Atrial natriuretic peptide and total exchangeable body sodium: Relationships in rats with chronic myocardial infarction

1988 ◽  
Vol 74 (6) ◽  
pp. 659-663 ◽  
Author(s):  
G. P. Hodsman ◽  
R. W. Harrison ◽  
E. Sumithran ◽  
C. I. Johnston
Keyword(s):  
Myocardial Infarction ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Left Ventricular ◽  
Right Atrial ◽  
Coronary Artery Ligation ◽  
Salt Diet ◽  
Body Sodium ◽  
Low Salt ◽  
Atrial Natriuretic

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.

Atrial natriuretic peptide transcription, storage, and release in rats with myocardial infarction

1987 ◽  
Vol 253 (6) ◽  
pp. H1449-H1455 ◽  
Author(s):  
R. E. Mendez ◽  
J. M. Pfeffer ◽  
F. V. Ortola ◽  
K. D. Bloch ◽  
S. Anderson ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Atrial Natriuretic Peptide ◽  
Infarct Size ◽  
Natriuretic Peptide ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Mrna Levels ◽  
Atrial Natriuretic

To study the role of atrial natriuretic peptide (ANP) in chronic heart failure, ANP synthesis, storage, and release were examined by measuring atrial ANP messenger ribonucleic acid (mRNA) levels and atrial and plasma ANP concentrations in rats with myocardial infarction produced by coronary artery ligation. Three groups were defined as the following: 1) controls, sham-operated, or operated, but noninfarcted; 2) moderate infarcts, involving 5-30% of the left ventricular circumference; and 3) large infarcts (greater than or equal to 30%). In addition, to determine a possible modulation by dietary Na intake on ANP levels in heart failure, plasma immunoreactive ANP (iANP) levels were measured in rats with and without infarcts given low, regular, or high Na intake for 2 wk, by which time all groups were in neutral balance. Plasma iANP levels varied directly with increasing infarct and atrial sizes, irrespective of Na intake. In contrast, atrial ANP concentration varied inversely with increasing infarct size. The ANP mRNA content index, a measure of total atrial ANP mRNA, was significantly increased in rats with large infarcts compared with control rats. These results indicate that in rats with myocardial infarction, the severity of left ventricular dysfunction, as inferred from infarct size, but not chronic Na intake, is the primary determinant of the extent of activation of the ANP system. Elevated circulating ANP levels are maintained through enhanced atrial synthesis and release. ANP may thus play an important role in the hemodynamic and renal adaptations to chronic heart failure.

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 ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Renal Clearance ◽  
Natriuretic Peptide ◽  
Renal Vein ◽  
Right Atrial ◽  
Sodium Restriction ◽  
Salt Restriction ◽  
Salt Diet ◽  
Low Salt ◽  
Atrial Natriuretic

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.

Changes of atrial natriuretic peptide in brain areas of rats with chronic myocardial infarction

1996 ◽  
Vol 270 (1) ◽  
pp. H312-H316 ◽  
Author(s):  
K. Hu ◽  
P. Gaudron ◽  
U. Bahner ◽  
M. Palkovits ◽  
G. Ertl
Keyword(s):  
Myocardial Infarction ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Sham Operation ◽  
Plasma Parameters ◽  
Brain Areas ◽  
Atrial Natriuretic

We measured immunoreactive atrial natriuretic peptide (ANP) in 18 selected, microdissected brain areas. Rats were studied 8 wk after coronary ligation or sham operation or as nonoperated control animals. In separate animals, hemodynamic and plasma parameters were measured. Rats with myocardial infarction had marked elevated right atrial and left ventricular end-diastolic pressure (2.6 +/- 0.6 and 16.2 +/- 3.1 mmHg, respectively; n = 15) vs. sham-operated rats (1.3 +/- 1.0 and 5.5 +/- 1.2 mmHg, n = 14; P < 0.05) and depressed maximal rate of pressure development (9,613 +/- 980 vs. 15,600 +/- 2,027 mmHg/s; P < 0.05) but similar arterial pressure (126 +/- 4 vs. 124 +/- 3 mmHg; P > 0.05). After myocardial infarction (n = 10), plasma ANP, renin activity, and angiotensin (ANG) II were elevated (53.1 +/- 16.2 pg/ml, 10.7 +/- 2.5 ng ANG I ml-1 h-1, and 219.6 +/- 11.0 fmol/ml, respectively) vs. sham rats (12.0 +/- 2.2 pg/ml, 5.7 +/- 0.7 ng ANG I ml-1, h-1, and 142.9 +/- 9.4 fmol/ml; n = 10; P < 0.05), whereas vasopressin and aldosterone levels remained unchanged among groups. In rats with myocardial infarction, a substantial decrease of ANP was found in the medial preoptic nucleus, the supraoptic nucleus, the subfornical organ, the paraventricular nucleus, and the locus ceruleus. These nuclei are involved in electrolyte, and fluid homeostasis, blood pressure regulation, and modulation of neuroendocrine systems. The mechanism of this reduction and the consequences for systemic adaption or decompensation remain unclear. However, the data suggest that myocardial infarction and chronic left ventricular dysfunction may induce changes of a neurotransmitter in brain.

Atrial natriuretic peptide, B-type natriuretic peptide, and serum collagen markers after acute myocardial infarction

2004 ◽  
Vol 96 (4) ◽  
pp. 1306-1311 ◽  
Author(s):  
Jarkko Magga ◽  
Mikko Puhakka ◽  
Seppo Hietakorpi ◽  
Kari Punnonen ◽  
Paavo Uusimaa ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Type I Collagen ◽  
Left Ventricular ◽  
Type I ◽  
Amino Terminal ◽  
Collagen Markers ◽  
Atrial Natriuretic

Experimental data suggest that atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) act locally as antifibrotic factors in heart. We investigated the interrelationships of natriuretic peptides and collagen markers in 93 patients receiving thrombolytic treatment for their first acute myocardial infarction (AMI). Collagen formation following AMI, evaluated as serum levels of amino terminal propeptide of type III procollagen, correlated with NH2-terminal proANP ( r = 0.45, P < 0.001), BNP ( r = 0.55, P < 0.001) and NH2-terminal proBNP ( r = 0.50, P < 0.01) on day 4 after thrombolysis. Levels of intact amino terminal propeptide of type I procollagen decreased by 34% ( P < 0.001), and levels of carboxy terminal cross-linked telopeptide of type I collagen (ICTP) increased by 65% ( P < 0.001). ICTP levels correlated with NH2-terminal proBNP ( r = 0.25, P < 0.05) and BNP ( r = 0.28, P < 0.05) on day 4. Our results suggest that ANP and BNP may act as regulators of collagen scar formation and left ventricular remodeling after AMI in humans. Furthermore, degradation of type I collagen is increased after AMI and may be regulated by BNP.

Mechanism for decrease in cardiac output with atrial natriuretic peptide in dogs

1989 ◽  
Vol 256 (3) ◽  
pp. H760-H765 ◽  
Author(s):  
R. W. Lee ◽  
S. Goldman
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Left Ventricular ◽  
Right Atrial ◽  
Total Blood Volume ◽  
Total Blood ◽  
Atrial Natriuretic

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.

Bovine atrial natriuretic peptide in heart failure

1990 ◽  
Vol 124 (3) ◽  
pp. 463-467 ◽  
Author(s):  
N. Takemura ◽  
H. Koyama ◽  
T. Sako ◽  
K. Ando ◽  
S. Motoyoshi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Plasma Concentration ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Right Atrium ◽  
Left Ventricular ◽  
Atrial Pressure ◽  
Right Atrial ◽  
The Right ◽  
Atrial Natriuretic

ABSTRACT The present study describes the concentration and molecular form of atrial natriuretic peptide (ANP) in Holstein dairy cattle with mild (bacterial endocarditis; BEC) or severe (dilated cardiomyopathy; DCM) heart failure. Significant increases in plasma concentration of ANP were observed in cattle with DCM (73·3 ± 16·02 pmol/l, n=4, P<0·01) and BEC (20·6± 3·45 pmol/l, n=7, P<0·05), when compared with those in control cattle (14·5± 1·84 pmol/l, n= 12). The concentration of ANP in cattle with DCM was significantly (P<0·01) higher compared with that in cattle with BEC. Plasma concentration of ANP correlated significantly with right atrial pressure (r =0·95, P<0·01) and left ventricular end-diastolic pressure (r= 0·84, P<0·01). Gel-permeation chromatography of ANP in plasma and the right atrium from control and cattle with BEC revealed a single peak corresponding to the elution position of authentic human ANP(99–126) in plasma, and two peaks corresponding to those of authentic human ANP(99–126) and pro-ANP in the atrial extract. In cattle with DCM, however, peaks corresponding to the elution positions of authentic human β-ANP and/or pro-ANP were detected in addition to the peak corresponding to ANP(99–126). The content of ANP in the right atrium of cattle with DCM was significantly (P<0·05) increased compared with that in control cattle and those with BEC. The present study therefore suggests that the synthesis and secretion of ANP might be stimulated by atrial distention induced by increased atrial pressure. This suggestion is supported by the fact that the middle molecular weight form of ANP, possibly corresponding to human β-ANP, was detected in both the plasma and atria of the cattle with severe heart failure. Journal of Endocrinology (1990) 124, 463–467

scholarly journals Insufficient secretion of atrial natriuretic peptide at acute phase of myocardial infarction

2000 ◽  
Vol 89 (2) ◽  
pp. 458-464 ◽  
Author(s):  
Keiko Maeda ◽  
Takayoshi Tsutamoto ◽  
Atsuyuki Wada ◽  
Naoko Mabuchi ◽  
Masaru Hayashi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Acute Phase ◽  
Plasma Levels ◽  
Chronic Phase ◽  
Left Ventricular ◽  
Group 2 ◽  
Group 1 ◽  
Atrial Natriuretic

To investigate the secretion of the plasma levels of atrial natriuretic peptide (ANP) in patients with acute myocardial infarction (AMI), we evaluated the relationship between plasma levels of ANP and pulmonary capillary wedge pressure (PCWP) in 45 consecutive patients during the acute phase of AMI (∼12 h after the attack) ( group 1) and compared data with those obtained after 1 mo ( group 2). In both groups 1and 2, plasma ANP levels significantly correlated with PCWP. The slope of the linear regression line between the PCWP and ANP in group 1 was significantly lower, by about one-third, than that in group 2. In addition, we examined changes in ANP levels and left ventricular end-diastolic pressure (LVEDP) over 180 min after AMI induced by injection of microspheres into the left coronary arteries of three dogs. The LVEDP and ANP levels 30 min after AMI were significantly higher than those before; however, despite the persistent high LVEDP during the 180 min after AMI, ANP levels decreased gradually and significantly to 63% of the peak level at 150 min. These findings suggest that the secretion of ANP during the acute phase of myocardial infarction may be insufficient relative to the chronic phase.

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