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)

Alpha atrial natriuretic peptide was measured in plasma in 7 patients with severe heart failure before and after the administration of the synthesized substance. An inverse correlation was found between basal plasma levels of alpha atrial natriuretic peptide and cardiac output. Incremental bolus injections of synthetic alpha atrial natriuretic peptide and the continuous infusion for 30 minutes resulted in a decrease of peripheral vascular resistance, an increase of cardiac output and a decrease of blood pressure. Plasma aldosterone was markedly reduced in each patient by the administration of atrial natriuretic peptide and a small but significant decrease of plasma cortisol was found. Diuresis, urinary sodium and potassium excretion were enhanced. No significant changes were observed concerning adrenocorticotropic hormone, plasma renin concentration, plasma norepinephrine and vasopressin and the plasma levels of 6-keto-prostaglandin F1-alpha and prostaglandin E2.
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PMID:Atrial natriuretic peptide in patients with severe heart failure. 294 71

Plasma atrial natriuretic peptide concentrations were measured by radioimmunoassay six to 77 weeks after operation in eight cardiac transplant recipients with no appreciable evidence of cardiac failure or rejection and in eight control subjects matched for age, sex, race, and blood pressure. Plasma atrial natriuretic peptide concentrations were significantly higher in the cardiac transplant recipients (mean 19.4 (SE 3.9) ng/l) than in the controls (7.3 (1.2) ng/l p less than 0.01). The mechanisms underlying these raised values were not clear. These findings suggest that the transplanted atria may secrete atrial peptides and also that innervation is not obligatory for secretion of atrial natriuretic peptides to occur. Before this can be confirmed, however, it remains to be established what the relative contribution of donor and recipient atrial tissue is to the secretion of these peptides.
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PMID:Raised concentrations of plasma atrial natriuretic peptides in cardiac transplant recipients. 294 5

We measured atrial natriuretic peptide (ANP) plasma levels in rats with experimental heart failure caused by left coronary artery ligation. ANP levels were clearly higher in infarcted rats (409 +/- 59 pg/ml; mean +/- S.E.M.) than in sham-operated controls (39 +/- 6 pg/ml). Moreover, plasma ANP levels increased progressively with the severity of cardiac dysfunction and size of infarct. Increased release of ANP in post-infarction heart failure appears to be a meaningful compensatory response to control rising preload. Our results are in keeping with evidence from human studies showing increased plasma concentration of ANP in patients with congestive heart failure. This model is a useful tool to further explore the role of ANP in heart failure.
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PMID:Elevated plasma atrial natriuretic peptide in rats with myocardial infarcts. 294 32

Serum levels of atrial natriuretic peptide (ANP) are elevated in chronic heart failure presumably due to dilatation of the left atrium resulting from increases in intracardiac pressures. To define the time course of changes in serum ANP levels and to determine the relationship to left ventricular end-diastolic pressure, rats were subjected to coronary artery ligation to produce myocardial infarction and left ventricular failure. Atrial natriuretic peptide levels were measured weekly for four weeks thereafter. In rats with myocardial infarction and elevation of left ventricular end-diastolic pressure there was no change in ANP levels at 7 and 14 days. However, at day 21 and 28, ANP levels were elevated more than 3 fold. There was a correlation between ANP levels and left ventricular end-diastolic pressures. There was no correlation between ANP levels and right atrial pressures or serum sodium concentrations. We conclude that the chronic elevation of left ventricular end-diastolic pressure is required to produce an increase in ANP after myocardial infarction which results in chronic heart failure.
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PMID:Atrial natriuretic peptide levels during development of chronic heart failure after myocardial infarction in rats. 295 58

Vasoconstrictory and vasodilatory hormone systems may be important in the regulation of peripheral vascular resistance and renal hemodynamics in the early phase of heart failure. The activity of the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous activity, and, as possible counterregulating systems, the activity of prostacyclin and atrial natriuretic peptide (ANP) were studied in 6 conscious dogs during the first 4 days of congestive heart failure in relation to hemodynamic changes and renal plasma flow. Congestive heart failure was induced by rapid right ventricular pacing, which caused a considerable decrease of cardiac output (-38%; p less than 0.05), oxygen saturation of the mixed venous blood (-13%; p less than 0.05), and mean arterial pressure (-24 mm Hg; p less than 0.05) on the 4th day. Mean pulmonary arterial pressure and mean pulmonary capillary wedge pressure increased (+4 mm Hg; p less than 0.05 and +7 mm Hg, respectively; p less than 0.05). Renal plasma flow was slightly reduced (N.S.), renal vascular resistance did not change. Peripheral vascular resistance showed a significant increase only on the 1st day. Sympathetic nervous activity was stimulated (from 175 +/- 31 pg/ml to 391 +/- 100 pg/ml; p less than 0.05), while plasma renin concentration was significantly suppressed on the 4th day (from 3.3 +/- 0.4 ngAI/ml/h to 1.9 +/- 0.5 ngAI/ml/h; p less than 0.05), and plasma aldosterone levels were decreased (from 108 +/- 12 pg/ml to 76 +/- 12 pg/ml; p less than 0.05). ANP increased 3-fold (p less than 0.05) and 6-keto-prostaglandin F1 alpha increased in 4 out of 6 dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic changes and renal plasma flow in early heart failure: implications for renin, aldosterone, norepinephrine, atrial natriuretic peptide and prostacyclin. 295 80

The plasma concentration of atrial natriuretic peptide (ANP) in 16 healthy subjects on a free diet was 41 +/- 23 pg ml-1 (mean +/- SD) when upright and 58 +/- 27 pg ml-1 in the supine position (P less than 0.05), which confirms the concept that the supine position raises plasma ANP. Water immersion to the neck for 2 h caused a brisk diuresis, natriuresis and raised plasma ANP in 8 healthy subjects, suggesting that ANP is a mediator of diuresis and natriuresis during immersion. Dynamic exercise (50-200 W per 4 min) on a bicycle ergometer caused a gradual increase in plasma ANP in 6 healthy males, with a close correlation between the increases in plasma ANP and heart rate (r = 0.96). Thus, plasma ANP levels are increased in healthy subjects by stimuli causing an increased preload and possibly by tachycardia itself. Markedly raised plasma levels of ANP were found in patients with congestive heart failure, and upright posture caused a further rise of plasma ANP which correlated with the increase in heart rate (r = 0.87). High plasma ANP concentrations were also found in 25 patients with end-stage renal failure maintained on haemodialysis. When these patients were subdivided into those with concomitant heart failure and those with normal cardiac function, changes in plasma ANP correlated with predialysis weight gain and weight loss during dialysis, but only in patients without heart failure. In 9 infants treated by operative or pharmacological closure of persistent ductus arteriosus, high pre-treatment plasma ANP values were lowered by successful therapy, and plasma ANP correlated with the degree of left atrial distension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma atrial natriuretic peptide in health and disease. 295 6

Plasma concentrations of atrial natriuretic peptide were measured in eight patients undergoing elective cardiac catheterisation and angiography. All patients had normal resting pressures in the cardiac chambers and no clinical evidence of heart failure. Plasma atrial natriuretic peptide rose significantly from the superior vena cava into the right atrium and right ventricle. The increase into the right atrium was variable, with no increase in three subjects, but there was a consistent increase in all subjects from the superior vena cava to to the right ventricle. These findings in the right atrium are probably caused by inadequate mixing and streaming of blood from the coronary sinus containing high concentrations of atrial natriuretic peptide. There was no increase in the concentration of natriuretic peptide from the pulmonary artery to the left ventricle, but the concentrations in the left ventricle were significantly higher than in the superior vena cava. These findings demonstrate that the heart secretes atrial natriuretic peptides in the absence of cardiac failure. Studies based on sampling of the right atrium will not accurately measure cardiac secretion of atrial natriuretic peptide and will therefore be likely to obscure the mechanisms responsible for regulating its secretion. The right ventricle and pulmonary artery are the best sampling sites to measure atrial natriuretic peptide release from the right atrium.
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PMID:Secretion of atrial natriuretic peptide from the heart in man. 295 78

Plasma atrial natriuretic peptide (ANP), a hormone secreted by the heart, is elevated in cardiac failure. In the aim to study the role of ANP in cardiac failure, the haemodynamic response to ANP was examined in rats with chronic heart failure produced by coronary artery ligation. Plasma ANP was clearly elevated in all infarcted rats before ANP injection as compared with controls. ANP lowered the blood pressure and impaired cardiac contractility, as measured by the maximal positive value of the first derivative of the pressure signal, in a dose-dependent manner. The blood pressure lowering effects of ANP were attenuated in rats with cardiac failure. We conclude that rats with experimentally induced heart infarct are partially resistant to the haemodynamic effects of ANP.
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PMID:Haemodynamic effects of atrial natriuretic peptide in rats with heart failure. 295 88

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

The relation of dyspnea of presumed cardiac origin to regional and global left ventricular (LV) function was evaluated among 67-year old men sampled from the general population of Gothenburg, Sweden. From a screened cohort of 644 men, 42 men with cardiac dyspnea and without obstructive pulmonary disease, and 45 controls were sampled. Dyspnea was measured and graded according to the World Health Organization standard. Two-dimensional and M-mode echocardiography, carotid pulse tracing, apexcardiography and phonocardiography were used to evaluate regional wall motion, systolic time intervals, LV ejection indices, wall stress, diastolic time intervals, direct and indirect indices of LV filling properties, and indices of pulmonary hypertension. The plasma concentrations of immunoreactive atrial natriuretic peptide (IrANP) and catecholamines were also assessed. The dyspneic men had more regional wall motion abnormalities than the controls. Systolic, as well as diastolic LV impairment, and increased LV mass were more abundant. Dyspnea grade was significantly related to either of these abnormalities in univariate analyses, and also in multivariate analyses when clinical information, such as chest X-ray, electrocardiogram, and clinical history were taken into account. Multivariate analyses of all the studied indices of cardiac function, together with clinical information, showed dyspnea grade to be significantly and independently related to mitral valve E-point to septal separation (EPSS), presence of akinetic segments, a history of angina pectoris, exercise capacity, and left atrial dimension. Taken together these variables explained 74% of dyspnea grade variance. There was also a relation between dyspnea grade and IrANP, which was independent of clinical findings, but only appeared under conditions of severe dyspnea. It is concluded that the degree of dyspnea is associated with a fairly similar progressive impairment of diastolic, regional and systolic function. In mild heart failure LV hypertrophy and diastolic abnormalities are more prevalent than systolic dysfunction. In severe dyspnea a mixture of regional, systolic, and diastolic abnormalities are present. A decrease of fractional shortening and increased levels of IrANP are late phenomena. EPSS may be a useful indicator of LV dysfunction in population studies.
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PMID:Relation between cardiac dyspnea and left ventricular function. A non-invasive study of 67-year-old men. 296 21


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