Prevalence of impaired renal water excretion and dilutional hyponatremia in cirrhotic patients

Recently developed radioimmunoassay (RIA) techniques were employed in a quantitative investigation of the renal actions of the avian antidiuretic hormone arginine vasotocin (AVT) in the conscious domestic fowl. Constant intravenous infusion of AVT at doses of 0.125-1.00 ng X kg-1 X min-1 was used to produce plasma AVT (PAVT) concentrations (verified by RIA) over the entire range of physiological PAVT levels in the domestic fowl. Comparison of the dose-response relationships between PAVT and glomerular and tubular mechanisms of antidiuresis revealed that tubular mechanisms are of primary importance and glomerular mechanisms of secondary importance in the conservation of water by the avian kidney. The greatest proportion of the total AVT-induced reduction in renal water excretion occurred at low physiological PAVT levels (less than 5 microU/ml), prior to any significant reduction in glomerular filtration rate (GFR), and appeared to be the exclusive result of tubular mechanisms of antidiuresis. At high PAVT levels (5-16 microU/ml), glomerular and tubular mechanisms overlapped, and their effects on water conservation could not be separated. Although GFR was reduced by nearly 30% at the highest dose of AVT, only minor additional amounts of water were conserved by the combined actions of glomerular and tubular mechanisms. Thus glomerular mechanisms appear to have only a minor secondary effect on water-conserving ability of the avian kidney.

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Effect of alpha- and beta-adrenergic stimulation on renal water excretion in man

Kidney International ◽

10.1038/ki.1974.106 ◽

1974 ◽

Vol 6 (4) ◽

pp. 247-253 ◽

Cited By ~ 22

Author(s):

Tomas Berl ◽

Judith A. Harbottle ◽

Robert W. Schrier

Keyword(s):

Adrenergic Stimulation ◽

Beta Adrenergic ◽

Water Excretion ◽

Renal Water Excretion

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Dendroaspis Natriuretic Peptide Administered Intracerebroventricularly Increases Renal Water Excretion

Clinical and Experimental Pharmacology and Physiology ◽

10.1046/j.1440-1681.2002.03631.x ◽

2002 ◽

Vol 29 (3) ◽

pp. 195-197 ◽

Cited By ~ 6

Author(s):

JongUn Lee ◽

Soo Wan Kim

Keyword(s):

Natriuretic Peptide ◽

Water Excretion ◽

Renal Water Excretion

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Total paracentesis in cirrhotic patients with tense ascites and dilutional hyponatremia

The American Journal of Gastroenterology ◽

10.1111/j.1572-0241.1999.01296.x ◽

1999 ◽

Vol 94 (8) ◽

pp. 2219-2223 ◽

Cited By ~ 17

Author(s):

Maria Carme Vila ◽

Susanna Coll ◽

Ricard Sola ◽

Montserrat Andreu ◽

Jordi Gana ◽

...

Keyword(s):

Cirrhotic Patients ◽

Dilutional Hyponatremia

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Neural Basis for Regulation of Vasopressin Secretion by Anticipated Disturbances in Osmolality

10.1101/2021.01.27.428388 ◽

2021 ◽

Author(s):

Angela Kim ◽

Joseph C. Madara ◽

Chen Wu ◽

Mark L. Andermann ◽

Bradford B. Lowell

Keyword(s):

Water Balance ◽

Arcuate Nucleus ◽

Feedback Regulation ◽

Neural Mechanisms ◽

Neuron Activity ◽

Neural Basis ◽

Water Excretion ◽

Hypothalamic Arcuate Nucleus ◽

Vasopressin Secretion ◽

Renal Water Excretion

AbstractWater balance, tracked by extracellular osmolality, is regulated by feedback and feedforward mechanisms. Feedback regulation is reactive, occurring as deviations in osmolality are detected. Feedforward or presystemic regulation is proactive, occurring when disturbances in osmolality are anticipated. Vasopressin (AVP) is a key hormone regulating water balance and is released during hyperosmolality to limit renal water excretion. AVP neurons are under feedback and feedforward regulation. Not only do they respond to disturbances in blood osmolality, but they are also rapidly suppressed and stimulated, respectively, by drinking and eating, which will ultimately decrease and increase osmolality. Here, we demonstrate that AVP neuron activity is regulated by multiple anatomically-and functionally-distinct neural circuits. Notably, presystemic regulation during drinking and eating are mediated by non-overlapping circuits that involve the lamina terminalis and hypothalamic arcuate nucleus, respectively. These findings reveal neural mechanisms that support differential regulation of AVP release by diverse behavioral and physiological stimuli.

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Mechanism of cold diuresis in the rat

AJP Renal Physiology ◽

10.1152/ajprenal.1983.244.2.f210 ◽

1983 ◽

Vol 244 (2) ◽

pp. F210-F216 ◽

Cited By ~ 5

Author(s):

M. L. Morgan ◽

R. J. Anderson ◽

M. A. Ellis ◽

T. Berl

Keyword(s):

Mean Arterial Pressure ◽

Arterial Pressure ◽

Plasma Osmolality ◽

Urine Osmolality ◽

Urine Flow ◽

Hemodynamic Parameters ◽

Water Excretion ◽

Urinary Osmolality ◽

6 Hydroxydopamine ◽

Renal Water Excretion

The effect of cold exposure (CE) on renal water excretion has not been clearly delineated. Conscious rats were exposed to decreased ambient temperature (15 degrees C). Forty-five minutes of CE resulted in reversible increases in urine flow and decreases in urine osmolality. The diuresis was not due to a diminished response to vasopressin (VP), as the antidiuresis associated with 500 microU of Pitressin given to water-diuresing rats was comparable at 15 and 30 degrees C. To determine whether the diuresis was due to intrarenal factors, glomerular filtration rate, renal blood flow, sodium excretion, and osmolar clearances were measured and found to be equivalent during control and cold conditions. To determine whether the observed diuresis was due to suppression of endogenous VP, VP-free Brattleboro rats undergoing a constant VP infusion were cold exposed. In these rats, CE was not associated with a change in either urine flow or urinary osmolality. This antidiuretic hormone-mediated mechanism was corroborated by a decrease in immunoassayable VP levels. To determine the mechanism whereby CE suppresses endogenous VP, plasma osmolality and hemodynamic parameters were measured. Although CE was not associated with a change in plasma osmolality, it did result in a significant increase in both mean arterial pressure and cardiac index. Pretreatment of rats with 6-hydroxydopamine prevented both the increase in mean arterial pressure and cold diuresis. We conclude that the diuresis observed upon exposure to 15 degrees C results from nonosmotic suppression of endogenous VP, as a consequence of the increase in mean arterial pressure.

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