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 possible role of the proximal tubule in the natriuresis which follows the administration of small doses of lithium, as used in lithium clearance studies, was investigated in 12 healthy males on a fixed sodium intake. Subjects were given placebo tablets, or 100 mg or 600 mg of lithium carbonate; renal function was assessed 3-6 h later. The 600-mg dose of lithium carbonate caused a 50-60% increase in sodium excretion, whereas the 100-mg dose was without effect. Creatinine clearance, used as an index of glomerular filtration rate, was unaffected by either dose. Three indices of end-proximal fluid delivery were used simultaneously: urine flow rate during suppression of vasopressin secretion (Vmax), phosphate clearance and lithium clearance (the latter only on the days on which lithium was administered). No effect of either dose of lithium on Vmax or phosphate clearance was evident; nor was there a difference between values for lithium clearance following the two doses. We conclude that administration of the standard 600-mg test dose of lithium carbonate does not affect proximal tubular function.
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PMID:The natriuretic effect of lithium in man: is the proximal tubule involved? 863 88

Using in situ hybridization methods that discriminate mRNAs encoding rat vasopressin V1a, V1b, V2 and oxytocin receptors in hepatic, brain and renal tissues, experiments were done to determine whether estrogen and/or progesterone influence renal vasopressin receptor (VR) or oxytocin receptor (OTR) transcripts. Estrogen induced OTR gene expression in the outer stripe of the outer medulla and increased expression of OTRs in macula densa cells. Outer stripe OTR mRNA peaked with 4 days of estrogen treatment, and decreased to undetectable levels with 31 days of treatment of ovariectomized females. Estradiol's induction of outer stripe OTR mRNA expression was blocked by the antiestrogen, tamoxifen, but was not affected by high levels of circulating oxytocin. A role for OTRs in regulating renal function independently of adrenal steroids was suggested by findings that adrenalectomized males showed high levels of OTR transcripts in outer stripe proximal tubule and cortical macula densa cells after 5 and 10 micrograms/100g of estradiol. Consistent with specialized roles for OTRs during female reproduction, OTR transcripts could not be detected in renal tissues of peri-parturient females, at times when OTR mRNA levels were very high in uterus. OTR gene expression in macula densa cells reappeared 4-8 days into lactation and attained control levels by day 20. Physiological experiments showed that estrogen + oxytocin decreased plasma [Na+] levels in ovariectomized rats at a time when proximal tubule OTR expression is maximal. These data are consistent with 1) cell-specific regulation by estrogen of renal OTR gene expression and 2) the possibility that OTRs may be important mediators of steroid-induced alterations in renal fluid and/or solute reabsorption.
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PMID:Oxytocin receptor gene expression in female rat kidney. The effect of estrogen. 871 83

1. Renal tubules and, in particular, the inner medullary collecting duct, produce endothelin and express cognate receptors. 2. Endothelins inhibit vasopressin-stimulated cAMP accumulation and water reabsorption in the collecting duct; endothelins may also inhibit sodium reabsorption in the proximal tubule and collecting duct. 3. Autocrine inhibition of sodium and water reabsorption in the inner medullary collecting duct by endothelin may play a role in maintaining extracellular fluid volume homeostasis. 4. Derangements in autocrine inhibition of sodium and water reabsorption in the inner medullary collecting duct by endothelin may be involved in the pathogenesis of the hypertensive state. 5. Nephron-derived endothelins may function in a paracrine manner to regulate interstitial, juxtaglomerular and vascular smooth muscle cell function.
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PMID:Endothelins: renal tubule synthesis and actions. 871 71

Aquaporins (AQPs) are a newly recognized family of transmembrane proteins that function as molecular water channels. At least four aquaporins are expressed in the kidney where they mediate rapid water transport across water-permeable epithelia and play critical roles in urinary concentrating and diluting processes. AQP1 is constitutively expressed at extremely high levels in the proximal tubule and descending limb of Henle's loop. AQP2, -3 and -4 are expressed predominantly in the collecting duct system. AQP2 is the predominant water channel in the apical plasma membrane and AQP3 and -4 are found in the basolateral plasma membrane. Short-term regulation of collecting duct water permeability by vasopressin is largely a consequence of regulated trafficking of AQP2-containing vesicles to and from the apical plasma membrane.
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PMID:Renal aquaporins. 874 83

Discovery of aquaporin water channel proteins has provided insight into the molecular mechanism of membrane water permeability. The distribution of known mammalian aquaporins predicts roles in physiology and disease. Aquaporin-1 mediates proximal tubule fluid reabsorption, secretion of aqueous humor and cerebrospinal fluid, and lung water homeostasis. Aquaporin-2 mediates vasopressin-dependent renal collecting duct water permeability; mutations or downregulation can cause nephrogenic diabetes insipidus. Aquaporin-3 in the basolateral membrane of the collecting duct provides an exit pathway for reabsorbed water. Aquaporin-4 is abundant in brain and probably participates in reabsorption of cerebrospinal fluid, osmoregulation, and regulation of brain edema. Aquaporin-5 mediates fluid secretion in salivary and lacrimal glands and is abundant in alveolar epithelium of the lung. Specific regulation of membrane water permeability will likely prove important to understanding edema formation and fluid balance in both normal physiology and disease.
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PMID:Pathophysiology of the aquaporin water channels. 881 12

Present package labeling for sevoflurane recommends the use of fresh gas flow rates of 2 L/min or more when delivering anesthesia with sevoflurane. This recommendation resulted from a concern about the potential nephrotoxicity of a degradation product of sevoflurane, "Compound A," produced by the action of carbon dioxide absorbents on sevoflurane. To assess the adequacy of this recommendation, we compared the nephrotoxicity of 8 h of 1.25 minimum alveolar anesthetic concentration (MAC) sevoflurane (n = 10) versus desflurane (n = 9) in fluid-restricted (i.e., nothing by mouth overnight) volunteers when the anesthetic was given in a standard circle absorber anesthetic system at 2 L/min. Subjects were tested for markers of renal injury (urinary albumin, glucose, alpha-glutathione-S-transferase [GST], and pi-GST; and serum creatinine and blood urea nitrogen [BUN]) before and 1, 2, 3, and/or 5-7 days after anesthesia. Desflurane did not produce renal injury. Rebreathing of sevoflurane produced average inspired concentrations of Compound A of 41 +/- 3 ppm (mean +/- SD). Sevoflurane was associated with transient injury to: 1) the glomerulus, as revealed by postanesthetic albuminuria; 2) the proximal tubule, as revealed by postanesthetic glucosuria and increased urinary alpha-GST; and 3) the distal tubule, as revealed by postanesthetic increased urinary pi-GST. These effects varied greatly (e.g., on postanesthesia Day 3, the 24-h albumin excretion was < 0.03 g (normal) for one volunteer; 0.03-1 g for five others; 1-2 g for two others; 2.1 g for one volunteer; and 4.4 g for another volunteer). Neither anesthetic affected serum creatinine or BUN, nor changed the ability of the kidney to concentrate urine in response to vasopressin, 5 U/70 kg subcutaneously (i.e., these measures failed to reveal the injury produced). In addition, sevoflurane, but not desflurane, caused small postanesthetic increases in serum alanine aminotransferase (ALT), suggesting mild, transient hepatic injury.
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PMID:Nephrotoxicity of sevoflurane versus desflurane anesthesia in volunteers. 945 67

Water channel aquaporin-1 (AQP1) is strongly expressed in kidney in proximal tubule and descending limb of Henle epithelia and in vasa recta endothelia. The grossly normal phenotype in human subjects deficient in AQP1 (Colton null blood group) and in AQP4 knockout mice has suggested that aquaporins (other than the vasopressin-regulated water channel AQP2) may not be important in mammalian physiology. We have generated transgenic mice lacking detectable AQP1 by targeted gene disruption. In kidney proximal tubule membrane vesicles from knockout mice, osmotic water permeability was reduced 8-fold compared with vesicles from wild-type mice. Although the knockout mice were grossly normal in terms of survival, physical appearance, and organ morphology, they became severely dehydrated and lethargic after water deprivation for 36 h. Body weight decreased by 35 +/- 2%, serum osmolality increased to >500 mOsm, and urinary osmolality (657 +/- 59 mOsm) did not change from that before water deprivation. In contrast, wild-type and heterozygous mice remained active after water deprivation, body weight decreased by 20-22%, serum osmolality remained normal (310-330 mOsm), and urine osmolality rose to >2500 mOsm. Urine [Na+] in water-deprived knockout mice was <10 mM, and urine osmolality was not increased by the V2 agonist DDAVP. The results suggest that AQP1 knockout mice are unable to create a hypertonic medullary interstitium by countercurrent multiplication. AQP1 is thus required for the formation of a concentrated urine by the kidney.
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PMID:Severely impaired urinary concentrating ability in transgenic mice lacking aquaporin-1 water channels. 946 75

One of the most important factors controlling blood pressure is the total body Na+ content, which depends upon Na+ intake and excretion. The kidney influences body Na+ content by regulating the tubular absorption of the Na+ filtered through the glomeruli. Thus, the regulation of Na+ absorption in the tubules of the kidney plays an important role in controlling blood pressure. More than 99% of the Na+ passing through the glomerulus is reabsorbed in the kidney. About 90% of the filtered Na+ through the glomerulus is reabsorbed in the proximal tubule and the ascending limb of the loop of Henle. The remainder of the Na+ absorption occurs in the distal nephron. This process is regulated by hormones such as aldosterone and antidiuretic hormone (ADH), and also by the osmolality of the plasma. These observations suggest that the regulation of Na+ transport in the distal nephron by hormones and osmolality plays an important role in the control of blood pressure. The distal nephron is composed of two different types of epithelial cells: the principal cell and the intercalated cell. The latter is also composed of two types of cells: alpha and beta intercalated cells. In addition to Na+ absorption, the distal-nephron epithelial cells also participate in K+ and H+ secretion. Na+ absorption is mediated through the principal cell, which also contributes to K+ secretion, whereas H+ is secreted through both types of intercalated cells, alpha and beta, in different ways. There are, in general, two steps in the transepithelial ion movement across the epithelium, including the distal-nephron epithelium. For example, in the case of Na+ absorption, one is the entry step of Na+ across the apical membrane and the other is the extrusion step of Na+ across the basolateral membrane. This means that there are two major regulatory sites of transepithelial Na+ absorption: namely, regulation of the entry and extrusion steps of Na+. It is generally thought that the entry step of Na+ across the apical membrane is the rate-limiting step in the transepithelial Na+ transport and that Na+ channels in the apical membrane play an important role as an entry step of Na+ and are regulated by hormones and plasma osmolality. In this review, we describe the regulatory mechanisms of Na+ absorption in renal distal-nephron epithelium by aldosterone, ADH and osmolality. Further, we will review the regulatory mechanisms of Cl- transport, which also plays an important role in Na+ transport as a major counter ion, and discuss other roles of Cl- in the active regulation of Na+ transport.
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PMID:Hormonal and osmotic regulation of NaCl transport in renal distal nephron epithelium. 953 74

During mixed gas saturation diving (to 3-49.5 ATA) daily urine flow increases by about 500 ml/day, with no changes in fluid intake and glomerular filtration rate. The diuresis is accompanied by a significant decrease in urine osmolality and increase in excretion of such solutes as urea, K+, Na+, Ca2+ and inorganic phosphate (Pi). The fall in urine osmolality is mainly due to a reduction of free water reabsorption which is associated with a suppression of insensible water loss and the attendant inhibition of antidiuretic hormone (ADH) system. The increase in urea excretion may be associated with a reduction of urea reabsorption at the collecting duct as a consequence of ADH suppression. The rise in K+ excretion is due to a facilitated K+ secretion at the distal tubule as a result of increased aldosterone, urine flow and excretion of impermeable anions such as Pi. The activation of aldosterone system is partly attributed to a transient dehydration induced by early hyperbaric diuresis. The increase in Na+ excretion in the face of enhanced aldosterone secretion indicates that the Na+ transport in the proximal tubule is markedly inhibited (by unknown mechanism). The Pi excretion increases with no changes in plasma level of parathyroid hormone (PTH), thus it may be due to an inhibition of Na(+)-Pi cotransport in the proximal tubule. The increase in Ca2+ excretion may be secondary to the inhibition of Na+ transport at the proximal tubule. Precise information on the proximal tubular Na+ transport is important to understand the mechanisms of impaired solute transport under hyperbaric conditions.
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PMID:Renal function in hyperbaric environment. 957 38

Renal effects of physiological amounts of vasopressin were studied in conscious dogs during servocontrolled overhydration (2% body wt). During infusion of vasopressin (50 pg . min-1 . kg body wt-1), plasma vasopressin concentration increased to 2.30 +/- 0.20 pg/ml compared with 0.12 +/- 0.03 pg/ml during control (water diuresis). With vasopressin infusion, urine flow was significantly lower (0.30 +/- 0.10 ml/min) and sodium excretion (UNaV) was significantly higher (58.0 +/- 15.8 micromol/min) than without vasopressin (4.6 +/- 0.4 ml/min and 14.4 +/- 4.1 micromol/min, respectively). Deamino-[Cys1,D-Arg8]vasopressin, a V2 receptor agonist (4 pg . min-1 . kg-1), mimicked the antidiuretic response (0.20 +/- 0.03 ml/min) without changing UNaV (9.7 +/- 4.4 micromol/min). Indomethacin given during arginine vasopressin (AVP) infusion suppressed prostaglandin E2 excretion, intensified the antidiuresis (0.10 +/- 0.02 ml/min), and abolished the natriuresis (13.4 +/- 3.7 micromol/min). During AVP infusion, UNaV was highly correlated (r = 0.85) with prostaglandin E2 excretion. Blood pressure, glomerular filtration rate, plasma atrial natriuretic peptide concentration, and the rate of proximal tubule reabsorption (derived from lithium clearance) were similar in all series. The data indicate that, in the dog, physiological amounts of vasopressin can induce natriuresis, probably through activation of non-V2 receptors and the intrarenal synthesis of prostaglandins.
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PMID:Mechanism of vasopressin natriuresis in the dog: role of vasopressin receptors and prostaglandins. 960 16


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