Renal Sodium Retention in Cirrhosis: Relation to Aldosterone and Nephron Site

1979 ◽  
Vol 56 (2) ◽  
pp. 169-177 ◽  
Author(s):  
S. P. Wilkinson ◽  
T. P. Jowett ◽  
J. D. H. Slater ◽  
V. Arroyo ◽  
H. Moodie ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Renal Excretion ◽  
Free Water ◽  
Sodium Reabsorption ◽  
Sodium Retention ◽  
Diluting Segment ◽  
Wide Range ◽  
Healthy Control ◽  
Renal Tubular ◽  
Range Of Values

1. In a group of patients with cirrhosis who showed a wide range of values for the rate of renal sodium excretion, the latter was found to be inversely related to both the plasma concentration and rate of renal excretion of aldosterone. However, for a given sodium excretion the values for aldosterone were significantly lower in the patients than for a group of healthy control subjects. These findings suggest either an increased renal tubular sensitivity to aldosterone or the participation of other factors in the pathogenesis of the sodium retention. 2. Based on measurements of the rate of urine flow and the clearances of free water and inulin during a maximal water diuresis, the fractional reabsorption of sodium by the ‘proximal’, ‘diluting segment’ and ‘distal’ segments of the nephron was estimated. For patients retaining sodium the enhanced reabsorption occurred at both proximal and distal sites, the latter being quantitatively more important. There was no significantly enhanced sodium reabsorption in the diluting segment.

Effect of catecholamines on tubular function in the isolated perfused rat kidney

1977 ◽  
Vol 233 (1) ◽  
pp. F39-F45 ◽  
Author(s):  
A. Besarab ◽  
P. Silva ◽  
L. Landsberg ◽  
F. H. Epstein
Keyword(s):  
Sodium Excretion ◽  
Constant Pressure ◽  
Rat Kidney ◽  
Free Water ◽  
Tubular Function ◽  
Sodium Reabsorption ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Beta Receptors ◽  
Renal Tubular

Addition of norepinephrine or epinephrine to the isolated rat kidney perfused at constant pressure resulted in an increase in sodium reabsorption and the excretion of a dilute urine with an increase in free water clearance. Vasopressin reversed the fall in urinary osmolarity but not the diminution in sodium excretion. The urinary changes produced by catecholamines were blocked by propranolol but not by phenoxybenzamine, suggesting that they were mediated, at least in part, by beta receptors. Similar though less pronounced changes in sodium excretion and urinary osmolarity were produced by isoproterenol and phenylephrine, while the combination of these drugs induced marked dilution of the urine. The results suggest that circulating catecholamines or adrenergic nerves innervating the kidney directly influence renal tubular function and might, therefore, participate in the regulation of sodium and water excretion by the kidneys.

Effect of acute unilateral renal denervation on tubular sodium reabsorption in the dog

1977 ◽  
Vol 232 (1) ◽  
pp. F16-F19
Author(s):  
G. Nomura ◽  
T. Takabatake ◽  
S. Arai ◽  
D. Uno ◽  
M. Shimao ◽  
...  
Keyword(s):  
Renal Denervation ◽  
Renal Plasma Flow ◽  
Free Water ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Water Diuresis ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Tubular Sodium Reabsorption ◽  
Renal Tubular

The effects of acute denervation of the kidney on renal tubular sodium and water excretion were studied in anesthetized, hypophysectomized, and cortisone-treated mongrel dogs during stable water diuresis produced by the infusion of 2.5% dextrose. In all experiments, denervation natriuresis, and diuresis were observed without significant change in glomerular filtration rate (GRF) and renal plasma flow (RPF). Fractional sodium delivery to the distal nephron (CNa + CH2O/100 ml GFR) and fractional free water clearance (CH23/100 ml GFR) was significantly greater in the denervated kidney compared with the innervated kidney (9.6+/-1.2 vs. 6.7+/-0.9% and 8.8+/-1.2 vs. 6.5+/-0.8%, respectively). Distal tubular sodium reabsorption (CH2O/(CNa + CH2O)) was not significantly different. We conclude that renal denervation primarily affects the proximal tubule as manifested by a decrease in the reabsorption of sodium and water. A small effect of denervation on the distal nephron is not completely ruled out.

Atrial natriuretic factor counteracts sodium-retaining actions of insulin in normal men

1993 ◽  
Vol 265 (3) ◽  
pp. R584-R590 ◽  
Author(s):  
J. A. Miller ◽  
S. Abouchacra ◽  
B. Zinman ◽  
K. L. Skorecki ◽  
A. G. Logan
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Low Dose ◽  
Diastolic Pressure ◽  
Sodium Reabsorption ◽  
Acute Administration ◽  
Sodium Retention ◽  
Natriuretic Factor ◽  
Normal Men ◽  
Atrial Natriuretic

It has been hypothesized that hyperinsulinemia is causally related to hypertension by its effect on renal sodium transport. To examine the relationship between the sodium-retaining actions of insulin and atrial natriuretic factor (ANF), 16 healthy subjects were studied on three occasions, approximately 1 wk apart, using standard clearance techniques to evaluate responses during the acute administration of insulin, low-dose ANF, or both. In study 1, the euglycemic clamp was used to increase plasma insulin 10-fold to an average of 320 +/- 14 (SE) pM. This maneuver produced an immediate and persistent fall in sodium excretion from 0.315 +/- 0.02 to 0.207 +/- 0.02 mmol/min (P < 0.001) independent of change in renal hemodynamics, lithium clearance, and catecholamines. The decline in sodium excretion was associated with a marked increase in fractional distal sodium reabsorption. Systolic and diastolic pressure did not change significantly. In study 2, low-dose ANF (0.3 pmol.kg-1.min-1) designed to raise plasma levels to twice baseline was administered simultaneously in a repeat of study 1. This maneuver abolished insulin-mediated sodium reabsorption. In study 3, low-dose ANF infusion alone produced no changes in tubular handling of sodium. Our findings indicate that insulin at levels found in hyperinsulinemic states caused sodium retention and that physiological increases in plasma ANF concentration abolished the sodium-retaining action of insulin. Our findings suggest that if hypertension is causally related to hyperinsulinemia, mechanisms besides renal sodium retention are responsible for the hypertensive properties of insulin.

Mechanisms of the antinatriuretic action of physiological doses of angiotensin II in man

1989 ◽  
Vol 76 (6) ◽  
pp. 653-658 ◽  
Author(s):  
Peter H. Seidelin ◽  
John J. McMurray ◽  
Allan D. Struthers
Keyword(s):  
Creatinine Clearance ◽  
Sodium Excretion ◽  
Free Water ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Distal Nephron ◽  
Aldosterone Secretion ◽  
Significant Fall ◽  
Parallel Change ◽  
Proximal Tubular

1. Angiotensin 11 (ANG II; 1 ng min−1 kg−1) or 5% (w/v) d-glucose (placebo) was infused in six normal male volunteers, pretreated with 500 mg of lithium carbonate, who were undergoing maximal water diuresis. 2. This dose of ANG II caused a circulating increment within the physiological range (27 ± 4 to 48 ± 9 pmol/l). 3. Compared with placebo, ANG II caused a significant fall in urinary sodium excretion (113 ± 13 to 82 ± 10 μmol/min). This antinatriuretic effect occurred without a fall in creatinine clearance (107 ± 3 versus 113 ± 3 ml/min). 4. ANG II caused a significant fall in fractional lithium clearance (28 ± 2 to 23 ± 2%). This may indicate a proximal tubular effect of ANG II. 5. ANG II also reduced fractional distal delivery [(sodium clearance plus free water clearance) divided by creatinine clearance], another measure of proximal tubular outflow. A parallel change in these two separate markers of proximal function supports an action of ANG II at this nephron segment. 6. Furthermore, the antinatriuretic effect of ANG II was unlikely to be due to stimulation of aldosterone secretion because (a) the fall in sodium excretion was temporally dissociated from the rise in aldosterone secretion, (b) potassium excretion also tended to fall during ANG II infusion and (c) aldosterone has a distal nephron effect, while, in this study, proximal nephron fractional reabsorption of sodium increased and distal nephron fractional reabsorption of sodium was unchanged. 7. These observations suggest that physiological increments in ANG II can have an antinatriuretic effect in man, which, at least initially, results from increased proximal tubular sodium reabsorption and is independent of the effect of aldosterone.

Studies on Mineralocorticoid ‘Escape’ in Cirrhosis

1979 ◽  
Vol 56 (5) ◽  
pp. 401-406 ◽  
Author(s):  
S. P. Wilkinson ◽  
I. K. Smith ◽  
Helen Moodie ◽  
Lucilla Poston ◽  
R. Williams
Keyword(s):  
Extracellular Fluid ◽  
Plasma Renin ◽  
Fluid Volume ◽  
The Other ◽  
Extracellular Fluid Volume ◽  
Sodium Reabsorption ◽  
Sodium Retention ◽  
Similar Extent ◽  
Water Diuresis ◽  
Diluting Segment

1. The mineralocorticoid 9α-fluorohydrocortisone was given to 12 patients with cirrhosis without ascites. In seven an ‘escape’ from its sodium-retaining effects was observed, the other five continuing to retain sodium. 2. Changes in plasma renin activity (PRA) and inulin clearance (Cinulin) were used in the assessment of possible changes in the ‘effective’ extracellular fluid volume. PRA fell and Cinulin increased to a similar extent in each of the two groups of patients. These findings do not support the concept that the failure to show the mineralocorticoid escape in some patients with cirrhosis is due to a failure of expansion of the effective extracellular fluid volume. 3. Sodium reabsorption in the different segments of the nephron as estimated by clearance techniques under conditions of maximal water diuresis showed that the greatest changes to account for both mineralocorticoid escape and sodium retention were in the part of the nephron beyond the diluting segment.

Renal Function in Saline-Loaded Dogs with Minimal Sodium Excretion

1973 ◽  
Vol 51 (2) ◽  
pp. 148-152 ◽  
Author(s):  
Mortimer Levy ◽  
Earle A. Lockhart
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Sodium Reabsorption ◽  
Sodium Retention ◽  
Arterial Blood ◽  
Saline Loading ◽  
Blood Pressure Fall ◽  
Pressure Fall

In this laboratory, dogs acutely saline-loaded to 7–8% body weight and treated with large doses of antidiuretic hormone and deoxycorticosterone acetate will excrete on the average 400–700 μequiv/min of sodium. We have been able to study five dogs, similarly treated, which for no apparent cause showed a trivial natriuretic response following comparable volume expansion. Postexpansion sodium excretion varied from 30 to 150 μequiv/min. Glomerular filtration rate and arterial blood pressure remained constant, but in each case p-aminohippurate clearance rate (CPAH) fell in response to acute saline loading. Renal vasodilatation with acetylcholine and elevation of perfusion pressure with noradrenaline reversed the sodium retention. Fractional reabsorption in the proximal tubule was normal, and the loop of Henle appeared to be the major nephron site responsible for the augmented sodium reabsorption. Constancy of arterial blood pressure, fall in CPAH, and response to altered intrarenal hemodynamics seem to characterize these saline-loaded dogs with minimal sodium excretion as a unique population.

Effects of α-adrenergic blockade on sodium excretion in normal and chronic salt retaining dogs

1976 ◽  
Vol 54 (3) ◽  
pp. 209-218 ◽  
Author(s):  
Shyan-Yih Chou ◽  
Paul H. Liebman ◽  
Leon F. Ferder ◽  
Daniel L. Levin ◽  
Roy J. Cacciaguida ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Urine Volume ◽  
Vena Cava ◽  
Free Water ◽  
Urinary Sodium Excretion ◽  
Blocking Agent ◽  
Major Effect ◽  
Sodium Reabsorption ◽  
Adrenergic Blockade ◽  
Free Water Clearance

The α-adrenergic blocking agent phenoxybenzamine (PBA) was administered intravenously (10 μg kg−1 min−1) during a steady state water diuresis under pentothal anesthesia to six normal dogs, six dogs with chronic thoracic inferior vena cava constriction and ascites (caval dogs) and seven dogs chronically salt depleted by sodium restriction and furosemide administration. In normal dogs urinary sodium excretion increased significantly from 265 ± 56 (SEM) to 370 ± 65 μequiv./min, whereas no increase in sodium excretion was noted in either caval dogs or salt depleted animals after PBA. In all three groups urine volume, fractional free water clearance and distal sodium load did not change significantly. In normal dogs, distal tubular sodium reabsorption decreased significantly from 73.4 ± 2.8% to 63.1 ± 4.0%, whereas no change was noted in caval or salt depleted dogs. Blood pressure and renal hemodynamics were not significantly altered by PBA administration in any group. These data demonstrate a natriuretic effect of α-adrenergic blockade in normal dogs with the major effect in the water clearing segment of the nephron. The absence of any effect in chronic caval or salt depleted dogs suggests that increased α-adrenergic activity does not play a significant role in the sodium retention of these animals.

A Role for Sodium-Retaining Steroids in the Regulation of Proximal Tubular Sodium Reabsorption in Man

1972 ◽  
Vol 42 (4) ◽  
pp. 423-432 ◽  
Author(s):  
John R. Gill ◽  
Catherine S. Delea ◽  
F. C. Bartter
Keyword(s):  
Flow Rate ◽  
Sodium Excretion ◽  
Free Water ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Diluting Segment ◽  
Free Water Clearance ◽  
Urinary Osmolality ◽  
Glomerular Filtrate ◽  
Water Clearance

1. The response to an infusion of 4% (w/v) fructose in water was determined in fifteen women on a daily sodium intake of 100 mEq/day. The results were compared with those obtained during a similar infusion on another day after treatment with deoxycorticosterone (20 mg/day; seven subjects), or spironolactone (200 mg/day; eight subjects), for 1 day before the day of study. 2. Treatment with deoxycorticosterone significantly (P < 0·01) decreased sodium excretion (from a mean value of 391 to 192 μEq/min) and urine flow rate (from 14·3 to 12·4 ml min−1 100 ml−1 of glomerular filtrate) without a change in urinary osmolality or the clearance of inulin. The steroid also increased the fractional reabsorption of sodium at the diluting segment of the nephron, but this increase in reabsorption was not sufficient to compensate for the decrease in delivery of sodium to the site, so that absolute free-water clearance decreased. 3. Treatment with spironolactone significantly (P < 0·01) increased sodium excretion (from 349 to 437 μEq/min) and urine flow rate (from 12·5 to 14·4 ml min−1 100 ml−1 of glomerular filtrate) with essentially no change in urinary osmolality or in inulin clearance. Spironolactone also decreased the fractional reabsorption of sodium at the diluting segment of the nephron, but the degree of inhibition of reabsorption was not sufficient to prevent an increase in free-water clearance as a result of increased delivery of sodium to the site. 4. The findings support the concept that changes in circulating aldosterone can alter the renal excretion of sodium in man by affecting its reabsorption in the proximal tubule as well as in the distal tubule.

Urinary hydroxyproline in infants with and without fractures/rickets

1990 ◽  
Vol 36 (4) ◽  
pp. 642-644 ◽  
Author(s):  
W W Koo ◽  
S K Krug Wispe ◽  
P Succop ◽  
A Champlin ◽  
R Sherman ◽  
...  
Keyword(s):  
Low Birthweight ◽  
Urinary Hydroxyproline ◽  
Vlbw Infants ◽  
Molar Ratios ◽  
Wide Range ◽  
Group A ◽  
Renal Tubular ◽  
Group B ◽  
Urinary Peptide ◽  
Range Of Values

Abstract Molar ratios of peptide-bound and free hydroxyproline:creatinine (OHPr:Cr) in urine were measured at 3, 6, 9, and 12 months of age in two groups of very-low-birthweight (VLBW less than or equal to 1500 g) infants. Group A (15 infants) had radiographically confirmed fractures and (or) rickets (F/R); Group B (17 infants) did not. The urinary peptide-bound OHPr:Cr ratio varied widely within groups and was greatest at three months in both groups: A = 0.81 +/- 0.45 and B = 0.55 +/- 0.32 (mean +/- SD). The ratio decreased with increasing postnatal age for each group but was not statistically different between groups throughout the study. The urinary free OHPr:Cr ratio also was greatest at age three months (A = 0.32 +/- 0.15 and B = 0.53 +/- 0.46), rapidly decreasing afterwards, and was not statistically different between groups throughout the study. We conclude that, in VLBW infants, bone turnover as indicated by the urinary peptide-bound OHPr:Cr ratio is highest during early infancy; however, the wide range of values for this ratio suggests that its use alone is not sufficient for detection of F/R in VLBW infants. The rapid decrease in free OHPr:Cr ratio is presumably related to the maturation of renal tubular function.

Alpha 2-adrenoceptors and sodium reabsorption in the isolated perfused rat kidney

1984 ◽  
Vol 247 (4) ◽  
pp. F680-F685 ◽  
Author(s):  
D. D. Smyth ◽  
S. Umemura ◽  
W. A. Pettinger
Keyword(s):  
Adenylate Cyclase ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Blocking Agent ◽  
Sodium Reabsorption ◽  
Sodium Retention ◽  
Sympathoadrenal System ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney

Alpha 2-Adrenoceptors are known to inhibit adenylate cyclase in a number of tissues, but their function in the kidney is unknown. Adenylate cyclase and sodium excretion were stimulated with furosemide (30 microM) in the rat kidney perfused with Krebs-Henseleit solution (albumin 6.5 g/100 ml, 36 degrees C). beta-Adrenoceptors and alpha 1-adrenoceptors were blocked by propranolol (100 nM) and prazosin (30 nM) in the perfusate. Urinary cAMP and sodium excretion increased with furosemide. Activation of alpha 2-adrenoceptors with epinephrine (28 nM) caused no change in perfusion pressure or flow but decreased urinary cAMP and sodium excretion. These effects of epinephrine were reversed by the alpha 2-selective adrenoceptor blocking agent yohimbine (300 nM). Thus, in the setting of furosemide-stimulated sodium excretion and an associated elevation of adenylate cyclase, alpha 2-adrenoceptor stimulation resulted in sodium retention and inhibition of adenylate cyclase. By this receptor mechanism the sympathoadrenal system may contribute to retention of sodium.

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