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.

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.

Atrial natriuretic peptide response to rapid atrial pacing in cardiac-denervated dogs

1989 ◽  
Vol 257 (1) ◽  
pp. R162-R167 ◽  
Author(s):  
T. D. Williams ◽  
K. P. Walsh ◽  
R. Canepa-Anson ◽  
M. I. Noble ◽  
A. J. Drake-Holland ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Flow Rate ◽  
Free Water ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Cardiac Denervation ◽  
Atrial Natriuretic

The effects of rapid atrial pacing on central hemodynamics, plasma hormones, and renal function were investigated in eight control and nine cardiac-denervated dogs under chloralose anesthesia. Pacing at approximately 250 ppm for 60 min caused similar increases in pulmonary wedge and right atrial pressures, systemic vascular resistance, and plasma atrial natriuretic peptide (ANP) in both groups. In control dogs, pacing produced a fall in both plasma vasopressin (AVP) and plasma renin activity (PRA) and a rise in urine flow rate associated with an increase in free water but not sodium clearance. In contrast, in cardiac-denervated dogs, both plasma AVP and PRA increased during pacing; urine flow rate did not change, and marked sodium retention occurred. This study supports the concept that the increase in urine flow during rapid atrial pacing is mediated by inhibition of renin and AVP secretion through intact cardiac nerves. The secretion of ANP is unaffected by cardiac denervation. The natriuretic and vasodilator actions of high plasma ANP concentrations during rapid atrial pacing can be inhibited either by neurally mediated cardiorenal effects in normal animals or by stimulation of the renin-angiotensin system after cardiac denervation.

Role of atrial natriuretic peptide in volume-expansion natriuresis

1986 ◽  
Vol 251 (2) ◽  
pp. R310-R313 ◽  
Author(s):  
T. R. Schwab ◽  
B. S. Edwards ◽  
D. M. Heublein ◽  
J. C. Burnett
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Urinary Sodium ◽  
Right Atrial ◽  
Fractional Excretion Of Sodium

Studies were performed to investigate the role of circulating atrial natriuretic peptide (ANP) in acute volume-expansion natriuresis. Sham-operated (SHAM, n = 6) and right atrial appendectomized (ATRX, n = 12) anesthetized rats underwent acute volume expansion with isoncotic albumin. After equilibration and control periods, volume expansion increased urine flow rate, urinary sodium excretion, fractional excretion of sodium, and circulating ANP. Absolute increases in urine flow rate (delta 46 +/- 4 SHAM; delta 25 +/- 5 microliter/min ATRX), urinary sodium excretion (delta 9.48 +/- 1.01 SHAM; delta 4.77 +/- 1.03 mueq/min ATRX), fractional excretion of sodium (delta 3.16 +/- 0.53 SHAM; delta 1.65 +/- 0.32% ATRX), and ANP (delta 303.3 +/- 35.9 SHAM; delta 156.6 +/- 26.0 pg/ml ATRX) were significantly reduced by right atrial appendectomy. No significant differences in mean arterial pressure, central venous pressure, or glomerular filtration rate during volume expansion were observed between groups. These studies support the hypothesis that right atrial appendectomy in the rat attenuates acute volume expansion-induced increases in circulating ANP and urinary sodium excretion and that the natriuresis of acute volume expansion is mediated in part by an increase in circulating ANP.

Hemodynamic and renal effects of low-dose infusions of atrial peptide in awake dogs

1988 ◽  
Vol 254 (2) ◽  
pp. R161-R169 ◽  
Author(s):  
P. Bie ◽  
B. C. Wang ◽  
R. J. Leadley ◽  
K. L. Goetz
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Urine Flow ◽  
Right Atrial ◽  
Experimental Protocols ◽  
Cardiac Filling ◽  
Left And Right ◽  
Atrial Natriuretic

The effects of alpha-human atrial natriuretic peptide (alpha-hANP) on cardiovascular and renal function in conscious dogs were evaluated in two experimental protocols. In one protocol, alpha-hANP was infused intravenously at increasing rates of 50, 100, and 200 ng.min-1.kg-1 (stepup infusion) during successive 20-min periods. The greatest responses occurred during the final 20-min period of the stepup infusion when the plasma concentration of immunoreactive atrial natriuretic peptide (irANP) was increased by 44-fold over preinfusion values; pressures in the aorta and both atria were decreased at this time, whereas glomerular filtration rate, urine flow, and sodium excretion were increased. In a second protocol, alpha-hANP was infused for 1 h at constant rates of either 12.5, 25, or 50 ng.min-1.kg-1; these constant infusions increased plasma irANP by 3-, 7-, and 12-fold, respectively. Each infusion rate decreased left and right atrial pressures and increased urine flow and sodium excretion. The two lowest infusion rates elevated plasma irANP to levels that would be expected to occur only during unusual physiological, or perhaps pathophysiological, conditions. The two highest infusion rates decreased plasma renin activity. Nevertheless, the accompanying maximal increases in sodium excretion were modest (41-72%). These data imply that small changes in circulating atrial peptides that presumably occur under normal physiological conditions would not have a dominant effect on the regulation of sodium excretion; the peptides may, however, play a modulatory role on sodium excretion under these conditions. It remains to be determined whether the ability of atrial peptides to lower cardiac filling pressures is of physiological significance.

Increased renal atrial natriuretic peptide synthesis in rats with deoxycorticosterone acetate-salt treatment

1996 ◽  
Vol 271 (4) ◽  
pp. F779-F789 ◽  
Author(s):  
Y. J. Lee ◽  
S. J. Shin ◽  
M. S. Tan ◽  
T. J. Hsieh ◽  
J. H. Tsai
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Excretion Rate ◽  
Rat Kidney ◽  
Urinary Sodium Excretion ◽  
Treated Group ◽  
Urinary Sodium ◽  
Deoxycorticosterone Acetate ◽  
Low Salt

To investigate the role of renal synthesis of atrial natriuretic peptide (ANP) as a contributor to the water-sodium homeostasis, we studied the effects of electrolyte-water imbalance on renal ANP mRNA levels, plasma ANP concentrations, and urinary ANP excretion rates by using reverse transcription-polymerase chain reaction (PCR) and radioimmunoassay. Male Wistar rates divided into the following three groups: 1) the control group, 2) deoxycorticosterone acetate (DOCA)-salt-treated group, and 3) low-salt-treated group. The urinary sodium excretion rate and urine volume in the DOCA-salt rats were significantly elevated at 2 days and for the 10-day study. The urinary ANP excretion rate in DOCA-salt rats was significantly increased at 2 days after treatment and was well correlated to the urinary sodium excretion rate (r = 0.76, P < 0.01). Plasma ANP levels in the DOCA-salt rats were elevated on the day of death. In contrast, plasma renin activities were markedly suppressed in DOCA-salt rats and increased in low-salt rats. By immunohistochemical study, immunoreactive ANP materials were mainly localized in the proximal and distal cortical tubules of the kidney. With the PCR cloning and sequencing technique, ANP cDNA was cloned from the rat kidney, and the sequences were identical to that of ANP identified in the atria. By semiquantitative PCR technique, the expression of ANP mRNA in the ventricle and renal cortex tissues was significantly enhanced in the DOCA-salt rats. Our results confirm that the rat kidney is a site of ANP synthesis and indicate that renal ANP synthesis is enhanced in a volume-expansion state. We propose that renal synthesized natriuretic peptide participates in the intrarenal regulation of water-electrolyte homeostasis and may contribute to renal adaptation during the mineralocorticoid escape phenomenon.

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.

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.

Sign in / Sign up

Export Citation Format

Share Document