Effect of Vasopressin on Uric Acid Excretion: Evidence for Distal Nephron Reabsorption of Urate in Man

1976 ◽  
Vol 51 (1) ◽  
pp. 33-40 ◽  
Author(s):  
A. Meisel ◽  
H. Diamond
Keyword(s):  
Flow Rate ◽  
Distal Part ◽  
Extracellular Fluid ◽  
Urine Flow ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Urine Flow Rate ◽  
Distal Nephron ◽  
Uric Acid Excretion ◽  
Urate Reabsorption

1. When changes in urine flow rate were induced by vasopressin administration in eight subjects, urate excretion decreased by a mean of 14% and was positively correlated with urine flow rate (r = 0·88, p < 0·01). The effect of vasopressin on urate excretion was not influenced by prior changes in extracellular fluid volume. 2. Mannitol administration in a dose sufficient to prevent vasopressin-induced alterations in urine flow rate blocked the effect of vasopressin on urate excretion. 3. Alterations in urate excretion produced by changes in extracellular fluid volume could be distinguished from the urate-retaining effect of vasopressin-mediated decrease in urine flow. Urate retention after vasopressin was entirely attributed to a decrease in pyrazinamide-suppressible urate excretion, consistent with either decreased secretion or enhanced post-secretory reabsorption of urate. 4. Since diminished urine flow rate in the distal part of the nephron is more likely to lead to enhanced reabsorption of urate, these results provide additional evidence for urate reabsorption in the distal part of the nephron.

Effect of urine flow rate on uric acid excretion in man

1972 ◽  
Vol 15 (4) ◽  
pp. 338-346 ◽  
Author(s):  
Herbert S. Diamond ◽  
Robert Lazarus ◽  
David Kaplan ◽  
David Halberstam
Keyword(s):  
Uric Acid ◽  
Flow Rate ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Acid Excretion ◽  
Uric Acid Excretion

scholarly journals Mechanisms of proximal tubule sodium transport regulation that link extracellular fluid volume and blood pressure

2010 ◽  
Vol 298 (4) ◽  
pp. R851-R861 ◽  
Author(s):  
Alicia A. McDonough
Keyword(s):  
Blood Pressure ◽  
Proximal Tubule ◽  
Flow Rate ◽  
Sodium Transport ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
The Body ◽  
Extracellular Fluid Volume ◽  
Ang Ii ◽  
Salt Diet

One-hundred years ago, Starling articulated the interdependence of renal control of circulating blood volume and effective cardiac performance. During the past 25 years, the molecular mechanisms responsible for the interdependence of blood pressure (BP), extracellular fluid volume (ECFV), the renin-angiotensin system (RAS), and sympathetic nervous system (SNS) have begun to be revealed. These variables all converge on regulation of renal proximal tubule (PT) sodium transport. The PT reabsorbs two-thirds of the filtered Na+ and volume at baseline. This fraction is decreased when BP or perfusion pressure is increased, during a high-salt diet (elevated ECFV), and during inhibition of the production of ANG II; conversely, this fraction is increased by ANG II, SNS activation, and a low-salt diet. These variables all regulate the distribution of the Na+/H+ exchanger isoform 3 (NHE3) and the Na+-phosphate cotransporter (NaPi2), along the apical microvilli of the PT. Natriuretic stimuli provoke the dynamic redistribution of these transporters along with associated regulators, molecular motors, and cytoskeleton-associated proteins to the base of the microvilli. The lipid raft-associated NHE3 remains at the base, and the nonraft-associated NaPi2 is endocytosed, culminating in decreased Na+ transport and increased PT flow rate. Antinatriuretic stimuli return the same transporters and regulators to the body of the microvilli associated with an increase in transport activity and decrease in PT flow rate. In summary, ECFV and BP homeostasis are, at least in part, maintained by continuous and acute redistribution of transporter complexes up and down the PT microvilli, which affect regulation of PT sodium reabsorption in response to fluctuations in ECFV, BP, SNS, and RAS.

scholarly journals Effect of flow rate and the extracellular fluid volume on proximal urate and water absorption

1980 ◽  
Vol 17 (2) ◽  
pp. 155-161 ◽  
Author(s):  
Harry O. Senekjian ◽  
Thomas F. Knight ◽  
Steven C. Sansom ◽  
Edward J. Weinman
Keyword(s):  
Water Absorption ◽  
Flow Rate ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume

scholarly journals Effects of nonsteroidal anti-inflammatory drugs on plasma volume and extracellular fluid volume in rats

1978 ◽  
Vol 28 ◽  
pp. 179
Author(s):  
Toshiaki Kadokawa ◽  
Kanno Hosoki ◽  
Kunihiko Takeyama ◽  
Hisao Minato ◽  
Masanao Shimizu
Keyword(s):  
Plasma Volume ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Control of atrial natriuretic factor release in conscious dogs

1986 ◽  
Vol 251 (5) ◽  
pp. R947-R956 ◽  
Author(s):  
K. M. Verburg ◽  
R. H. Freeman ◽  
J. O. Davis ◽  
D. Villarreal ◽  
R. C. Vari
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Isotonic Saline ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Conscious Dogs ◽  
Base Line ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The aim of this study was to examine the changes in the concentration of plasma immunoreactive atrial natriuretic factor (iANF) that occur in response to expansion or depletion of the extracellular fluid volume in conscious dogs. The plasma iANF concentration was also measured postprandially after the ingestion of a meal containing 125 meq of sodium. Postprandial plasma iANF increased 45% (P less than 0.05) above the base-line concentration, and this increase was accompanied by a brisk natriuresis. After a low-sodium meal, however, plasma iANF and sodium excretion failed to increase. The plasma iANF concentration increased from 57 +/- 5 to 139 +/- 36 pg/ml (P less than 0.05) immediately after volume expansion with intravenous isotonic saline infusion (2.5% body wt) administered over a 30-min period; plasma iANF remained elevated at 90 +/- 14 pg/ml (P less than 0.05) for an additional 30 min before returning toward preinfusion levels. Plasma iANF decreased 45% from 78 +/- 17 to 43 +/- 7 pg/ml (P less than 0.05) in response to the administration of ethacrynic acid (2.0 mg/kg, iv bolus) that produced an estimated 15% depletion of intravascular volume. In additional experiments the infusion of synthetic alpha-human ANF at 100 and 300 ng X kg-1 X min-1 increased (P less than 0.05) both the plasma iANF concentration and the urinary excretion of iANF. This study demonstrates that the secretion of ANF is consistently influenced by changes in the extracellular fluid volume. Furthermore, the results support the concept that ANF functions to increase postprandial sodium excretion following the ingestion of a high-sodium meal.

Homeostatic potassium excretion in fed and fasted sheep

1988 ◽  
Vol 254 (2) ◽  
pp. R357-R380 ◽  
Author(s):  
L. Rabinowitz ◽  
D. M. Green ◽  
R. L. Sarason ◽  
H. Yamauchi
Keyword(s):  
Flow Rate ◽  
Urine Flow ◽  
Plasma Aldosterone ◽  
Urine Flow Rate ◽  
Potassium Excretion ◽  
Adult Sheep ◽  
Blood Ph ◽  
Low Levels ◽  
K Concentration ◽  
Filtered Load

In unanesthetized adult sheep, following intake of a daily meal, there was a peak in K excretion. The maximum and minimum rates of K excretion following meals were directly related to meal K content. On days without meals, no peak in K excretion occurred. Changes in K excretion on fed and fast days occurred without changes in the low levels of plasma aldosterone and were poorly correlated with urine or blood pH, urine flow rate, Na excretion, or the filtered load of K, but they correlated well with fractional K excretion. Plasma K did not change on fast days. Plasma K increased on some, but not all, fed days. Increases in plasma K that occurred on fed days were insufficient to account for the concurrent kaliuresis. Infusion of aldosterone or isotonic NaCl failed to alter K excretion in fed or fasted sheep. Infusion of isotonic NaCl + aldosterone hypertonic Na2SO4 + aldosterone increased K excretion in fasted but not fed sheep. Infusion of K in the rumen of fed and fasted sheep elevated rumen K concentration and led to increases in K excretion that could not be explained by increases in plasma K. The mechanisms responsible for the homeostatic changes in K excretion on fed and fast days were not ascertained but may importantly depend on sensors of enteric K content.

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