Contributions of glomerular and tubular mechanisms to antidiuresis in conscious domestic fowl

1985 ◽  
Vol 249 (6) ◽  
pp. F842-F850 ◽  
Author(s):  
J. N. Stallone ◽  
E. J. Braun
Keyword(s):  
Water Conservation ◽  
Domestic Fowl ◽  
Arginine Vasotocin ◽  
Quantitative Investigation ◽  
Secondary Importance ◽  
Water Excretion ◽  
Avian Kidney ◽  
Combined Actions ◽  
A Minor ◽  
Renal Water Excretion

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.

Effect of a selective octapeptide analogue of somatostatin on renal water excretion in the dog

Metabolism ◽  
1985 ◽  
Vol 34 (5) ◽  
pp. 408-409 ◽  
Author(s):  
Theodore Mountokalakis ◽  
Mortimer Levy
Keyword(s):  
Water Excretion ◽  
Renal Water Excretion

scholarly journals Intensive Care Unit Acquired Hypernatremia after Major Surgery is Associated with Urine Concentrating Defect: An Observational Study

2020 ◽  
Author(s):  
Philipp Deetjen ◽  
Ulrich Jaschinski ◽  
Axel Heller
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Water Balance ◽  
Water Conservation ◽  
Sodium Excretion ◽  
Free Water ◽  
Major Surgery ◽  
Surgical Intensive Care Unit ◽  
Surgical Intensive Care ◽  
Water Excretion

Abstract Background: Although intensive care acquired hypernatremia is a common event, limited knowledge exists about the pathogenesis of this disorder. The present study attempts to show that patients undergoing major surgery develop hypernatremia in the presence of both high salt and volume load and concentration disorder of the kidney with insufficient sodium excretion.Methods: In a retrospective study, all patients who were admitted to a 40-bed tertiary surgical intensive care unit of a university hospital from July 2019 to December 2019 with major surgery were examined. Hypernatremia was defined as a sodium value exceeding 145 mmol/l. In addition to the analysis of all patients, complete water and salt balances were performed in a smaller subgroup with 142 patients.Results: 23.9% of patients undergoing major surgery developed hypernatremia, whereby hypernatremia was associated with increased mortality. Patients with hypernatremia showed a renal concentration defect with decreased urine sodium concentration (65 (IQR: 44.8-90) mmol/l vs 78 (IQR: 46-107) mmol/l, p = 0.007) and decreased urine osmolality (514 (IQR: 465-605) mmol/l vs 602 (IQR: 467-740) mmol/l, p < 0.001). In the subgroup of patients with complete sodium and water balance, a positive salt and water balance was observed. After propensity score matching, we found a significantly increased electrolyte free water clearance (1020 ±1740 ml vs -560 ±1620 ml, p <0.001) in the hypernatremia group, together with an inadequately lower total sodium urine excretion (401 ±303 mmol vs 593 ±400 mmol, p = 0.02). Conclusion: The present study shows that postoperative hypernatremia is associated with an imbalance between perioperative salt and water load and renal sodium and water handling with inadequately low renal sodium excretion and inadequately high renal water excretion. The underlying renal concentration disorder may be explained by a defect in a natriuretic-ureotelic response a recently described renal urea-mediated water conservation mechanism after salt exposure.

Disorders of Water Balance

2017 ◽  
Author(s):  
Richard H Sterns ◽  
Stephen M. Silver ◽  
John K. Hix ◽  
Jonathan W. Bress
Keyword(s):  
Water Balance ◽  
Water Intake ◽  
Serum Sodium ◽  
Water Conservation ◽  
Free Water ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Water Losses ◽  
Water Excretion ◽  
Impaired Water

Guided by the hypothalamic antidiuretic hormone vasopressin, the kidney’s ability to conserve electrolyte–free water when it is needed and to excrete large volumes of water when there is too much of it normally prevents the serum sodium concentration from straying outside its normal range. The serum sodium concentration determines plasma tonicity and affects cell volume: a low concentration makes cells swell, and a high concentration makes them shrink. An extremely large water intake, impaired water excretion, or both can cause hyponatremia. A combination of too little water intake with too much salt, impaired water conservation, or excess extrarenal water losses will result in hypernatremia. Because sodium does not readily cross the blood-brain barrier, an abnormal serum sodium concentration alters brain water content and composition and can cause serious neurologic complications. Because bone is a reservoir for much of the body’s sodium, prolonged hyponatremia can also result in severe osteoporosis and fractures. An understanding of the physiologic mechanisms that control water balance will help the clinician determine the cause of impaired water conservation or excretion; it will also guide appropriate therapy that can avoid the life-threatening consequences of hyponatremia and hypernatremia.

Stimulation of avian renal phosphate secretion by parathyroid hormone

1981 ◽  
Vol 241 (3) ◽  
pp. F263-F272 ◽  
Author(s):  
R. F. Wideman ◽  
E. J. Braun
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Phosphate ◽  
Domestic Fowl ◽  
Inorganic Phosphate ◽  
Minor Component ◽  
Sodium Potassium ◽  
Tubule Lumen ◽  
Tubular Transport ◽  
A Minor ◽  
Stimulation Of

Phosphate buffers (ammonium, sodium, potassium, and calcium phosphate, pH 5.5, 7.2, 8.5) and 32P were infused unilaterally into the renal portal systems of intact, parathyroidectomized (PTX), and parathyroid hormone-infused (PTH) domestic fowl to study the secretory flux for inorganic phosphate (Pi). Urine samples were collected simultaneously from both kidneys, with the uninfused kidney serving as a control for the portal-perfused kidney (modified Sperber technique). No consistent unilateral excess of Pi or 32P excretion occurred for any of the experimental groups. For intact birds, fractional 32P excretion by both kidneys (FE32p) was identical to fractional Pi excretion (FEpi) (determined by chemical analysis) and reflected net reabsorption (0.64). However, during PTH infusion, FE32p was 0.82 (net reabsorption) while FEPi was 1.21 (net secretion). These results indicate that a) the peritubular-to-lumen flux for Pi and 32P is a minor component of net tubular transport, regardless of the parathyroid status, counterion availability, or peritubular Pi concentration; b) plasma Pi and 32P enter the tubule lumen predominantly by filtration; c) PTH stimulates tubular Pi secretion; and d) the secreted Pi is derived from an organic or inorganic pool that does not readily equilibrate with infused 32P (or presumably peritubular Pi).

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

1974 ◽  
Vol 6 (4) ◽  
pp. 247-253 ◽  
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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