scholarly journals Role of plasma vasopressin in the impairment of water excretion in nephrotic syndrome

1984 ◽  
Vol 25 (2) ◽  
pp. 422-429 ◽  
Author(s):  
Mario Usberti ◽  
Stefano Federico ◽  
Sergio Meccariello ◽  
Bruno Cianciaruso ◽  
Mario Balletta ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Water Excretion ◽  
Plasma Vasopressin

Elevation of Plasma Vasopressin in Spontaneous Migraine

Cephalalgia ◽  
1991 ◽  
Vol 11 (6) ◽  
pp. 249-250 ◽  
Author(s):  
KK Hampton ◽  
A Esack ◽  
RC Peatfield ◽  
PJ Grant
Keyword(s):  
Blood Flow ◽  
Acute Attack ◽  
Peripheral Blood Flow ◽  
Posterior Pituitary ◽  
Water Excretion ◽  
Paired Samples ◽  
Plasma Vasopressin ◽  
Antidiuretic Effect ◽  
Renal Water Excretion

Vasopressin is a vasoactive hormone secreted from the posterior pituitary. At low concentration its role is in regulating renal water excretion, but at higher concentrations it has a number of extrarenal actions, including effects on blood flow. To investigate the role of vasopressin in spontaneous migraine, paired samples were collected from 14 subjects (a) during an acute attack of spontaneous migraine, and (b) when symptom-free for at least seven days. During an attack, vasopressin was consistently raised (median (range) 3.5 (1.2–9.6) pg/ml v 0.5 (0.5–1.1) pg/ml, p < 0.001). The highest vasopressin concentration occurred in the only patient who vomited. The results suggest vasopressin rises during an attack of spontaneous migraine, and this may, in part, be related to emesis. In the majority, vasopressin levels only rose sufficiently to have some renal antidiuretic effect, although in some these levels could have been sufficient to cause alteration in peripheral blood flow. Release of vasopressin may be responsible for the facial pallor and antidiuresis observed in migraine.

The influence of vasopressin on oxytocin-induced changes in urine flow in the male rat

1982 ◽  
Vol 100 (2) ◽  
pp. 216-220 ◽  
Author(s):  
Mary L. Forshing ◽  
M.J. Brimble ◽  
R. J. Balment
Keyword(s):  
Urine Flow ◽  
Male Rat ◽  
Water Excretion ◽  
Plasma Vasopressin ◽  
Renal Receptor ◽  
Diuretic Response ◽  
Long Evans ◽  
Induced Changes ◽  
Renal Water Excretion

Abstract. Oxytocin administration in rats infused with hypotonic saline is associated with a saliuresis and altered renal water excretion. The role of vasopressin in determining the pattern of oxytocin-induced changes in urine flow was investigated in Long Evans and vasopressin-deficient Brattleboro rats, which exhibit contrasting diuretic and antidiuretic responses to oxytocin. Ethanol anaesthesia and water loading in Long Evans suppressed plasma vasopressin levels and was associated with an antidiuretic response to oxytocin. Vasopressin administration in the Brattleboro rat reversed the oxytocin-induced antidiuresis normally observed in vasopressin dificiency. These results taken with previous observations, have been interpreted as indicative that oxytocin acts as a weak agonist at the renal vasopressin receptor. When plasma vasopressin is suppressed or absent oxytocin acts as a weak antidiuretic agent, but in the presence of higher vasopressin levels a diuretic response to oxytocin is seen which follows displacement of vasopressin, the more potent antidiuretic agent, from the renal receptor.

scholarly journals Role of Plasma Vasopressin in Impaired Water Excretion of Glucocorticoid Deficiency

1978 ◽  
Vol 62 (4) ◽  
pp. 738-744 ◽  
Author(s):  
John Boykin ◽  
Antoine Detorrenté ◽  
Abby Erickson ◽  
Gary Robertson ◽  
Robert W. Schrier
Keyword(s):  
Water Excretion ◽  
Plasma Vasopressin ◽  
Glucocorticoid Deficiency ◽  
Impaired Water

Lack of effect of chronic renal denervation on altered sodium reabsorption during increased ureteral pressure

1980 ◽  
Vol 58 (5) ◽  
pp. 477-483 ◽  
Author(s):  
D. R. Wilson ◽  
M. Cusimano ◽  
U. Honrath
Keyword(s):  
Isotonic Saline ◽  
Urine Osmolality ◽  
Tubular Reabsorption ◽  
Renal Nerves ◽  
Sodium Reabsorption ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Water Excretion ◽  
Renal Nerve Activity

The role of the renal nerves in the altered sodium reabsorption which occurs during increased ureteral pressure was studied using clearance techniques in anaesthetized rats undergoing diuresis induced by isotonic saline infusion. In rats with a sham denervated kidney, an ipsilateral increase in ureteral pressure to 20 cm H2O resulted in a marked and significant decrease in sodium and water excretion, increased fractional sodium reabsorption, and increased urine osmolality with no significant change in glomerular filtration rate. A similar significant ipsilateral increase in tubular reabsorption of sodium occurred in rats with chronically denervated kidneys during increased ureteral pressure. The changes in tubular reabsorption were rapidly reversible after return of ureteral pressure to normal. These experiments indicate that enhanced tubular reabsorption of sodium during an ipsilateral increase in ureteral pressure is not mediated by increased renal nerve activity. During the antinatriuresis of increased ureteral pressure there was a decrease in the fractional reabsorption of sodium from the opposite normal kidney. The role of the renal nerves in this compensatory change in function in the opposite kidney was studied in two further groups of animals. The renal response to a contralateral increase in ureteral pressure was similar in denervated and sham-denervated kidneys. The results indicate that altered renal nerve activity, through ipsilateral or contralateral renorenal reflexes, is not responsible for the changes in tubular reabsorption of sodium which occur during increased ureteral pressure induced by partial ureteral obstruction.

Role of Plasma Vasopressin in Changes of Water Balance Accompanying Acute Alcohol Intoxication

1995 ◽  
Vol 19 (3) ◽  
pp. 759-762 ◽  
Author(s):  
Hanna Taivainen ◽  
Kalevi Laitinen ◽  
Riitta Tahtela ◽  
Kalervo Kiianmaa ◽  
Matti J. Valimaki
Keyword(s):  
Water Balance ◽  
Alcohol Intoxication ◽  
Acute Alcohol Intoxication ◽  
Plasma Vasopressin

scholarly journals Role of ‘catalytic’ iron in an animal model of minimal change nephrotic syndrome

1996 ◽  
Vol 49 (2) ◽  
pp. 370-373 ◽  
Author(s):  
Norishi Ueda ◽  
Radhakrishna Baliga ◽  
Sudhir V. Shah
Keyword(s):  
Animal Model ◽  
Nephrotic Syndrome ◽  
Minimal Change Nephrotic Syndrome ◽  
Minimal Change

scholarly journals Evidence for a role of angiotensin converting enzyme 2 in proteinuria of idiopathic nephrotic syndrome

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Roberta da Silva Filha ◽  
Sérgio Veloso Brant Pinheiro ◽  
Thiago Macedo e Cordeiro ◽  
Victor Feracin ◽  
Érica Leandro Marciano Vieira ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Idiopathic Nephrotic Syndrome ◽  
Renin Angiotensin System ◽  
Cross Sectional Study ◽  
Healthy Controls ◽  
Ang Ii ◽  
Cross Sectional ◽  
Angiotensin Converting Enzyme 2 ◽  
Inflammatory Molecules

AbstractIntroduction: Renin angiotensin system (RAS) plays a role in idiopathic nephrotic syndrome (INS). Most studies investigated only the classical RAS axis. Therefore, the aims of the present study were to evaluate urinary levels of RAS molecules related to classical and to counter-regulatory axes in pediatric patients with INS, to compare the measurements with levels in healthy controls and to search for associations with inflammatory molecules, proteinuria and disease treatment. Subjects and methods: This cross-sectional study included 31 patients with INS and 19 healthy controls, matched for age and sex. Patients and controls were submitted to urine collection for measurement of RAS molecules [Ang II, Ang-(1-7), ACE and ACE2] by enzyme immunoassay and cytokines by Cytometric Bead Array. Findings in INS patients were compared according to proteinuria: absent (<150 mg/dl, n = 15) and present (≥150 mg/dl, n = 16). Results: In comparison to controls, INS patients had increased Ang II, Ang-(1-7) and ACE, levels while ACE2 was reduced. INS patients with proteinuria had lower levels of ACE2 than those without proteinuria. ACE2 levels were negatively correlated with 24-h-proteinuria. Urinary concentrations of MCP-1/CCL2 were significantly higher in INS patients, positively correlated with Ang II and negatively with Ang-(1-7). ACE2 concentrations were negatively correlated with IP-10/CXCL-10 levels, which, in turn, were positively correlated with 24-h-proteinuria. Conclusion: INS patients exhibited changes in RAS molecules and in chemokines. Proteinuria was associated with low levels of ACE2 and high levels of inflammatory molecules.

scholarly journals New Aspects of Pathogenesis and Treatment of Membranous Glomerulopathy After the MENTOR Study

2020 ◽  
pp. 46-53
Author(s):  
Maurizio Salvadori ◽  
Aris Tsalouchos
Keyword(s):  
Nephrotic Syndrome ◽  
Adrenocorticotropic Hormone ◽  
Glomerular Diseases ◽  
The Past ◽  
Superior Efficacy ◽  
Novel Drugs ◽  
Membranous Glomerulopathy ◽  
Blocking Mechanisms ◽  
Antigenic Epitopes

Membranous nephropathy (MN) is the major cause of nephrotic syndrome in adults, accounting for 20% of cases with an annual incidence of 1 per 100,000 population. In the past 10 years, the role of podocytes has been identified. Environmental triggers in genetically predisposed patients can activate podocytes to exhibit antigenic epitopes, including PLA2R, THBS1, and NELL1, which become targets of specific autoantibodies with subsequent complement activation. The discovery of these mechanisms has opened a new horizon in the treatment of MN, and novel drugs are available with more specific mechanisms of action. Rituximab, a monoclonal antibody directed against CD20 expressed on B lymphocytes, has been used in several trials and appears to induce remission of nephrotic syndrome in 60% of patients (GEMRITUX trial). The recently published results of the MENTOR trial documented the superior efficacy of rituximab in patients observed for up to 24 months. In MN, the concept of targeting disease control has introduced novel therapies with specific blocking mechanisms, such as belimumab; nonspecific blocking mechanisms, such as those against adrenocorticotropic hormone; and new therapeutic options, such as ofatumumab, bortezomib, and eculizumab, which have recognised the pathological processes involved in the glomerular diseases.

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