Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diuretic and natriuretic effects of r-alpha-ANP (99-126) were investigated in rats with chronic ischaemic heart failure (IHF) produced by left coronary artery ligation. The plasma concentration of immunoreactive ANP (IrANP) was significantly higher, 91.8 +/- 16.0 pm in the IHF rats compared to 31.0 +/- 4.9 pm in sham-operated controls. In the control rats, ANP infusion (0.25-1.0 micrograms kg 1 mm 1) increased urine flow rate (V) and urinary sodium (UNa V) excretion. At the highest dose level, both V and UNa V were increased approximately fivefold. The diuresis and natriuresis seen in the control group after the infusion of ANP were blunted in the IHF rats. A bilateral surgical renal denervation in the IHF rats did not alter the renal dopamine levels, but induced a significant decrease in renal noradrenaline content, and almost completely restored the renal responsiveness to the ANP infusions. We conclude that renal denervation reversed the blunted renal excretory response to ANP in IHF rats. Thus, in experimental IHF, there seems to be a functional antagonism between efferent renal sympathetic nerve activity and ANP.
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PMID:Renal interaction between sympathetic activity and ANP in rats with chronic ischaemic heart failure. 252 11

The nature of plasma cardiodilatin, the amino-terminal product of the human pro-atrial natriuretic peptide, was investigated by two separate radioimmunoassays directed against the N-terminal and the putative C-terminal of the cardiodilatin molecule: ANP-[Asn1-Lys16] and ANP-[Lys87-Arg98], respectively. Serial dilutions of normal and cardiac failure plasma exhibited parallelism with the synthetic peptide standard curves in both assays. The concentrations of N- and C-terminal cardiodilatin-immunoreactivity equivalents (-IE) were significantly higher in cardiac failure patients. N-terminal-IE: 912 +/- 87, normal subjects 129 +/- 13 (mean +/- SEM); C-terminal-IE: 7979 +/- 1784, normal subjects 895 +/- 213 (both p less than 0.001). Although the concentrations determined by the two assays were not identical, significant correlations were found between them in both normal subjects (r = .69, p less than 0.001) and cardiac failure patients (r = .72, p less than 0.01). Characterisation by gel permeation and fast protein liquid chromatography demonstrated coelution of the N- and C-terminal cardiodilatin immunoreactivities in a single chromatographic peak. These results suggest that the circulating cardiodilatin in normal subjects and patients with cardiac failure contains the entire prohormone amino-terminal sequence ANP-[Asn1-Arg98].
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PMID:Pro-atrial natriuretic peptide (1-98): the circulating cardiodilatin in man. 252 25

We have established an easily reversible acute heart failure model in beagle canines by reversible aortic or mitral regurgitation (AR or MR). To cause reversible AR, a basket catheter was inserted into the left ventricle from the apex and fixed at the aortic valve in 10 canines. To cause MR, a basket catheter was inserted into the left atrium via the pulmonary vein and fixed at the mitral valve in 10 canines. The regurgitation by AR or MR was caused by extending the tip basket wire, and the recovery from the regurgitation was immediately possible by closing it. Left atrial pressure (LAP), right atrial pressure (RAP) and pulmonary artery pressure (PAP) were increased significantly during AR or MR, and decreased to the normal level after the release of AR or MR. Using these reversible acute heart failure models, the effects of both advancing and restoring acute heart failure by the secretion of ANP were examined by observing the changes of ANP concentration and its molecular forms in the plasma and left atrial tissue in the same canine. Plasma ANP concentration showed a reversible change. In group analysis, plasma ANP concentration did not correlate with LAP or RAP, but in each canine it showed high correlations with LAP (r = 0.70 approximately 0.94, 0.82 +/- 0.07) and RAP (r = 0.60 approximately 0.93, 0.79 +/- 0.08), having a different slope in each regression line. The ANP concentration in the atrial tissue was decreased during AR or MR, but the low level was maintained after AR or MR. The main molecular form of ANP in the plasma was alpha-ANP and that in the tissue was gamma-ANP. In summary, the tissue storage of ANP was decreased because the ANP secretion caused by stimulation of acute heart failure exceeded its production. The ANP secretion was decreased by the subsequent elimination of heart failure, but the production was not stimulated rapidly, because the tissue content remained unchanged.
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PMID:[The concentration of atrial natriuretic peptide (ANP) in plasma and atrial tissue of canines with acute heart failure induced by reversible aortic or mitral regurgitation]. 253 Jan 21

An age-related dependence of plasma ANP levels was studied in 163 healthy children (94 boys, 69 girls) between the ages of day 1 and 16 yr. In neonates during the first 2-4 days of life, significantly higher plasma ANP plasma levels (range 129-356 pg/ml, mean 227) were found compared with older infants and children (p less than 0.001). Beyond the neonatal period through adolescence no significant difference in ANP concentrations could be found between the various age groups. Plasma ANP levels ranged between 2 and 109 pg/ml (mean 47) for all age groups after the newborn period. ANP levels were also determined in 15 adult volunteers and in arterial and venous cord blood of 16 healthy newborns, and concentrations were similar to those found in children. In addition, plasma ANP levels were measured in 40 children with various cardiac diseases; 22 of 40 patients exhibited ANP levels above the upper normal range seen in control children. Of these 22 patients all except two children revealed clinical signs of heart failure. In contrast 15 of 17 children without heart failure showed plasma ANP levels within the range of control children. ANP plasma levels ranged between 93 and 967 pg/ml (mean 284) in patients with heart failure and between 15 and 118 pg/ml (mean 57) in patients without heart failure, respectively. Increased ANP levels in neonates and cardiac patients may result from increased atrial distention and reflect a compensatory mechanism to improve cardiac function by reducing pre- and afterload.
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PMID:Comparison of plasma atrial natriuretic peptide levels in healthy children from birth to adolescence and in children with cardiac diseases. 294 47

The plasma alpha-atrial natriuretic polypeptide (alpha-ANP) concentration in the peripheral veins of children with congenital heart diseases was measured by radioimmunoassay and compared with cardiac catheterization data. Every patient with heart failure had a higher alpha-ANP concentration (132.1 to 858.7 pg/mL) than the upper limit of the normal range (11.7 to 98.7 pg/mL), whereas more than half of the patients without heart failure had a normal alpha-ANP concentration. Although none of the 13 children with atrial septal defect had heart failure, their mean (+/- SD) plasma alpha-ANP concentration (99.4 +/- 40.7 pg/mL) was significantly higher than that in control children (44.6 +/- 22.3 pg/mL). The plasma alpha-ANP concentration was significantly correlated with the pulmonary blood flow/systemic blood flow (Qp/Qs) ratio in the children with atrial septal defect. In the 34 children with ventricular septal defect the plasma alpha-ANP concentration increased in relation to increasing size of the defect. The plasma alpha-ANP concentration was significantly correlated with the Qp/Qs ratio, pulmonary artery pressure, and left atrial pressure, estimated from mean pulmonary artery wedge pressure, in the children with ventricular septal defect. In the children with tetralogy of Fallot, the mean plasma alpha-ANP concentration was normal, and mean right and left atrial pressures were not increased. The elevated alpha-ANP concentration in the three patients with heart failure decreased after their conditions improved with various treatments. Thus the measurement of alpha-ANP concentration may be valuable in evaluating the presence or absence of heart failure and the response to treatment in children with congenital heart diseases. Distention of the right and left atrial might induce the release of alpha-ANP in patients with atrial and ventricular septal defects, respectively.
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PMID:Relationship between plasma atrial natriuretic polypeptide concentration and hemodynamic measurements in children with congenital heart diseases. 295 77

Research on the physiological role of atrial peptides in man is limited, and the potential for these peptides, or more stable analogues, in therapeutics is uncertain. It is clear, however, that plasma levels of immunoreactive atrial natriuretic peptide (IR-ANP) are increased in volunteers taking a high sodium diet, and are elevated in patients with heart failure, chronic renal failure, and primary aldosteronism. There is suggestive evidence that IR-ANP levels are increased also in essential hypertension, although overlap with normotensives is considerable. Injection or infusion of atrial peptides into man results in a diuresis, an increased output of urine electrolytes, a fall in blood pressure and a rise in heart rate, suppression of aldosterone and sometimes of renin also, and stimulation of norepinephrine. In essential hypertensives, urinary effects may be greater than in normotensives. Heart failure patients show a rise in cardiac output and falls in both systemic and pulmonary arterial pressure. Over the next few years and especially if specific antagonists can be developed, the physiologic and pathophysiologic roles of atrial peptides in normal man and in clinical disorders should be clarified. It is possible that stable analogues of atrial peptides will find a place in the treatment of cardiac failure, renal failure, and perhaps hypertension.
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PMID:Atrial natriuretic peptides in man. 296 23

Serum ANP levels were measured by radioreceptor assay in 40 patients with various forms of secondary hypertension and 6 patients with heart failure. In addition, serum ANP was determined in 4 patients with renal artery stenosis before and after dilatation, as well as in 5 anephric patients before and after haemodialysis. Our results showed elevated serum ANP level in most patients with various forms of secondary hypertension and chronic heart failure. A distinction between these two groups and a control group of healthy individuals was not possible due to the wide range and occasional normal levels in the first two groups. ANP levels in patients with renal stenosis decreased after dilatation but there was no correlation with the success of this procedure. A positive correlation between ANP and plasma renin level was detectable in patients with renal artery stenosis, but was also elevated in anephric patients with absent renin production. In summary, our results show that measurements of serum-ANP are of little significance in the diagnosis of hypertension and chronic cardiac failure.
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PMID:[Diagnostic value of atrial natriuretic peptide in hypertension and heart insufficiency]. 296 83

The muscle cells of cardiac atria contain many secretory granula with a prohormone of 126 amino acids (ANF(1-126)). Distension of the atria causes exocytosis of the granula with cleavage of the prohormone into the hormone ANF(99-126) or alpha-ANP and the N-terminal fragment ANF(1-98) with an as yet unknown role. The plasma concentration of the hormone in normal man is in the range of 10 pM (30 pg/ml) with a plasma half-life of several minutes and a release rate of 2-3 ng/kg per minute. The plasma concentration changes in parallel with the intake of sodium chloride and is elevated acutely by all interventions which increase the blood volume, or which cause its redistribution towards the cardiopulmonary compartment. Infusions of the hormone cause diuresis and natriuresis, inhibition of the renin-angiotensin-aldosterone system and of sympathetic activity and augmentation of tissue filtration. Thus, a hormonal feedback loop for cardiac unloading by limiting the plasma volume could be assumed. However, the ANF infusion rates necessary for eliciting these actions in man induce ANF plasma concentrations above physiological levels. On the other hand, a physiological role of the hormone in this regulation is suggested by observations during long-term administration of the hormone, which demonstrate actions of the hormone at physiological plasma levels. Furthermore, experiments with injection of ANF antibodies indicate a synergistic action of ANF, together with reflexes in response to atrial distension. ANF acts by activating specific high affinity membrane receptors, resulting in intracellular cGMP formation and cGMP release into plasma and urine. These ANF receptors are "down-regulated" by infusions of the hormone and by chronic volume expansion. In fetal circulation and in congestive heart failure, there is also augmented prohormone synthesis in the cardiac ventricles, which may then contribute to the release of the hormone. Although during cardiac failure the ANF plasma levels are augmented up to 30-fold, and the atrial prohormone content is reduced, there is no indication for an exhaustion of hormone synthesis or for resetting of stimulated hormone release. In addition to its role as a peripheral hormone for "cardiac unloading", ANF occurs in the central nervous system as a neuropeptide, which might also be involved in blood pressure and volume regulation.
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PMID:[Atrial natriuretic hormone in the human]. 296 72

The human heart secretes ANP, mainly or exclusively as the 1-28-amino-acid alpha-hANP. Secretion is increased when there is hypervolemia of the central circulation, either acute or chronic, the stimulus being, it is presumed, atrial stretch. The clearance rate of alpha-hANP has been documented in healthy volunteers but not in patients with clinical disorders. Injection or infusion of atrial peptides into normal humans has clear-cut hemodynamic, renal, and hormone effects. However, the doses used have been high and the results do not allow extrapolation to the realms of physiology. Patients with essential hypertension appear to have exaggerated renal responses to administered alpha-hANP, although the number of subjects studied is small and matching with normotensive controls was imperfect. By contrast, cardiac failure is characterized by impaired renal responses to atrial peptides. The place of atrial peptides in human physiology and pathophysiology is not clear and will require very low-dose infusion studies under exacting experimental conditions or the development of a specific inhibitor of circulating ANP. In theory, atrial peptides might find a place in therapeutics, most likely in cardiac failure or renal failure, but also essential hypertension if an orally active agonist can be developed.
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PMID:Human studies with atrial natriuretic factor. 296 67

The atrial hormonal system consists of 126 amino acid-containing prohormone (proANP) stored in the secretory granules of atrial myocytes and 28 amino acid-containing hormone (ANP) that is secreted into the bloodstream in response to raised atrial pressure. ANP participates in the homeostasis of body fluid volume through its main receptor-mediated effects; natriuresis, inhibition of renin and aldosterone secretion, and vasodilation. It counteracts the renin-angiotensin system with the putative primary role of regulating the circulating blood volume. Although in man, the physiologic volume stimuli lead to relatively modest increases of ANP secretion, its plasma level undergoes striking changes in pathology. Marked elevations in conditions accompanied by fluid retention, most conspicuously in heart failure and renal failure, have been explained as a compensatory reaction to volume overload. The recent data suggest a decreased target organ responsiveness as one of the causes of a relative inefficiency of the high circulating levels of ANP in inducing an appropriate natriuresis in these volume overload conditions. The well established radioimmunoassay and the more recent methods of plasma ANP measurement are reviewed, and the authors' results with a commercial RIA are presented.
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PMID:Atrial natriuretic peptide: blood levels in human disease and their measurement. 296 16


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