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Effect of selective angiotensin antagonists on the antidiuresis produced by angiotensin-(1-7) in water-loaded rats

Baracho,N.C.V.; Simões-e-Silva,A.C.; Khosla,M.C.; Santos,R.A.S.
Fonte: Associação Brasileira de Divulgação Científica Publicador: Associação Brasileira de Divulgação Científica
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/09/1998 EN
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In the present study we evaluated the nature of angiotensin receptors involved in the antidiuretic effect of angiotensin-(1-7) (Ang-(1-7)) in water-loaded rats. Water diuresis was induced in male Wistar rats weighing 280 to 320 g by water load (5 ml/100 g body weight by gavage). Immediately after water load the rats were treated subcutaneously with (doses are per 100 g body weight): 1) vehicle (0.05 ml 0.9% NaCl); 2) graded doses of 20, 40 or 80 pmol Ang-(1-7); 3) 200 nmol Losartan; 4) 200 nmol Losartan combined with 40 pmol Ang-(1-7); 5) 1.1 or 4.4 nmol A-779; 6) 1.1 nmol A-779 combined with graded doses of 20, 40 or 80 pmol Ang-(1-7); 7) 4.4 nmol A-779 combined with graded doses of 20, 40 or 80 pmol Ang-(1-7); 8) 95 nmol CGP 42112A, or 9) 95 nmol CGP 42112A combined with 40 pmol Ang-(1-7). The antidiuretic effect of Ang-(1-7) was associated with an increase in urinary Na+ concentration, an increase in urinary osmolality and a reduction in creatinine clearance (CCr: 0.65 ± 0.04 ml/min vs 1.45 ± 0.18 ml/min in vehicle-treated rats, P<0.05). A-779 and Losartan completely blocked the effect of Ang-(1-7) on water diuresis (2.93 ± 0.34 ml/60 min and 3.39 ± 0.58 ml/60 min, respectively). CGP 42112A, at the dose used, did not modify the antidiuretic effect of Ang-(1-7). The blockade produced by Losartan was associated with an increase in CCr and with an increase in sodium and water excretion as compared with Ang-(1-7)-treated rats. When Ang-(1-7) was combined with A-779 there was an increase in CCr and natriuresis and a reduction in urine osmolality compared with rats treated with Ang-(1-7) alone. The observation that both A-779...

Corticotropin-releasing hormone causes antidiuresis and antinatriuresis by stimulating vasopressin and inhibiting atrial natriuretic peptide release in male rats

Gutkowska, J.; Jankowski, M.; Mukaddam-Daher, S.; McCann, S. M.
Fonte: The National Academy of Sciences Publicador: The National Academy of Sciences
Tipo: Artigo de Revista Científica
Publicado em 04/01/2000 EN
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In both normally hydrated and volume-expanded rats, there was a biphasic effect of corticotropin-releasing hormone (CRH) (1–10 μg, i.v.) on renal function. Within the first hour, CRH caused antidiuresis, antinatriuresis, and antikaliuresis together with reduction in urinary cGMP output that, in the fourth hour, were replaced by diuresis, natriuresis, and kaliuresis accompanied by increased cGMP output. Plasma arginine vasopressin (AVP) concentrations increased significantly within 5 min, reached a peak at 15 min, and declined by 30 min to still-elevated values maintained for 180 min. Changes in plasma atrial natriuretic peptide (ANP) were the mirror image of those of AVP. Plasma ANP levels were correlated with decreased ANP in the left ventricle at 30 min and increased ANP mRNA in the right atrium at 180 min. All urinary changes were reversed by a potent AVP type 2 receptor (V2R) antagonist. Control 0.9% NaCl injections evoked an immediate increase in blood pressure and heart rate measured by telemetry within 3–5 min. This elevation of blood pressure was markedly inhibited by CRH (5 μg). We hypothesize that the effects are mediated by rapid, direct vasodilation induced by CRH that decreases baroreceptor input to the brain stem...

Norepinephrine inhibition of vasopressin antidiuresis

Fisher, D. A.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /03/1968 EN
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The effect of norepinephrine on exogenous vasopressin antidiuresis was investigated in water-loaded subjects. After an initial 2 to 3 hr period of water loading (phase 1), 10-100 mU of vasopressin per hr were infused at a constant rate for 1 hr (phase 2) followed by infusion of 10-100 mU of vasopressin per hr plus 600 μg of l-norepinephrine per hr for 1 hr (phase 3). Endogenous creatinine clearance, osmolal clearance, and free water clearance (in milliliters/minute) and sodium and chloride excretion (in milliequivalents/minute) were measured. In 10 subjects given 10-20 mU of vasopressin per hr during phases 2 and 3, free water clearance decreased significantly from phase 1 to phase 2 (9.3 to 0.15, P = 0.001) and increased during phase 3 norepinephrine infusion to 4.7 ml/min (P = 0.001). A comparable decrease in phase 2 free water clearance was observed in four subjects given 50 or 100 mU of vasopressin per hr during phases 2 and 3 (P < 0.01); however, the phase 3 norepinephrine infusion in these subjects was not associated with an increase in free water clearance. Creatinine clearance, osmolal clearance, and sodium and chloride excretion were unchanged throughout the studies in both groups of subjects.

Role of renal aquaporins in escape from vasopressin-induced antidiuresis in rat.

Ecelbarger, C A; Nielsen, S; Olson, B R; Murase, T; Baker, E A; Knepper, M A; Verbalis, J G
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em 15/04/1997 EN
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The purpose of this study was to investigate whether escape from vasopressin-induced antidiuresis is associated with altered regulation of any of the known aquaporin water channels. After 4-d pretreatment with 1-deamino-[8-D-arginine]-vasopressin (dDAVP) by osmotic mini-pump, rats were divided into two groups: control (continued dDAVP) and water-loaded (continued dDAVP plus a daily oral water load). A significant increase in urine volume in the water-loaded rats was observed by the second day of water loading, indicating onset of vasopressin escape. The onset of escape coincided temporally with a marked decrease in renal aquaporin-2 protein (measured by semiquantitative immunoblotting), which began at day 2 and fell to 17% of control levels by day 3. In contrast, there was no decrease in the renal expression of aquaporins 1, 3, or 4. The marked suppression of whole kidney aquaporin-2 protein was accompanied by a concomitant suppression of whole kidney aquaporin-2 mRNA levels. Immunocytochemical localization and differential centrifugation studies demonstrated that trafficking of aquaporin-2 to the plasma membrane remained intact during vasopressin escape. The results suggest that escape from vasopressin-induced antidiuresis is attributable...

Drinking and antidiuresis elicited by isoprenaline in the dog

Fitzsimons, J. T.; Szczepańska-Sadowska, Ewa
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /06/1974 EN
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1. Isoprenaline hydrochloride injected subcutaneously or infused intravenously caused drinking and simultaneous antidiuresis in the dog. The minimal effective dose was between 20 and 50 μg per dog.

Nitric oxide inhibition and the impact on renal nerve-mediated antinatriuresis and antidiuresis in the anaesthetized rat

Bagnall, NM; Dent, PC; Walkowska, A; Sadowski, J; Johns, EJ
Fonte: Blackwell Science Inc Publicador: Blackwell Science Inc
Tipo: Artigo de Revista Científica
EN
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The contribution of nitric oxide (NO) to the antinatriuresis and antidiuresis caused by low-level electrical stimulation of the renal sympathetic nerves (RNS) was investigated in rats anaesthetized with chloralose–urethane. Groups of rats, n = 6, were given i.v. infusions of vehicle, l-NAME (10 μg kg−1 min−1), 1400W (20 μg kg−1 min−1), or S-methyl-thiocitrulline (SMTC) (20 μg kg−1 min−1) to inhibit NO synthesis non-selectively or selectively to block the inducible or neuronal NOS isoforms (iNOS and nNOS, respectively). Following baseline measurements of blood pressure (BP), renal blood flow (RBF), glomerular filtration rate (GFR), urine flow (UV) and sodium excretion (UNaV), RNS was performed at 15 V, 2 ms duration with a frequency between 0.5 and 1.0 Hz. RNS did not cause measurable changes in BP, RBF or GFR in any of the groups. In untreated rats, RNS decreased UV and UNaV by 40–50% (both P < 0.01), but these excretory responses were prevented in l-NAME-treated rats. In the presence of 1400W i.v., RNS caused reversible reductions in both UV and UNaV of 40–50% (both P < 0.01), while in SMTC-treated rats, RNS caused an inconsistent fall in UV, but a significant reduction (P < 0.05) in UNaV of 21%. These data demonstrated that the renal nerve-mediated antinatriuresis and antidiuresis was dependent on the presence of NO...

Absence of Antidiuresis during Administration of Prostaglandin F2α

Roberts, G.; McGarry, J.; Turnbull, A. C.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em 18/04/1970 EN
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Water diuresis was induced in six patients in mid-pregnancy. Three were then given oxytocin and the remainder prostaglandin F2α (PGF2α), both drugs being infused intravenously in doses used to induce labour at term. Pronounced antidiuresis occurred with oxytocin, whereas PGF2α showed no such effect. The probable absence of any risk of water intoxication when using PGF2α in inducing labour may be of particular value when maternal pre-eclampsia or renal disease is present.

A small cell bronchogenic carcinoma associated with tumoral hypophosphataemia and inappropriate antidiuresis.

Robin, N.; Gill, G.; van Heyningen, C.; Fraser, W.
Fonte: BMJ Group Publicador: BMJ Group
Tipo: Artigo de Revista Científica
Publicado em /10/1994 EN
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A patient is described with small cell carcinoma of the lung, associated with profound hypophosphataemia and hyponatraemia. Increased phosphate excretion and inappropriately high urine osmolality were observed. The abnormalities are consistent with tumoral hypophosphataemia and inappropriate antidiuresis. These tumour-related metabolic abnormalities have only been described once before with this malignancy.

Dissociation between the secretion and renal action of endogenous atrial natriuretic peptide in the syndrome of inappropriate antidiuresis.

Eadington, D. W.; Cowan, F. M.
Fonte: BMJ Group Publicador: BMJ Group
Tipo: Artigo de Revista Científica
Publicado em /01/1990 EN
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A patient is described with the syndrome of inappropriate antidiuresis (SIAD) and renal sodium retention secondary to a lymphoma. The basal atrial natriuretic peptide (ANP) level and the ANP response to volume expansion were normal (age adjusted) but the natriuretic effect of ANP was attenuated by an unidentified factor. The case emphasizes the dominance of circulating volume over plasma tonicity in the regulation of ANP secretion.

Administration of D-Alanine-[Ang-(1-7)] (A-779) Prior to Pregnancy in Sprague Dawley Rats Produces Antidiuresis in Late Gestation

Joyner, J; Neves, LAA; Ferrario, CM; Brosnihan, KB
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em //2008 EN
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We previously demonstrated that angiotensin-(1-7) [Ang-(1-7)], which is increased in the kidney and urine during pregnancy, influences normal fluid expansion of pregnancy. These previous studies were completed by chronic administration of the Ang-(1-7) receptor antagonist D-Alanine-[Ang-(1-7)] (A-779) at a dose of 48 μg/kg/hr after the start of pregnancy (gestational days 11-19). To further explore the role of Ang-(1-7) on kidney function during early, middle, and late pregnancy, Sprague Dawley rats were chronically pretreated 8 days prior to pregnancy and throughout pregnancy (gestational days 0-19) with vehicle or A-779 at a dose of 24 μg/kg/hr. Metabolic studies were completed in virgin animals and throughout pregnancy (gestational days 4-5, 14-15, and 18-19). Chow consumption and water intake increased throughout pregnancy while the difference between intake and output (balance) was increased only at late (day 19) pregnancy with both vehicle and A-779 administration. Urine volume and urinary osmolality were significantly increased and decreased respectively throughout pregnancy in vehicle treated rats only. In late (19 day) pregnancy, A-779 administration significantly decreased chow consumption and water intake. In virgin animals...

Agonist-Independent Interactions between β-Arrestins and Mutant Vasopressin Type II Receptors Associated with Nephrogenic Syndrome of Inappropriate Antidiuresis

Kocan, Martina; See, Heng B.; Sampaio, Natália G.; Eidne, Karin A.; Feldman, Brian J.; Pfleger, Kevin D. G.
Fonte: The Endocrine Society Publicador: The Endocrine Society
Tipo: Artigo de Revista Científica
EN
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Nephrogenic syndrome of inappropriate antidiuresis is a recently identified genetic disease first described in two unrelated male infants with severe symptomatic hyponatremia. Despite undetectable arginine vasopressin levels, patients have inappropriately concentrated urine resulting in hyponatremia, hypoosmolality, and natriuresis. It was found that each infant had a different mutation of the vasopressin type II receptor (V2R) at codon 137 where arginine was converted to cysteine or leucine (R137C or R137L), resulting in constitutive signaling. Interestingly, a missense mutation at the same codon, converting arginine to histidine (R137H), leads to the opposite disease phenotype with a loss of the kidney’s ability to concentrate urine resulting in nephrogenic diabetes insipidus. This mutation is associated with impaired signaling, although whether this is predominantly due to impaired trafficking to the plasma membrane, agonist-independent internalization, or G protein uncoupling is currently unclear. Using bioluminescence resonance energy transfer and confocal microscopy, we demonstrate that both V2R-R137C and V2R-R137L mutants interact with β-arrestins in an agonist-independent manner resulting in dynamin-dependent internalization. This phenotype is similar to that observed for V2R-R137H...

Interferon-alpha is a predisposing risk factor for carbamazepine-induced hyponatremia: A case of syndrome of inappropriate antidiuresis caused by interferon-alpha therapy

Tanaka, Midori; Kamoi, Kyuzi; Takahashi, Toru
Fonte: Dove Medical Press Publicador: Dove Medical Press
Tipo: Artigo de Revista Científica
Publicado em 30/11/2009 EN
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A 31-year-old man had been treated with carbamazepine (CBZ) for 6 years and warfarin with bucolome for 2 years before developing hyponatremia 7 days after an injection of interferon-alpha 2b and starting oral ribavirin for chronic hepatitis C virus infection. Despite the hyponatremia, urinary osmolality exceeded plasma osmolality, and urinary excretion volume decreased markedly after water loading. Restriction of water intake and administration of dimethylchlortetracycline improved the hyponatremia, and lithium therapy maintained the normonatremia for one year. The hyponatremia recovered 6 months after the interferon-alpha 2b therapy was completely stopped. In the present case, the syndrome of inappropriate antidiuresis may have been caused by the effect of interferon-alpha 2b on the renal distal tubules that had been sensitized by CBZ. Patients on CBZ therapy should be carefully observed for the development of hyponatremia when they are started on interferon-alpha 2b injections.

Functional Characterization of Vasopressin Type 2 Receptor Substitutions (R137H/C/L) Leading to Nephrogenic Diabetes Insipidus and Nephrogenic Syndrome of Inappropriate Antidiuresis: Implications for TreatmentsS⃞

Rochdi, Moulay D.; Vargas, Gabriel A.; Carpentier, Eric; Oligny-Longpré, Geneviève; Chen, Stanford; Kovoor, Abraham; Gitelman, Stephen E.; Rosenthal, Stephen M.; von Zastrow, Mark; Bouvier, Michel
Fonte: The American Society for Pharmacology and Experimental Therapeutics Publicador: The American Society for Pharmacology and Experimental Therapeutics
Tipo: Artigo de Revista Científica
Publicado em /05/2010 EN
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Substitution of arginine-137 of the vasopressin type 2 receptor (V2R) for histidine (R137H-V2R) leads to nephrogenic diabetes insipidus (NDI), whereas substitution of the same residue to cysteine or leucine (R137C/L-V2R) causes the nephrogenic syndrome of inappropriate antidiuresis (NSIAD). These two diseases have opposite clinical outcomes. Still, the three mutant receptors were shown to share constitutive β-arrestin recruitment and endocytosis, resistance to vasopressin-stimulated cAMP production and mitogen-activated protein kinase activation, and compromised cell surface targeting, raising questions about the contribution of these phenomenons to the diseases and their potential treatments. Blocking endocytosis exacerbated the elevated basal cAMP levels promoted by R137C/L-V2R but not the cAMP production elicited by R137H-V2R, demonstrating that substitution of Arg137 to Cys/Leu, but not His, leads to constitutive V2R-stimulated cAMP accumulation that most likely underlies NSIAD. The constitutively elevated endocytosis of R137C/L-V2R attenuates the signaling and most likely reduces the severity of NSIAD...

Pramipexole as a possible cause of the syndrome of inappropriate antidiuresis

Arai, Motomi; Iwabuchi, Masayasu
Fonte: BMJ Publishing Group Publicador: BMJ Publishing Group
Tipo: Artigo de Revista Científica
Publicado em 26/03/2009 EN
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A 60-year-old man with Parkinson’s disease developed hyponatraemia with low plasma osmolarity, urine hyperosmolarity and an elevated urine sodium concentration. Plasma vasopressin (AVP) level was five times the upper normal limit and a diagnosis of the syndrome of inappropriate antidiuresis (SIAD) was made. Although the patient was treated with levodopa/carbidopa 500 mg/50 mg, entacapone 400 mg, seregiline 5 mg, cabergoline 1 mg, pergolide 250 μg and pramipexole 3 mg, SIAD resolved after the dose reduction of pramipexole. Dopamine is reported to facilitate AVP secretion through activation of D4 receptors. The hD4:hD2L pKi ratio calculated from published data is 0.017 for cabergoline, 0.44 for pergolide, 1.1 for ropinirole and 13 for pramipexole. The hD4:hD2 pKi ratio of dopamine is reported to be 1. Accordingly, pramipexole has a higher selectivity for D4 receptor than other dopamine agonists. Pramipexole is likely to increase AVP secretion, which is a prerequisite for developing SIAD.

Sex differences in vasopressin V2 receptor expression and vasopressin-induced antidiuresis

Liu, Jun; Sharma, Nikhil; Zheng, Wei; Ji, Hong; Tam, Helen; Wu, Xie; Manigrasso, Michaele B.; Sandberg, Kathryn; Verbalis, Joseph G.
Fonte: American Physiological Society Publicador: American Physiological Society
Tipo: Artigo de Revista Científica
EN
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The renal vasopressin V2 receptor (V2R) plays a critical role in physiological and pathophysiological processes associated with arginine vasopressin (AVP)-induced antidiuresis. Because clinical data suggests that females may be more prone to hyponatremia from AVP-mediated antidiuresis, we investigated whether there are sex differences in the expression and function of the renal V2R. In normal Sprague-Dawley rat kidneys, V2R mRNA and protein expression was 2.6- and 1.7-fold higher, respectively, in females compared with males. To investigate the potential physiological implications of this sex difference, we studied changes in urine osmolality induced by the AVP V2R agonist desmopressin. In response to different doses of desmopressin, there was a graded increase in urine osmolality and decrease in urine volume during a 24-h infusion. Females showed greater mean increases in urine osmolality and greater mean decreases in urine volume at 0.5 and 5.0 ng/h infusion rates. We also studied renal escape from antidiuresis produced by water loading in rats infused with desmopressin (5.0 ng/h). After 5 days of water loading, urine osmolality of both female and male rats escaped to the same degree physiologically, but V2R mRNA and protein in female kidneys was reduced to a greater degree (−63% and −73%...

Nephrogenic Syndrome of Inappropriate Antidiuresis

Morin, D.; Tenenbaum, J.; Ranchin, B.; Durroux, T.
Fonte: Hindawi Publishing Corporation Publicador: Hindawi Publishing Corporation
Tipo: Artigo de Revista Científica
EN
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Mutations in the vasopressin V2 receptor gene are responsible for two human tubular disorders: X-linked congenital nephrogenic diabetes insipidus, due to a loss of function of the mutant V2 receptor, and the nephrogenic syndrome of inappropriate antidiuresis, due to a constitutive activation of the mutant V2 receptor. This latter recently described disease may be diagnosed from infancy to adulthood, as some carriers remain asymptomatic for many years. Symptomatic children, however, typically present with clinical and biological features suggesting inappropriate antidiuretic hormone secretion with severe hyponatremia and high urine osmolality, but a low plasma arginine vasopressin level. To date, only two missense mutations in the vasopressin V2 receptor gene have been found in the reported patients. The pathophysiology of the disease requires fuller elucidation as the phenotypic variability observed in patients bearing the same mutations remains unexplained. The treatment is mainly preventive with fluid restriction, but urea may also be proposed.

Persistent elevation of urine aquaporin-2 during water loading in a child with nephrogenic syndrome of inappropriate antidiuresis (NSIAD) caused by a R137L mutation in the V2 vasopressin receptor

Cheung, Clement C; Cadnapaphornchai, Melissa A; Ranadive, Sayali A; Gitelman, Stephen E; Rosenthal, Stephen M
Fonte: BioMed Central Publicador: BioMed Central
Tipo: Artigo de Revista Científica
EN
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Nephrogenic Syndrome of Inappropriate Antidiuresis (NSIAD) is a novel disease caused by a gain-of-function mutation in the V2 vasopressin receptor (V2R), which results in water overload and hyponatremia. We report the effect of water loading in a 3-year old boy with NSIAD, diagnosed in infancy, to assess urine aquaporin-2 (AQP2) excretion as a marker for V2R activation, and to evaluate the progression of the disease since diagnosis. The patient is one of the first known NSIAD patients and the only patient with a R137L mutation. Patient underwent a standard water loading test in which serum and urine sodium and osmolality, serum AVP, and urine AQP2 excretion were measured. The patient was also evaluated for ad lib fluid intake before and after the test. This patient demonstrated persistent inability to excrete free water. Only 39% of the water load (20 ml/kg) was excreted during a 4-hour period (normal ≥ 80-90%). Concurrently, the patient developed hyponatremia and serum hypoosmolality. Serum AVP levels were detectable at baseline and decreased one hour after water loading; however, urine AQP2 levels were elevated and did not suppress normally during the water load. The patient remained eunatremic but relatively hypodipsic during ad lib intake. In conclusion...

Retrospective Evaluation of Standard Diagnostic Procedures in Identification of the Causes of New-Onset Syndrome of inappropriate Antidiuresis

Hsu, Chih-Yang; Chen, Chieh-Liang; Huang, Wei-Chieh; Lee, Po-Tsang; Fang, Hua-Chang; Chou, Kang-Ju
Fonte: Ivyspring International Publisher Publicador: Ivyspring International Publisher
Tipo: Artigo de Revista Científica
Publicado em 10/01/2014 EN
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Background: Many diagnostic procedures are conducted in patients with syndrome of inappropriate antidiuresis (SIAD). However, the contribution in identification of the cause of SIAD remains unknown.

Mechanism of antidiuresis caused by bendroflumethiazide in conscious rats with diabetes insipidus

Grønbeck, Lene; Marples, David; Nielsen, Søren; Christensen, Sten
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /02/1998 EN
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The mechanism underlying the antidiuretic effect of thiazide diuretics in diabetes insipidus (DI) is unknown. This study addressed two specific questions: is the reduction in urine flow rate (V) related to a decrease in the delivery of fluid from the pars recta of the proximal tubules ('distal delivery'), and are there any changes in the expression and/or intracellular distribution of vasopressin stimulated water channels (AQP2) in the collecting ducts, during chronic thiazide-induced antidiuresis?Nine Brattleboro rats with vasopressin-deficient DI were treated for 5 days with bendroflumethiazide (BFTZ), 9 mg kg−1 day−1 orally, and 9 Brattleboro rats were left untreated. BFTZ-treated DI rats showed a fall in V from ∼200 to ∼75 ml day−1 and an increase in urine osmolality from ∼130 to ∼400 mosmol kg−1.BFTZ-induced antidiuresis was associated with a persistent loss of sodium, but not of potassium. After 5 days of treatment, clearance studies in conscious rats showed a tendency towards decreases in effective renal plasma flow (−7%), GFR (−12%) and lithium clearance (CLi; used as marker for distal delivery) (−25%), compared with untreated controls, but none of these changes were statistically significant. There was no apparent relationship between CLi and V in BFTZ-treated or untreated DI rats.BFTZ treatment did not change the expression of AQP2 in homogenates of cortex...

Clofibrate-Induced Antidiuresis

Moses, Arnold M.; Howanitz, Joan; Gemert, Marcia Van; Miller, Myron
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /03/1973 EN
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Normal subjects and patients with antidiuretic hormone (ADH) deficiency were studied to determine the mechanism of the antidiuretic action of clofibrate. Before clofibrate treatment, the patients' ability to concentrate urine with a standardized dehydration procedure correlated with the amount of ADH which was excreted. During clofibrate administration all six patients with ADH deficiency developed an antidiuresis which was like that of ADH, since there was no change in sodium, potassium, total solute, or creatinine excretion. There was a correlation between the patients' ability to concentrate urine during dehydration and the subsequent response to clofibrate, and the excretion of ADH during dehydration correlated with the excretion of ADH on clofibrate therapy. Clofibrate-induced antidiuresis in these patients was partially overcome by ethanol and by water loading. Clofibrate interfered with the ability of patients and subjects to excrete a water load and prevented the water load from inhibiting ADH excretion in the normal subjects. These studies suggested that clofibrate was acting through endogenous ADH and this thesis was supported by the failure of clofibrate to produce an antidiuresis when injected into rats with total ADH deficiency (Brattleboro strain) although an antidiuresis was produced in water-loaded normal rats. When the drug was injected into Brattleboro rats with exogenous ADH...