Cardiac Secretion and Renal Clearance of Atrial Natriuretic Peptide in Normal Man: Effect of Salt Restriction

1989 ◽  
Vol 77 (6) ◽  
pp. 605-610 ◽  
Author(s):  
Krishnankutty Sudhir ◽  
Peter Friberg ◽  
Ian T. Meredith ◽  
Robyn L. Woods ◽  
Murray D. Esler ◽  
...  

1. Previous studies of endogenous atrial natriuretic peptide (ANP) in humans have examined changes in plasma levels, rather than regional secretion and clearance of the peptide. Using arterial and selective venous catheterization and sampling, and measurement of regional organ flow, we measured haemodynamics, cardiac secretion of ANP and renal clearance of ANP in six healthy volunteers at rest, on a normal sodium diet 2. Salt restriction decreases plasma concentrations of ANP. We assessed the contribution of the heart and kidney to this decrease, by measuring cardiac secretion and renal clearance of ANP at the termination of a low salt diet 3. Twenty-four hour urinary sodium excretion fell on the low salt diet from 163 to 29 mmol/day [standard error of the difference (sed) ± 14, P < 0.001]. Body weight decreased on salt restriction from 76.4 to 75.4 kg (sed ± 0.33, P < 0.05). Brachial mean arterial pressure fell by 6% (P < 0.05), but right atrial pressure was unchanged. Renal vein plasma renin activity increased by 56% with sodium restriction (P < 0.01), whereas arterial ANP concentrations fell by 39% (P < 0.05) 4. Coronary sinus ANP levels fell from 417 to 268 pg/ml (sed ± 74, P < 0.05), whereas renal vein concentrations were unaltered. There was a 47% decrease in cardiac secretion of ANP in the low salt state (P < 0.05). Net extraction of ANP across the kidney (about two-thirds) and renal clearance of ANP were unchanged on the low salt diet. Thus decreased plasma ANP with sodium restriction is due to reduced cardiac secretion.

1988 ◽  
Vol 74 (6) ◽  
pp. 659-663 ◽  
Author(s):  
G. P. Hodsman ◽  
R. W. Harrison ◽  
E. Sumithran ◽  
C. I. Johnston

1. The relationship between plasma atrial natriuretic peptide (ANP) and body sodium was determined in rats 1 month after myocardial infarction induced by coronary artery ligation. After operation rats received a normal or a low salt diet, and total exchangeable body sodium was measured sequentially. 2. Rats with infarction receiving a normal salt intake did not retain sodium when compared with sham-operated controls. Rats receiving a low salt diet had a 10% decrease in body sodium (P < 0.01). The decrease was the same in rats with infarction as in controls. 3. Plasma ANP was similar in control rats irrespective of salt status. Plasma ANP levels were markedly elevated in rats with infarction irrespective of salt status (P < 0.01). 4. The rise in plasma ANP was correlated with cardiac hypertrophy and infarct size in animals fed both normal and low salt diets. However, there was no relationship between plasma ANP and exchangeable body sodium. 5. These results suggest that in this model of heart failure plasma ANP is raised by increased left atrial stretch in proportion to the severity of left ventricular dysfunction. In contrast, plasma ANP concentrations do not appear to be elevated as a consequence of increased right atrial pressure caused by sodium retention and expanded extracellular volume.


1987 ◽  
Vol 72 (2) ◽  
pp. 201-208 ◽  
Author(s):  
L. R. Solomon ◽  
J. C. Atherton ◽  
H. Bobinski ◽  
R. Green

1. The effect of changes of dietary sodium chloride intake and posture on plasma atrial natriuretic peptide concentration and renal function was studied in 11 normal human volunteers. 2. Plasma atrial natriuretic peptide concentration was higher in the upright posture on a high than it was on a medium or low salt diet. On the medium and high but not on the low salt diet the concentration increased significantly on adoption of the supine posture. 3. Creatinine, sodium, lithium and fractional lithium clearances, fractional distal sodium excretion and total distal water and sodium reabsorption, which were estimated by the lithium clearance technique, were significantly higher on the high than on the low salt diet. The medium salt intake gave intermediate values. 4. Heart rate while upright was significantly higher on the low than on either the medium or the high salt diets. Systolic blood pressure was unaffected by salt intake. Diastolic blood pressure in the supine position was significantly higher on the low than on the medium or high salt diets. 5. Both plasma noradrenaline concentrations and plasma renin activity were significantly higher on the low than on the high salt diet. Values on the medium salt intake were intermediate. Plasma concentrations of both hormones were higher in the upright than in the supine posture on all three salt intakes. 6. The data are consistent with the hypothesis that atrial natriuretic peptide contributes to the cardiovascular and renal adjustments to changes in dietary sodium chloride, and the possible role of the peptide is discussed.


1988 ◽  
Vol 255 (6) ◽  
pp. E934-E941
Author(s):  
R. L. Woods

To quantify the role of the kidney in whole body metabolic clearance rate (MCR) from plasma of atrial natriuretic peptide (ANP), synthetic alpha-human ANP-(1-28) was infused at 200 ng/min to steady-state conditions in chronically instrumented one-kidney conscious dogs. Clearances were measured in dogs with a normally filtering kidney and they were also measured after the glomerular filtration rate (GFR) was reduced to close to zero by acutely inflating a cuff around the renal artery (RAC), which resulted in minimal urine production and renal blood flow reduction to 59% of the resting level. In normal dogs, MCR was 1,090 +/- 134 ml/min with renal clearance rate (RCR) contributing only 13.9%. After RAC, MCR fell to 864 +/- 151 ml/min, due in part to a fall in RCR (-41.5 +/- 12.9 ml/min), but mostly due to a fall in "rest of the body" (total renal) clearance of ANP. The reduced GFR accounted for virtually all the fall in RCR. Normal plasma ANP half-life was 59.6 +/- 7.9 s. In conclusion, MCR of ANP was very high, approaching the cardiac output, suggesting that most of ANP is cleared in one circulation through peripheral tissues. GFR contributed significantly to RCR (approximately 30%) but the contribution of the kidney to whole body MCR was small relative to rest of the body clearance of ANP.


1988 ◽  
Vol 254 (2) ◽  
pp. R161-R169 ◽  
Author(s):  
P. Bie ◽  
B. C. Wang ◽  
R. J. Leadley ◽  
K. L. Goetz

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.


1989 ◽  
Vol 256 (3) ◽  
pp. H760-H765 ◽  
Author(s):  
R. W. Lee ◽  
S. Goldman

To examine the mechanism by which atrial natriuretic peptide (ANP) decreases cardiac output, we studied changes in the heart, peripheral circulation, and blood flow distribution in eight dogs. ANP was given as a bolus (3.0 micrograms/kg) followed by an infusion of 0.3 microgram.kg-1.min-1. ANP did not change heart rate, total peripheral vascular resistance, and the first derivative of left ventricular pressure but decreased mean aortic pressure from 91 +/- 4 to 76 +/- 3 mmHg (P less than 0.001) and cardiac output from 153 +/- 15 to 130 +/- 9 ml.kg-1.min-1 (P less than 0.02). Right atrial pressure and left ventricular end-diastolic pressure also decreased. Mean circulatory filling pressure decreased from 7.1 +/- 0.3 to 6.0 +/- 0.3 mmHg (P less than 0.001), but venous compliance and unstressed vascular volume did not change. Resistance to venous return increased from 0.056 +/- 0.008 to 0.063 +/- 0.010 mmHg.ml-1.kg.min (P less than 0.05). Arterial compliance increased from 0.060 +/- 0.003 to 0.072 +/- 0.004 ml.mmHg-1.kg-1 (P less than 0.02). Total blood volume and central blood volume decreased from 82.2 +/- 3.1 to 76.2 +/- 4.6 and from 19.8 +/- 0.8 to 17.6 +/- 0.6 ml/kg (P less than 0.02), respectively. Blood flow increased to the kidneys. We conclude that ANP decreases cardiac output by decreasing total blood volume. This results in a lower operating pressure and volume in the venous capacitance system with no significant venodilating effects. Cardiac factors and a redistribution of flow to the splanchnic organs are not important mechanisms to explain the decrease in cardiac output with ANP.


PEDIATRICS ◽  
1988 ◽  
Vol 82 (4) ◽  
pp. 639-643
Author(s):  
Suguru Matsuoka ◽  
Yoshihide Kurahashi ◽  
Yohko Miki ◽  
Masuhide Miyao ◽  
Yasuhiro Yamazaki ◽  
...  

The plasma level of human α-atrial natriuretic peptide was measured in healthy children and patients, 1 month to 15 years of age, with congenital heart diseases. Significant increases were found in patients with a ventricular septal defect, tricuspid valve atresia, patent ductus arteriosus, and atrial septal defect but not in those with pulmonary valve stenosis or tetralogy of Fallot. The levels were significantly higher in children with ventricular septal defects (221 ± 123 pg/mL) or patent ductus arteriosus (124 ± 38 pg/mL) than in those with atrial septal defects (65 ± 42 pg/mL) (P &lt; .01). The increased levels appeared to be correlated with enlargement of the left atrium (r = .85, P &lt; .01) but not with the right atrial size or the mean right atrial pressure. They were higher in younger than in older healthy infants, but this age difference did not affect the results. These findings indicate that human α-atrial natriuretic peptide is released into the circulation in response to chronic atrial expansion in patients with congenital heart disease and may have an important role in volume homeostasis.


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