/- 3), despite a fourfold increase in Purea. We conclude the following. 1) Inhibitor actions on urea transport in the IMCD are similar to those in red blood cells and toad bladder, suggesting that the urea transporter could be a membrane protein similar to that in the other tissues. 2) Inhibition of Purea by phloretin without an effect on vasopressin-stimulated water permeability supports the view that the urea pathway is not the vasopressin-stimulated water channel. 3) The ability of AVP to increase Purea without an effect on the inhibitory K1/2 for thiourea indicates that AVP probably does not act by altering the binding affinity of individual transporters for urea.
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PMID:Inhibition of urea transport in inner medullary collecting duct by phloretin and urea analogues. 250 65

High concentrations of organic solutes are present in the medulla of the antidiuretic kidney. However, their role in and response to acute changes in the diuretic state are unknown. In this study the organic solute content of the renal medulla was determined from extracts with the use of high-performance liquid chromatography following the acute dilution of the medullary interstitium during various forms of diuresis. After acute infusion of saline and furosemide, inner medullary urea, sodium, inositol, sorbitol, and betaine decrease significantly with no change in glycerophosphorylcholine (GPC) content. After diuresis, inner medullary urea and sodium contents eventually returned to control levels, although inositol, sorbitol, and betaine contents still remained low. Addition of antidiuretic hormone to the saline/furosemide infusion gave similar results. In contrast, induction of diuresis from mannitol infusion caused an acute decrease in all 4 organic solutes, whereas glucose infusion caused an acute decrease in all organic solutes except sorbitol. These data demonstrate that a decrease in all four organic solutes can accompany medullary dilution. However, GPC and sorbitol do not decrease when diuresis is induced by furosemide or glucose, respectively. In addition, the recovery of these compounds in a normally functioning kidney after diuresis is much slower than the regeneration of the sodium chloride and urea gradients.
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PMID:Acute regulation of the predominant organic solutes of the rabbit renal inner medulla. 250 89

To assess whether intracerebroventricular osmoreceptors are involved in vasopressin (AVP) and atrial natriuretic peptide (ANP) release and in the pressor response to centrally administered hypertonic NaCl, artificial cerebrospinal fluid (ACSF) or ACSF made hypertonic by adding 0.2 M NaCl, 0.4 M mannitol, and 0.4 M glucose in isotonic ACSF or 0.4 M urea was infused into the 3rd ventricle of conscious rats. In addition, intravenous infusion of [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]AVP (TMeAVP), a V1-AVP antagonist, was given in rats receiving intracerebroventricular infusion of 0.2 M NaCl in isotonic ACSF. Intracerebroventricular 0.2 M NaCl, 0.4 M mannitol, and 0.4 M glucose in isotonic ACSF increased plasma AVP and mean arterial pressure (MAP) without changing heart rate (HR) or plasma ANP. Urea at 0.4 M decreased plasma AVP and ANP with a slight rise in MAP but no change in HR. ACSF alone did not affect plasma AVP, ANP, MAP, or HR. Intravenous TMeAVP attenuated the pressor response to infusion of 0.2 M NaCl in isotonic ACSF, decreased plasma ANP, but did not affect HR. These results indicate that central osmoreceptors are involved in the release of AVP and in the pressor response to centrally administered hypertonic NaCl.
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PMID:Responses of vasopressin, atrial natriuretic peptide, and blood pressure to central osmotic stimulation. 252 77

A placebo-controlled, randomized, crossover study was conducted to assess a possible effect of a dihydropyridine Ca-entry blocker, nifedipine, on urinary concentration ability in nine healthy men under a water-deprivated condition. Placebo and nifedipine (20 mg) were orally administered on two separate occasions, at least one week apart, after the urinary osmolarity was stabilized. Urinary osmolarity, osmolar clearance, negative free water clearance, urine volume, urinary solutes (Na, K and urea), creatinine clearance and plasma vasopressin (AVP) were measured during the postdose 3-hour period and compared with those during the respective predose (baseline) period. Urinary osmolarity decreased by nifedipine from 1047.2 +/- 34.4 to 873.0 +/- 38.3 mOsm/kg (mean +/- SEM) at 2 hours postdose (P less than 0.05). Mean % decrease in urinary osmolarity at 1 to 3 hours after nifedipine was significantly (P less than 0.01) greater than after placebo. Urine volume significantly (P less than 0.01) increased from the baseline of 0.49 +/- 0.06 to 1.1 +/- 0.15 ml/min at 2 hours after nifedipine. Relationship between osmolar clearance and negative free water clearance relative to glomerular filtration rate observed during the postnifedipine phase was significantly (P less than 0.01) shifted downward compared with that derived from the pooled data unrelated to nifedipine dosing. No significant drug effect was detected on plasma AVP. Both placebo and nifedipine dosed during the continued water deprivation and stabilized urinary osmolarity condition caused an increase in the urinary excretions of solutes. The results indicate that nifedipine inhibits urinary concentration. This does not appear to be due to the inhibition of AVP secretion from the hypophysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of nifedipine on urinary concentrating ability: a placebo controlled study. 259 85

Water transport occurs in all biological membranes. A few selected membranes in the kidney, amphibian urinary bladder, and erythrocyte have very high water permeability and are thought to contain specialized water transporting units termed "water channels." The known biophysical properties of membranes containing water channels are a high osmotic water permeability coefficient (Pf), an osmotic-to-diffusional water permeability coefficient ratio (Pf/Pd) greater than unity, a low activation energy (Ea), and inhibition by mercurial compounds. The biochemical and molecular characteristics of water channel pathways are not known at present. Established and new methods to measure Pf and Pd in kidney tubules and in isolated membrane vesicles from kidney cells are reviewed and evaluated. In the mammalian proximal tubule, a high Pf results from transcellular movement of water across highly permeable apical and basolateral membranes containing water channels. It has been assumed that proximal tubule Pf is unregulated; however, recent results indicate that apical water channels are retrieved by endocytosis and that Pf is decreased fivefold with increasing transepithelial osmotic gradients. In the thin and thick ascending limbs, Pf is nearly the lowest of all biological membranes and is not subject to regulation. In contrast, collecting tubule Pf is subject to hormonal regulation by vasopressin. Vasopressin binding to receptors located at the basal membrane of principal cells initiates adenosine 3',5'-cyclic monophosphate production, which is thought ultimately to activate the exocytic insertion of intracellular vesicles containing water channels into the cell apical membrane. Vasopressin-induced endosomes from kidney collecting tubule and toad urinary bladder contain functional water channels but no proton pumps or urea transporters, supporting a membrane shuttle hypothesis that is selective for water channels. Future directions for the isolation and molecular cloning of kidney water channels are evaluated.
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PMID:Mechanisms and regulation of water permeability in renal epithelia. 268 34

Changes in blood, serum, and urine parameters that are usually associated with fluid and electrolyte balance were studied in 45 volunteers who ran the 1987 Pittsburgh Marathon. There were 39 males and 6 females. The mean age was 39.3 years. Their mean fluid intake was 1650 cc and the mean finishing time was 4 hours and 1 minute. The race was run in the rain with a temperature of 46 degrees F. When the prerace and postrace values of the runners were compared, significant increases were noted in the serum sodium, potassium, blood urea nitrogen (BUN), creatinine, uric acid, creatine phosphokinase (CPK), protein, plasma renin, vasopressin, and urinary potassium. Significant decreases were found in weight, blood pressure, and urinary sodium. No significant differences were noted in serum chloride, serum glucose, and hemoglobin/hematocrit. The mean weight loss of 1.9 kg was less than weight losses reported in marathons run under warmer conditions.
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PMID:Fluid and electrolyte balance during a cool weather marathon. 269 76

This chapter shows how the mammalian kidney is able to regulate the excretion of water independently from that of solutes. For this function, which derives from several evolutionary steps among vertebrates, it takes advantage of the diluting ability of the thick ascending limb to produce osmotic energy which is then used to concentrate solutes in the urine. This concentration is permitted by a highly sophisticated architecture of nephrons and vessels in the renal medulla, combined with special permeability characteristics of the different nephron segments and specific hormonal regulation. Two different types of loops of Henle and several well-insulated vascular compartments contribute to this process. The major nitrogenous waste product, urea, is concentrated by an indirect process involving a transfer of osmotic energy from the outer to the inner medulla. As known for several decades, concentrating function is primarily regulated by the effect of antidiuretic hormone (ADH) on water permeability of the collecting duct. However, as discovered more recently, it is also largely dependent upon the effect of the same hormone on urea permeability in the terminal collecting duct. In addition, recent investigations have revealed a much more complex hormonal regulation of the concentrating process than previously thought. ADH itself acts on many other structures in the kidney, and many other hormones and mediators, the secretion of which is not thought to be influenced by the water status, do affect urine concentration either directly or by their interaction with ADH. Rodents display a wide spectrum of morphological and functional renal adaptations improving water conservation. Their study has brought a better understanding of the significant steps and anatomical structures that contribute to the concentrating process. Finally, it is also apparent that the capacity to concentrate urine is influenced in individual animals of a given species by the availability of water, by specific feeding patterns, and by the protein content of the diet.
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PMID:The role of the kidney in the maintenance of water balance. 269 39


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