Urine Reinfusion Diuresis and Natriuresis in Rats: Role of Water, Electrolytes and Urea

1979 ◽  
Vol 57 (2) ◽  
pp. 187-193
Author(s):  
R. A. Norman ◽  
T. G. Coleman ◽  
P. R. Kastner
Keyword(s):  
Flow Rate ◽  
Sodium Excretion ◽  
Infusion Rate ◽  
Ringer Solution ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Urinary Volume ◽  
Natriuretic Factors

1. The purpose of this study was to determine the role of reinfused water, electrolytes and urea in the diuresis and natriuresis of urine reinfusion. 2. Three groups of rats underwent 5 h of urine reinfusion. The first group served as a control, and during urine reinfusion the urinary volume and sodium excretion increased to 10 or 12 times control values. 3. In a second group, urine reinfusion was followed by 2 h of infusion of Ringer solution at a rate equal to the urine flow rate; 71% of the diuresis and 75% of the natriuresis resulting from urine reinfusion were maintained. 4. In a third group, urine reinfusion was followed by infusion of Ringer solution with urea added. The infusion rate was equal to urine flow rate and the concentration of urea was equal to that in the urine; 98% of the diuresis and 102% of the natriuresis were maintained. 5. These results indicate that the majority of urine-reinfusion diuresis and natriuresis is due to reinfused volume and electrolytes, and the remainder, in these experiments at least, could be explained by the reinfused urea. Therefore there was no need to postulate additional urinary natriuretic factors to explain the results of urine reinfusion.

Blunted natriuresis to atrial natriuretic peptide in chronic sodium-retaining disorders

1987 ◽  
Vol 252 (5) ◽  
pp. F865-F871 ◽  
Author(s):  
J. P. Koepke ◽  
G. F. DiBona
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Atrial Natriuretic

Renal responses to atrial natriuretic peptide were examined in conscious dogs with congestive heart failure (tricuspid insufficiency) and in conscious rats with nephrotic syndrome (adriamycin). Heart-failure dogs displayed elevated atrial pressure and heart weights, blunted natriuresis to a saline load, and ascites. Nephrotic rats displayed proteinuria, hypoproteinemia, sodium retention, and ascites. In control animals, atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion. Although atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion in conscious heart-failure dogs and nephrotic rats, the responses were markedly blunted. In heart-failure dogs, infusion of atrial natriuretic peptide increased plasma concentrations of norepinephrine and epinephrine. In nephrotic rats, renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide. Mean arterial pressure, glomerular filtration rate, and p-aminohippurate clearance were affected similarly by atrial natriuretic peptide in heart-failure dogs or nephrotic rats vs. control animals. Conscious congestive heart-failure dogs and conscious nephrotic rats have blunted diuretic and natriuretic responses to atrial natriuretic peptide.

Excretion of endogenous digoxin-like immunoreactive factors in human urine is a function of urine flow rate.

1988 ◽  
Vol 34 (5) ◽  
pp. 960-964 ◽  
Author(s):  
B A Siegfried ◽  
R Valdes
Keyword(s):  
Urinary Excretion ◽  
Flow Rate ◽  
Human Urine ◽  
Sodium Excretion ◽  
Salt Intake ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Healthy Humans

Abstract We studied the effect of varying water and salt intake on the renal excretion of endogenous digoxin-like immunoreactive factors (DLIF). DLIF were measured in human urine and serum by competitive displacement of 125I-labeled digoxin from anti-digoxin antibodies. Diuresis was selectively induced in normal healthy humans by acute water ingestion, and natriuresis was preferentially induced by acute saline ingestion. We found the amount of endogenous immunoreactivity excreted in urine to be correlated with urine flow rate but not with urinary sodium excretion. Urinary excretion of DLIF, normalized to creatinine, was 3.6-fold greater at a urine flow rate of 5.5 mL/min than at 0.5 mL/min. On the other hand, saline intake increased urine flow rate 1.9-fold and increased sodium excretion threefold, but did not affect urinary excretion of DLIF. Fractional excretion of DLIF was linearly related to fractional excretion of water. This study demonstrates that normalization of DLIF values to urinary creatinine does not make DLIF excretion independent of urine flow rate and underscores the need for information on urine flow rate when DLIF measurements in urine are being interpreted.

Natriuretic and diuretic effects of infusion of atrial natriuretic factor in conscious dogs

1989 ◽  
Vol 257 (4) ◽  
pp. F565-F573
Author(s):  
J. Ohanian ◽  
M. A. Young ◽  
Y. T. Shen ◽  
R. Gaivin ◽  
S. F. Vatner ◽  
...  
Keyword(s):  
Amino Acid ◽  
Arterial Pressure ◽  
Flow Rate ◽  
Plasma Levels ◽  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Conscious Dogs ◽  
Natriuretic Factor

We studied the effects of 30-min infusions of the synthetic 25-amino acid atrial natriuretic factor [ANF-(102-126)] and the 28-amino acid ANF-(99-126) at 0.1 and 0.3 micrograms.kg-1.min-1 on urine flow rate, sodium excretion, and arterial pressure in conscious dogs. Each dose was administered on a separate day following a 1-h stabilization period. We also compared the effects of 60-min infusions of ANF, 0.01 micrograms.kg-1.min-1, or water infusion on separate days in conscious dogs. Arterial pressure was reduced in a dose-dependent fashion, reaching statistical significance at a dose of 0.3 micrograms.kg-1.min-1. During the 0.01-micrograms.kg-1.min-1 infusion, the plasma concentration of ANF rose approximately threefold (from 68 +/- 7 to 207 +/- 14 pg/ml), with no change in urine flow rate, sodium excretion, or arterial pressure. At a dose of 0.1 micrograms.kg-1.min-1, urine flow increased (P less than 0.05) by 0.41 +/- 0.15 ml/min, and sodium excretion rose by 72 +/- 24 mu eq/min, but not significantly, whereas plasma ANF levels rose to 1,236 +/- 229 pg/ml. At the highest dose of ANF (0.3 micrograms.kg-1.min-1) urine flow rose by 0.62 +/- 0.16 ml/min, P less than 0.05, and sodium excretion rose by 139 +/- 30 mu eq/min, P less than 0.05, whereas plasma levels of ANF rose to 2,436 +/- 320 pg/ml. In contrast, volume loading with dextran increased urine flow by 3.5 +/- 1.3 ml/min, P less than 0.05, and sodium excretion by 439 +/- 147 mu eq/min, P less than 0.05, whereas ANF rose to only 320 +/- 69 pg/ml. These results suggest that, in the conscious dog, ANF does not cause significant diuretic or natriuretic effects until plasma levels are markedly above those observed in physiological conditions. A possible explanation for the difference between this and previous studies is that the renal effects of ANF, at physiological plasma levels, are indirect and thus dependent on autonomic and hormonal (angiotensin, vasopressin, and aldosterone levels) factors governing the renal function of the animal.

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.

Atrial natriuretic peptide, right atrial pressure, and sodium excretion rate in the rat

1987 ◽  
Vol 253 (5) ◽  
pp. F969-F975 ◽  
Author(s):  
T. A. Fried ◽  
M. A. Ayon ◽  
G. McDonald ◽  
A. Lau ◽  
T. Inagami ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Excretion Rate ◽  
Balloon Catheter ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Right Atrial

This study examined the relationship between right atrial pressure (RAP), urine flow rate, sodium excretion rate, and plasma atrial natriuretic peptide (ANP) levels after an acute Ringer expansion. Two groups of rats had their RAP monitored and balloon catheters placed in their thoracic inferior venae cavae. In one group the balloon remained deflated, and in the second group the balloon was inflated during the volume expansion in an attempt to prevent the rise in RAP. The peak RAP was 7.3 +/- 0.8 mmHg when the balloon remained deflated and 3.5 +/- 0.6 mmHg in the group with the balloon catheter inflated (P less than 0.005). The corresponding peak ANP levels were 682 +/- 140 and 223 +/- 40 pg/ml. There was a significant correlation between the peak RAP and ANP levels (r = 0.754; P less than 0.05). The inflation of the balloon catheter significantly decreased the urine flow rate and the urine sodium excretion rate. A final group of animals had 200 microliters of rabbit serum containing antibody to ANP infused before the volume expansion. The antibody-treated animals had significantly lower urine flow and sodium excretion rates than nonantibody-treated control rats. We conclude that ANP is one of the factors which allows the rat to excrete an acute Ringer expansion.

The Role of Prostaglandins in Glucagon-Induced Natriuresis

1980 ◽  
Vol 58 (5) ◽  
pp. 393-401 ◽  
Author(s):  
M. A. Kirschenbaum ◽  
E. T. Zawada
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Prostaglandin E ◽  
Excretion Rates

1. Three groups of anaesthetized dogs were studied to determine the role of renal prostaglandins in glucagon-induced natriuresis. 2. Urine flow, sodium and prostaglandin E excretion rates increased significantly in the experimental kidney with glucagon infusion (0.20 μg/min) into the renal artery. These changes were completely reversed after the administration of either of two inhibitors of prostaglandin synthesis. 3. Infusion of glucagon (0.20 μg/min) after the administration of either of the prostaglandin synthetase inhibitors failed to increase either urine flow rate or sodium excretion above control values and failed to elevate urine prostaglandin E excretion rates. 4. Infusion of glucagon (0.75–1.25 μg/min) resulted in significant elevations in urine flow rate, glomerular filtration rate, renal plasma flow, urine sodium and prostaglandin E excretion rates. 5. The data presented indicate that the diuresis and natriuresis seen with the infusion of glucagon (0.20 μg/min) are accompanied by an increase in urine prostaglandin E excretion and are reversed by the administration of inhibitors of prostaglandin synthesis, suggesting that the increased urine flow and sodium excretion rates are dependent on prostaglandin-mediated mechanisms. The administration of glucagon in higher doses appears to be associated with alterations in electrolyte excretion and glomerular filtration rate, which presumably is related to factors other than prostaglandin synthesis and release.

Influence of serotonergic mechanisms on the urine flow rate in male rats

2014 ◽  
Vol 307 (10) ◽  
pp. R1239-R1250 ◽  
Author(s):  
Wen-Jia Fan ◽  
Shih-Ching Chen ◽  
Tsung-Hsun Hsieh ◽  
Chien-Hung Lai ◽  
You Shuei Lin ◽  
...  
Keyword(s):  
Flow Rate ◽  
Silent Period ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Male Rats ◽  
External Urethral Sphincter ◽  
Voiding Function ◽  
Pressure Threshold ◽  
Burst Period

This study extensively examined the role of a 5-HT1A receptor in controlling voiding function in anesthetized male rats. A simultaneous recording of the intravesical pressure (IVP), external urethral sphincter (EUS)-electromyography (EMG), and urine flow rate (UFR) during continuous cystometry was used. 8-Hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), a 5-HT1A receptor agonist, significantly improved the voiding efficiency, as detected by increases in the evoked contraction amplitude, EUS burst period, and silent period, and decreases in the volume threshold, pressure threshold, and residual volume. Interestingly, the UFR during voiding was reduced by 8-OH-DPAT, as evidenced by decreases in the maximal UFR and mean UFRs of the voiding period, spike duration, and interspike interval. Conversely, treating rats with WAY-100635, a 5-HT1A antagonist, produced effects opposite to those produced by 8-OH-DPAT. These findings suggest that 8-OH-DPAT improved the voiding efficiency by enhancing the detrusor contractile ability and prolonging EUS burst period, which would compensate for the lower UFR, resulting from urethral smooth muscle contractions and longer EUS silent periods during voiding. The present study contributes to our understanding of the role of 5-HT1A receptors in controlling the urine flow rate in male rats.

Renorenal reflex responses to mechano- and chemoreceptor stimulation in the dog and rat

1984 ◽  
Vol 246 (1) ◽  
pp. F67-F77 ◽  
Author(s):  
U. C. Kopp ◽  
L. A. Olson ◽  
G. F. DiBona
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Renal Blood Flow ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Urine Flow Rate

The renal functional effects of renal mechano- (MR) and chemoreceptor (CR) stimulation were examined in dogs and rats. In dogs increasing ureteral pressure (increases UP) increased ipsilateral (ipsi) renal blood flow and renin secretion rate, decreased contralateral (contra) renal blood flow, but did not affect contra renal excretion or renin secretion rate. Increasing renal venous pressure (increases RVP) increased ipsi renin secretion rate but did not affect contra renal function. Retrograde ureteropelvic perfusion with 0.9 M NaCl at unchanged UP did not affect either ipsi or contra renal function. In rats,increases UP and retrograde ureteropelvic perfusion with 0.9 M NaCl at unchanged UP did not affect mean arterial pressure, heart rate, contra renal blood flow, or glomerular filtration rate but increased contra urine flow rate and urinary sodium excretion. Increasing ureteral pressure with 0.1 M NaCl increased contra urine flow rate and urinary sodium excretion, whereas retrograde ureteropelvic perfusion with 0.1 M NaCl was without effect. Thus increases UP and retrograde ureteropelvic perfusion with 0.9 M NaCl stimulated renal MR and CR, respectively. The contra diuretic and natriuretic responses to renal MR and CR stimulation were abolished by either ipsi or contra renal denervation. Renal MR and CR stimulation increased ipsi afferent renal nerve activity (RNA) and decreased contra efferent RNA. These results indicate that in dogs renal MR stimulation results in a modest contralateral excitatory renorenal reflex, whereas in rats renal MR and CR stimulation produce a contralateral inhibitory renorenal reflex.

Prostaglandin-dependent polyuria in hypercalcemia

1981 ◽  
Vol 241 (3) ◽  
pp. F224-F230 ◽  
Author(s):  
E. R. Serros ◽  
M. A. Kirschenbaum
Keyword(s):  
Flow Rate ◽  
Plasma Osmolality ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Prostaglandin E ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Final Group ◽  
Thirst Mechanism

The present experiments examined the role of prostaglandin biosynthesis in the increase in urine flow rate seen in rats with hypercalcemia induced by the administration of 1,25-dihydroxycholecalciferol. In a first group, rats receiving the vitamin D metabolite developed hypercalcemia, polyuria, and increased urine prostaglandin E excretion. Indomethacin resulted in a fall in urine prostaglandin E excretion. A second group was fluid restricted to ascertain whether increased thirst could be an etiologic mechanism of the polyuria. This resulted in a trivial fall in urine flow rate despite a fall in body weight and a rise in both urine and plasma osmolality. In a final group, prostaglandin inhibition restored the vasopressin sensitivity of the hypercalcemic kidney. Accordingly, the polyuria seen in hypercalcemic rats after the administration of 1,25-dihydroxycholecalciferol is associated with an increase in urine prostaglandin E excretion and can be reversed by inhibition of prostaglandin synthesis. In addition, this polyuria can occur independent of the thirst mechanism. Finally, there is evidence that the vasopressin resistance of the hypercalcemic kidney could be reversed by prostaglandin inhibition.

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