Pathogenesis of solute-free water retention in experimental ascitic cirrhosis: is vasopressin the only culprit?

2015 ◽  
Vol 130 (2) ◽  
pp. 117-124 ◽  
Author(s):  
Giovanni Sansoè ◽  
Manuela Aragno ◽  
Raffaella Mastrocola ◽  
Maurizio Parola
Keyword(s):  
Antidiuretic Hormone ◽  
Water Retention ◽  
Renal Excretion ◽  
Free Water ◽  
Experimental Cirrhosis ◽  
Advanced Cirrhosis ◽  
Adrenoceptor Agonists ◽  
Sympatholytic Agents ◽  
Dilutional Hyponatraemia

Adrenergic hyper-function reduces renal excretion of water. In advanced cirrhosis, hypersecretion of vasopressin (antidiuretic hormone or ADH) is considered the cause of dilutional hyponatraemia. We show that in experimental cirrhosis sympatholytic agents (α2A-adrenoceptor agonists) are as effective as V2 antagonists to blunt water retention.

Overexpression of kidney neutral endopeptidase (EC 3.4.24.11) and renal function in experimental cirrhosis

2006 ◽  
Vol 290 (6) ◽  
pp. F1337-F1343 ◽  
Author(s):  
G. Sansoè ◽  
M. Aragno ◽  
R. Mastrocola ◽  
J. C. Cutrin ◽  
S. Silvano ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Specific Inhibitor ◽  
Free Water ◽  
Plasma Renin ◽  
Neutral Endopeptidase ◽  
Experimental Cirrhosis ◽  
Proximal Tubule Cells ◽  
Advanced Cirrhosis ◽  
Normal Humans ◽  
Renal Proximal Tubule Cells

Neutral endopeptidase degrades atrial natriuretic peptide (ANP) and bradykinin and may generate endothelin-1 from big-endothelin. In advanced cirrhosis, sodium retention is accompanied by elevated plasma ANP levels, and infusion of ANP causes hypotension, but in normal humans increasing the concentration of ANP through the inhibition of neutral endopeptidase, localized in renal proximal tubule cells, causes natriuresis without any arterial pressure drop. The purpose of this study was the assessment of kidney neutral endopeptidase expression and responses to candoxatrilat (a specific inhibitor of this enzyme) in rats with CCl4-induced cirrhosis. Two groups of control rats ( n = 5) were injected with vehicle or 3 mg/kg candoxatrilat. Three groups of cirrhotic rats with ascites ( n = 10) received vehicle alone or 3 or 10 mg/kg candoxatrilat. In cirrhotic rats, Western blot analysis revealed a 170% increase in renal neutral endopeptidase protein content ( P < 0.03), mainly in the proximal nephron and macula densa, and both candoxatrilat dosages increased plasma ANP levels, urinary volume, and urinary excretion of sodium, ANP, and cGMP compared with vehicle alone (all P < 0.03). Candoxatrilat (10 mg/kg) also reduced tubular solute-free water reabsorption ( P < 0.03) in cirrhotic rats, but renal blood flow, arterial pressure, and plasma renin activity were unaffected. Neutral endopeptidase inhibition has natriuretic and aquaretic actions in cirrhosis without any effect on blood pressure and kidney perfusion due to a significant overexpression of this enzyme in renal cortex.

Temporal relationship between the impairment of free water excretion and antidiuretic hormone hypersecretion in rats with experimental cirrhosis

1987 ◽  
Vol 93 (3) ◽  
pp. 498-505 ◽  
Author(s):  
J. Camps ◽  
J. Solá ◽  
V. Arroyo ◽  
R.M. Pérez-Ayuso ◽  
J. Gaya ◽  
...  
Keyword(s):  
Antidiuretic Hormone ◽  
Temporal Relationship ◽  
Free Water ◽  
Experimental Cirrhosis ◽  
Water Excretion

scholarly journals Severe Persistent Hyponatremia: A Rare Presentation of Biliary Fluid Loss

2019 ◽  
Vol 7 ◽  
pp. 232470961986937
Author(s):  
Asim Kichloo ◽  
El-Amir Zain ◽  
M. Zatmar Khan ◽  
Farah Wani ◽  
Jagmeet Singh
Keyword(s):  
Antidiuretic Hormone ◽  
Water Retention ◽  
Hormone Secretion ◽  
Free Water ◽  
Acalculous Cholecystitis ◽  
Fluid Loss ◽  
Rare Presentation ◽  
Arterial Blood ◽  
Cholecystostomy Tube ◽  
Acute Hyponatremia

Hypotonic hyponatremia is caused by a serum sodium level of <135 mEq/L in the setting of excess solute loss accompanied by free water retention because of antidiuretic hormone release, subsequent to decreased effective arterial blood volume. Acute hyponatremia can have various neurological manifestations, including drowsiness, lethargy, coma, seizures, respiratory depression, and even death. In this article, we present a case of a 41-year-old man who presented with hyponatremia as a result of sodium containing biliary fluid loss and resultant renal free water retention in response to increased antidiuretic hormone secretion. He underwent placement of a cholecystostomy tube for acalculous cholecystitis and was found to be persistently hyponatremic despite repletion with sodium-containing fluids. Once the cholecystostomy tube was removed, the patient’s sodium levels improved, and his symptoms resolved. Our case highlights choleuresis as an unusual but significant cause of hyponatremia in patients who have external biliary drainage.

Renal Nerves Are Not Involved in Sodium and Water Retention during Mechanical Ventilation in Awake Dogs 

1998 ◽  
Vol 89 (4) ◽  
pp. 942-953 ◽  
Author(s):  
Willehad Boemke ◽  
Martin O. Krebs ◽  
Kourosh Djalali ◽  
Harald Bunger ◽  
Gabriele Kaczmarczyk
Keyword(s):  
Mechanical Ventilation ◽  
Continuous Positive Airway Pressure ◽  
Antidiuretic Hormone ◽  
Airway Pressure ◽  
Water Retention ◽  
Positive Airway Pressure ◽  
Surgical Stress ◽  
Urine Volume ◽  
Plasma Renin ◽  
Renal Nerves

Background The role of renal nerves during positive end-expiratory pressure ventilation (PEEP) has only been investigated in surgically stressed, anesthetized, unilaterally denervated dogs. Anesthesia, sedation, and surgical stress, however, decrease urine volume and sodium excretion and increase renal sympathetic nerve activity independent of PEEP. This study investigated in awake dogs the participation of renal nerves in mediating volume and water retention during PEEP. Methods Eight tracheotomized, trained, awake dogs were used. The protocol consisted of 60 min of spontaneous breathing at a continuous positive airway pressure of 4 cm H2O, followed by 120 min of controlled mechanical ventilation with a mean PEEP of 15-17 cm H2O (PEEP), and 60 min of continuous positive airway pressure. Two protocols were performed on intact dogs, in which volume expansion had (hypervolemic; electrolyte solution, 0.5 ml x kg(-1) x min(-1)) and had not (normovolemic) been instituted. This was repeated on the same dogs 2 or 3 weeks after bilateral renal denervation. Results Hypervolemic dogs excreted more sodium and water than did normovolemic dogs. There was no difference between intact and renal-denervated dogs. Arterial pressure did not decrease when continuous positive airway pressure was switched to PEEP. Plasma renin activity, aldosterone, and antidiuretic hormone concentrations were greater in normovolemic dogs. The PEEP increased aldosterone and antidiuretic hormone concentrations only in normovolemic dogs. Conclusions In conscious dogs, renal nerves have no appreciable contribution to sodium and water retention during PEEP. Retention in normovolemic dogs seems to be primarily caused by an activation of the renin-angiotensin system and an increase in the antidiuretic hormone. Excretion rates depended on the volume status of the dogs.

scholarly journals Influenza A: another cause of SIADH?

2018 ◽  
pp. bcr-2018-226154
Author(s):  
Simon Mifsud ◽  
Maria Alessandra Zammit ◽  
Ramon Casha ◽  
Claudia Fsadni
Keyword(s):  
Case Report ◽  
Respiratory Tract ◽  
Antidiuretic Hormone ◽  
Influenza A ◽  
Respiratory Tract Infections ◽  
Hormone Secretion ◽  
Antidiuretic Hormone Secretion ◽  
Osmotic Stimulus ◽  
Tract Infections ◽  
Dilutional Hyponatraemia

The syndrome of inappropriate antidiuretic hormone (SIADH) secretion is a frequent cause of hyponatraemia. It is a dilutional hyponatraemia secondary to impaired urinary dilution in the absence of renal disease or any identifiable non-osmotic stimulus known to induce antidiuretic hormone secretion. SIADH can arise secondary to various respiratory tract infections; however, the association between SIADH and influenza A infection is described in only a few cases in the literature. The authors present a case report of influenza A that may have caused a profound SIADH-related hyponatraemia.

scholarly journals Vasopressin-induced hyponatremia in a patient with pulmonary hypertension and right heart failure treated for septic shock

2018 ◽  
Vol 5 (3) ◽  
pp. 36
Author(s):  
Andrew Peters ◽  
Yevgeniy Brailovsky ◽  
Vladimir Lakhter ◽  
Paul R. Forfia
Keyword(s):  
Heart Failure ◽  
Water Retention ◽  
Sodium Level ◽  
Serum Sodium Level ◽  
Free Water ◽  
Right Heart Failure ◽  
Vasodilatory Shock ◽  
Right Heart ◽  
Electrolyte Effects ◽  
Rapid Correction

We report a case of a 55-year-old woman who developed hyponatremia after the initiation of exogenous vasopressin to treat vasodilatory shock. Discontinuation of exogenous vasopressin therapy, without any other changes in medical therapy or the patient’s condition, led to a rapid correction in the serum sodium level along with a marked increase in urine output. Increased free water retention due to exogenous vasopressin administration may have contributed to hyponatremia in this patient. This case illustrates the potential for vasopressin to have potent and unintended renal and electrolyte effects in patients treated for vasodilatory shock.

Interaction of somatostatin with PTH and AVP: renal effects.

1979 ◽  
Vol 237 (5) ◽  
pp. E428
Author(s):  
N Brautbar ◽  
B S Levine ◽  
J W Coburn ◽  
C R Kleeman
Keyword(s):  
Antidiuretic Hormone ◽  
Arginine Vasopressin ◽  
Free Water ◽  
Treated Group ◽  
Free Water Clearance ◽  
Parathyroid Extract ◽  
Renal Tubular ◽  
Vehicle Treated Group ◽  
Experimental Group ◽  
Antidiuretic Action

Six conscious intact dogs were studied to evaluate the interactions of somatostatin (SRIF) with exogenous antidiuretic hormone arginine vasopressin (AVP). SRIF administration caused a significant increase in free water clearance compared to a vehicle-treated group: -0.91 (+/- 0.41 SD) ml/min to 0.21 (+/- 0.32 SD) ml/min in the experimental group (P less than 0.01) versus 0.21 (+/- 0.81 SD) ml/min to -0.21 (+/- 0.68 SD) ml/min in the control (P greater than 0.5). Six conscious, thyroparathyroidectomized dogs were studied to test the interaction of SRIF and parathyroid extract (PTE). There were no significant changes in the phosphaturic and hypocalciuric effects of PTE with SRIF administration. We conclude that acute systemic SRIF administration interferes with the antidiuretic action of AVP, probably at the renal-tubular level, but does not antagonize the renal actions of PTE.

Synthesis of new exenatide analogs and investigation of their influence on glycemia and renal function in rats

2011 ◽  
Vol 57 (3) ◽  
pp. 42-47
Author(s):  
A E Bogolepova ◽  
A V Kutina ◽  
A S Marina ◽  
S K Nikol'skaia ◽  
E I Shakhmatova ◽  
...  
Keyword(s):  
Renal Excretion ◽  
Free Water ◽  
Potassium Ions ◽  
Magnesium Ions ◽  
Glucose Loading ◽  
Rat Models ◽  
Renal Functions ◽  
In Vivo Testing ◽  
Physiologically Active Compounds

New analogs of exenatide with amino acid substitutions at 14, 35, and 39 have been synthesized. They were shown to be more stable than original exenatide in aqueous solutions. In vivo testing on rat models of glucose loading showed that exenatide and its novel analogs possess hypoglycemic activity and stimulate renal excretion of sodium and magnesium ions and osmotically free water but have virtually no effect on the elimination of potassium ions. Experiments with isolated skin and urinary bladder preparations from male frogs showed that exenatide and its analogs promote biosynthesis of physiologically active compounds modulating renal functions.

The blockade of the vascular effect of antidiuretic hormone (ADH) decreases arterial pressure in experimental cirrhosis with asches

1989 ◽  
Vol 9 ◽  
pp. S19 ◽  
Author(s):  
J. Clària ◽  
W. Jiménez ◽  
V. Arryo ◽  
C. López ◽  
G. La Villa ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Antidiuretic Hormone ◽  
Vascular Effect ◽  
Experimental Cirrhosis
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