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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study plasma levels of atrial natriuretic peptide and of the catecholamines epinephrine and norepinephrine were investigated in hypertensive patients (HT) (n = 30). 22 normotensive patients (NT) served as controls. Hypertensives showed an elevated ANP-level in comparison with controls (46.8 +/- 3.3 vs. 36.8 +/- 3.3 pg/ml, M +/- SEM, p less than 0.01). When patients with myocardial infarction or with reduced ejection fraction were excluded, the same relation was demonstrated (49.3 +/- 3.2 vs. 33.6 +/- 2.0 pg/ml, p less than 0.01). Plasma norepinephrine was 230.8 +/- 52.3 pg/ml in HT compared with 138.0 +/- 19.6 pg/ml in NT (p less than 0.05). Epinephrine was 70.8 +/- 10.5 vs. 54.8 +/- 9.7 pg/ml in HT and NT. To exclude an increased left ventricular enddiastolic - and hence left atrial - pressure as the cause for the elevation of ANP and norepinephrine, HT and NT were matched for the same levels of enddiastolic pressure (LVEDP) (n = 18). For each level of LVEDP ANP was higher in HT than in NT (p less than 0.01). The same held true for norepinephrine (p less than 0.05) and to a lesser extent for epinephrine (p = 0.09). Our results demonstrate that patients with essential hypertension exhibit markedly elevated levels for ANP and catecholamines which is not due to myocardial failure. We propose that the increased secretion of the vasodilatory hormone ANP serves as counterregulation against the vasoconstrictor norepinephrine. The endocrine function of the heart may play a pivotal role in the modulation of sympathetic activity.
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PMID:[Elevated levels of atrial natriuretic peptide and plasma catecholamines in arterial hypertension--indications for an interaction]. 297 96

Neurohormonal activation may provide a pathophysiological link between acute myocardial infarction and chronic congestive heart failure, and modulation of neurohormonal activity may be an important therapeutic target in these conditions. Plasma neurohormones were studied in 55 patients with acute myocardial infarction. Angiotensin II, noradrenaline and ANP were elevated in the early phase but tended to normalize during the first week in patients without signs of heart failure. In patients with heart failure angiotensin II and noradrenaline remained elevated for 1 month and ANP for 4-6 months. During head-up tilt, angiotensin II and noradrenaline increased most in patients with heart failure. In patients with a first myocardial infarction there was a positive correlation between sustained neurohormonal activity and infarct size. Almost complete suppression of plasma ACE activity was achieved within 30 min in 48 patients treated with intravenous enalaprilat, initiated within 24 h from the onset of infarction. The drug was tolerated in dosages of 1.0-1.2 mg given over 1-2h. Patients with systolic blood pressure between 100 and 110 mmHg incurred a greater risk of hypotension than those with higher blood pressure at baseline. Tolerance was not worse among patients treated with intravenous diuretics, metoprolol or nitroglycerin. A total of 98 patients were randomized to treatment with enalapril or placebo, initiated within 24 h from onset of infarction and continued for 4-6 months. During treatment there were no significant differences in plasma levels of angiotensin II, aldosterone, ANP or catecholamines between groups. Echocardiographic recordings were performed in 28 patients. Among patients on placebo there was a positive correlation between plasma levels of noradrenaline at days 5-7 and the increase in left ventricular volumes during the study period, and an inverse correlation between plasma aldosterone at days 5-7 and the increase in left ventricular ejection fraction during the study. No such correlation was found among patients on enalapril. ANP levels at 1 month correlated inversely with the left ventricular ejection fraction at the same time. Plasma neurohormones were measured in 223 patients with mild or moderately severe chronic heart failure, randomized to treatment with ramipril or placebo for 3 months. There was wide variation in hormone levels. Noradrenaline and aldosterone correlated inversely with exercise duration at baseline. Noradrenaline correlated positively with the degree of symptoms. Aldosterone and ANP were reduced with ramipril compared with placebo. Noradrenaline was reduced among patients with baseline levels in the highest tertile. Plasma hormones were also measured at peak exercise in 54 patients. Hormonal levels at rest correlated strongly with those at peak exercise.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurohormonal activation in patients with acute myocardial infarction or chronic congestive heart failure. With special reference to treatment with angiotensin converting enzyme inhibitors. 759 49

1. Long-term volume homeostasis is linked very closely to long-term arterial pressure control through the renal-body fluid feedback mechanism. A key feature of this control system is the ability of the kidneys to respond to changes in arterial pressure by altering renal excretion of salt and water, often referred to as renal-pressure natriuresis. 2. Quantitative studies indicate that ANP secretion is relatively sensitive to changes in atrial pressure and that the rate of hormonal secretion does not adapt to continuous long-term stimulation. 3. Under normal conditions, the renal-body fluid feedback mechanism for arterial pressure control is very efficient in minimizing changes in body fluid volumes during alterations in sodium intake. Therefore, only small changes in atrial pressure and ANP secretion occur. Alterations in plasma ANP concentration within physiological levels have little effect on renal-pressure natriuresis and, therefore, have little impact on volume homeostasis. 4. When the renal-body fluid feedback mechanism for arterial pressure control is impaired and body fluid volumes are elevated, such as in heart failure, large increases in atrial pressure and ANP secretion occur. The resultant pathophysiological plasma levels of ANP exert sustained natriuretic effects and chronically shift renal-pressure natriuresis to lower arterial pressures. In the absence of this chronic effect of ANP on renal-pressure natriuresis, reduced arterial pressure in compensated heart failure would result in protracted retention of salt and water and additional increments in body fluid volumes.
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PMID:Role of atrial natriuretic peptide in long-term volume homeostasis. 776 35

Brain and atrial natriuretic peptides (BNP and ANP) are cardiac hormones with diuretic, natriuretic, and vasodilatory activities. Cardiomyopathic hamsters are widely used animal models of heart failure. Due to the structural divergence of BNP among species, examination on pathophysiological roles of BNP using cardiomyopathic hamsters is so far impossible. We therefore isolated hamster BNP and ANP cDNAs, and investigated synthesis and secretion of these peptides in normal and cardiomyopathic hamsters. The COOH-terminal 32-residue peptide of cloned hamster preproBNP with 122 amino acids, preceded by a single arginine residue, supposedly represents hamster BNP showing < 50% homology to rat BNP. Alpha-hamster ANP, 28-residue peptide, is identical to alpha-rat ANP. In hamsters, BNP and ANP occur mainly in the ventricle and the atrium, respectively. The 32-wk-old hypertrophic cardiomyopathic BIO14.6 strain exhibited ventricular hypertrophy. The 32-wk-old dilated cardiomyopathic BIO53.58 strain remained at the stage without apparent heart failure. In BIO14.6 and BIO53.58 strains at this age, ventricular BNP and ANP gene expressions are augmented, and the plasma BNP concentration is elevated to 136 and 108 fmol/ml, respectively, three times greater than the elevated plasma ANP concentration, which well mimics changes of the plasma BNP and ANP concentrations in human heart failure. Cardiomyopathic hamsters, therefore, are useful models to investigate the implication of BNP in human cardiovascular diseases.
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PMID:Molecular cloning of hamster brain and atrial natriuretic peptide cDNAs. Cardiomyopathic hamsters are useful models for brain and atrial natriuretic peptides. 808 46

The cardiovascular and diuretic actions of carperitide were studied in experimental animals. Carperitide relaxed various canine arteries and veins that were contracted by high K+ or norepinephrine. Carperitide stimulated particulate guanylate cyclase from rat thoracic aortas. Carperitide had almost no effect on coronary perfusion pressure or heart rate, but caused a slight decrease in contractile force in isolated guinea pig hearts. Carperitide tended to decrease isoproterenol-induced renin release from isolated rat kidney slices and elicited decreases in angiotensin II-induced aldosterone release from bovine zona glomerulosa cells. Intravenous injection of carperitide elicited decreases in arterial blood pressure and total peripheral resistance in the anesthetized and conscious dogs. Carperitide also elicited transient increases in cardiac output and coronary blood flow followed by slight decreases in them. Intravenous infusion of carperitide elicited decreases in pulmonary capillary wedge pressure, pulmonary pressure and right atrial pressure in association with elevating plasma carperitide (ANP like immuno-reactivity) level in dogs with heart failure induced by coronary artery occlusion and saline loading. These results suggest that carperitide decreases both preload and afterload and can improve the untoward hemodynamic alterations in animals with acute experimental heart failure.
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PMID:[Effect of carperitide (alpha-human atrial natriuretic polypeptide) on the cardiovascular system in experimental animals]. 833 Aug 1

In chronic heart failure diuretic drugs improve central hemodynamic variables and cardiac pumping secondary to altered plasma and extracellular volumes; humoral markers of these changes include increased plasma renin and aldosterone levels. The latter increases are maximal over the first week but decline with chronic therapy. The plasma alpha-ANP levels show a reciprocal effect; these data are compatible with a rapid contraction of the plasma volume which is sustained during chronic therapy. The acute hemodynamic actions of diuretic agents reflect both immediate and direct vascular actions and also effects secondary to diuresis (volume redistribution). At rest substantial reductions in pulmonary "wedge" pressure (-29%), with a consequent fall in cardiac output (-10%), are described. Total systemic vascular resistance initially increases but "reverse autoregulation" over subsequent weeks returns this elevation gradually towards control values. Tolerance to these initial hemodynamic effects does not occur with maintained therapy; moreover, echocardiographic markers of contractility and exercise capacity may increase. The early venodilator effects of diuretic drugs can be attributed to prostaglandin release and the initial pressor actions to activation of the renin angiotensin system; these vascular actions may have limited relevance to long-term beneficial effects on hemodynamics. Direct pulmonary vasodilation and improved pulmonary compliance remain an interesting finding. Although most patients are both symptomatically and hemodynamically improved at rest, the actions during exercise are more varied. Some individuals with severely impaired left ventricular function show little hemodynamic improvement, whereas those with milder dysfunction usually benefit; in the main this is probably related to the latter being on a steeper cardiac function curve.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Central hemodynamic effects of diuretic therapy in chronic heart failure. 843 76

In summary, ANP exerts its action in the kidney directly and indirectly. Its qualitative importance in body fluid regulation remains unsettled. It appears that its role is more important in pathophysiological conditions such as CHF in which plasma ANP is elevated. Paradoxically, kidneys in heart failure, nephrosis and diabetes are characterized by diminished responsiveness to exogenous ANP. Further studies are needed to ascertain whether this involves an alteration at the receptor or postreceptor site. The cellular mechanisms for receptor regulation and postreceptor signalling in physiology and pathophysiology need further investigation. Finally, a paracrine mode for the action of ANP and other natriuretic peptides has been proposed. Whether they act locally to facilitate sodium excretion and how much importance they have compared to circulating ANP remain to be clarified. The potential role of ANP as a growth inhibitor is also intriguing.
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PMID:Biological significance of atrial natriuretic peptide in the kidney. 844 32

Recent studies suggest that plasma levels of alpha-hANP may reflect the severity of heart failure, but mechanism whereby ANP secretion increase is not known. Changes in alpha-hANP concentration in the arterial (A-ANP) and coronary sinus blood (CS-ANP) during and after the cardiopulmonary bypass (CPB) were measured to investigate the role of ANP in patients undergoing cardiac surgery. Fifteen patients were divided into 2 group; Group I, valvular heart disease (n = 9), Group II, coronary artery disease (n = 6). Both A-ANP and CS-ANP were significantly higher in the Group I than Group II before and during CPB. The difference between two groups decreased and was insignificant after CPB. The CS-ANP was twice as high as A-ANP at simultaneous sampling point. Significant correlations between the changes in PCWP (delta PCWP) and delta A-ANP (p < 0.01), delta RAP and delta A-ANP (p < 0.02) and an inverse linear correlation between CI and A-ANP (p < 0.01) were observed. Not a significant correlation was found between ANP and urine volume, urinary sodium excretion and other renal functional parameters during and after CPB. Hypothermia and the use of mannitol in large quantities were considered to be factors. In the Group I, A-ANPs were also measured in the postoperative follow-up period. A-ANP remained elevated above 100 pg/ml in patients with poor and decreased below 100 pg/ml with good prognostic signs 3 to 6 months postoperatively. From these results, it is suggested that alpha hANP is secreted from the atrial wall to the coronary sinus vein and the levels of alpha-hANP in the perioperative and follow-up period after heart surgery, especially in the valvular heart disease, are considered to reflect the cardiac performance.
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PMID:[Changes of alpha hANP concentration in arterial and coronary sinus blood during and after cardiopulmonary bypass]. 851 51

N-terminal parts of proatrial natriuretic polypeptide have been proposed to be sensitive and specific markers of congestive heart failure (CHF). A prerequisite for use of a clinical marker is knowledge of day-to-day variation and dependence on age and sex. Immunoreactive N-terminal proatrial natriuretic polypeptide (31-67) (ir-N-ANP(31-67)) was measured in a clinically relevant population of healthy individuals. A total of 21 females (mean age 52 years, range 42-76) and 26 males (mean age 54 years, range 42-73), without cardiovascular disease, were included in the study. No correlation was found between ir-N-ANP(31-67) and sex. A statistically significant positive linear correlation (ir-N-ANP pmol 1(-1) = 182+ (8.2 x age in years) (p = 0.004) was found between age and ir-N-ANP(31-67). For the youngest subjects (42 years) the expected mean ir-N-ANP(31-67) was 530 pmol 1(-1), and for the oldest subjects (76 years) it was 800 pmol 1(-1). For all the subjects, the median ir-N-ANP(31-67) was found to be 626 pmol 1(-1) (range 300-1151). The day-to-day variation was studied and no significant difference was found in the plasma concentration of two samples taken 2-5 days apart. Of the individual day-to-day variation, 95% would be expected to be in the interval from -244 to 188 pmol 1(-1) (mean +/- 2 x SD). We conclude that ir-N-ANP(31-67) rises with age. The age-dependent rise in ir-N-ANP(31-67) is modest, but should be taken into consideration in order to use ir-N-ANP(31-67) as a diagnostic marker of CHF. The day-to-day variation is found to be rather high and cannot be neglected if N-ANP(31-67) is to be used as a marker of asymptomatic heart failure.
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PMID:Proatrial natriuretic polypeptide (31-67) in healthy individuals: day-to-day variation and influence of sex and age. 854 4

The objective of the study was the evaluation of natriuretic peptides in ischemic heart disease. Atrial and brain peptides (ANP, BNP) were elevated in patients with ischemic heart failure, as compared with patients with angina without over failure, and controls (p < 0.01). BNP/ANP ratio was higher in NYHA class IV than in class III patients (2.67 +/- 0.87 vs. 1.52 +/- 0.59, respectively). Patients in the angina group, in whom elevated BNP or ANP was found, had subclinical systolic or diastolic dysfunction. There was inverse correlation between BNP, ANP and the left-ventricular ejection fraction (each r = 0.78, p < 0.001). We conclude that BNP is elevated as a result of myocardial dysfunction, but not of ischemia and seems to be a better index of disease stage and prognosis than ANP.
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PMID:Brain and atrial natriuretic peptides in patients with ischemic heart disease with and without heart failure. 863 Oct 38


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