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)

Atrial natriuretic factor (ANF) binding sites have been shown to be present on human platelet membranes. We investigated the effect of an infusion of ANF 5 pmol.kg-1.min-1 on platelet aggregation in whole blood ex-vivo in 8 normal volunteers. Spontaneous platelet aggregation, collagen (0.6-2 micrograms.m.-1)-induced or ADP (0.5-2.0 microM)-induced aggregation was not affected by ANF. Plasma aldosterone was however significantly attenuated by ANF. These results show that a pharmacological dose of ANF does not affect platelet aggregation in man. These results suggest that the high plasma levels of ANF normally achieved in chronic heart failure or acute myocardial infarction are unlikely to contribute to the platelet hyperractivity, often observed in these conditions.
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PMID:Effect of atrial natriuretic factor on platelet function in whole blood ex-vivo in man. 215 20

The cardiovascular reflexes have the key role in the rapid adjustments of the circulatory system in response to daily stresses such as standing and muscular exercise. Arterial and cardiopulmonary mechanoreceptors continuously signal to the cardiovascular centers in the brain the moment to moment pressure changes in the larger arteries, atria and ventricles and exert a tonic restraint on the sympathetic noradrenergic outflow. Depending on the stress, the vasomotor centers adjust this outflow, both qualitatively and quantitatively, to the heart and to the different vascular beds to maintain an appropriate arterial blood pressure. In addition, the sympathetic nerves modulate renin release from the juxtaglomerular cells and receptors at the veno-atrial junctions regulate vasopressin release from the posterior pituitary. Congestive heart failure is characterized by excessive neuro-humoral excitation as evidenced by direct recordings of sympathetic activity and by increased plasma levels of catecholamines, renin, angiotensin II and arginine vasopressin. The evidence indicates that this is a consequence of the reduced ability of the arterial and cardiopulmonary mechanoreceptors to inhibit the vasomotor centers. The cause(s) of this diminished circulatory control requires further studies. The cardiac glycosides, which normally cause vasoconstriction, cause vasodilatation in patients with heart failure. This is attributed to sensitization of the mechanoreceptors. The term atrial natriuretic factor refers to a family of peptide hormones released when the atrial myocytes are stimulated by an increase in transmural pressure. They cause diuresis, natriuresis and vasorelaxation. In severe congestive heart failure, the plasma levels are increased and this helps to compensate for the increased neurohumoral activation by inhibiting the renin-angiotensin system and enhancing sodium and water excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heart failure: role of cardiovascular reflexes. 215 12

Ibopamine is a novel oral dopamine analogue with positive inotropy and diuretic effects. In a double-blind, randomized study, the drug was investigated in 10 patients (mean age 49 +/- 10 years, six male, four female) with mild heart failure (NYHA classes II: six patients, III: four patients). Effects of single oral doses of 200 mg ibopamine, of 40 mg furosemide, and of 200 mg ibopamine plus 40 mg furosemide were compared in each patient at 3-day-intervals. One h after application, systolic and diastolic blood pressure increased from 119 +/- 11 to 124 +/- 8, and from 75 +/- 4 to 80 +/- 6 mm Hg (p less than 0.01) in the ibopamine group, while changes in both other groups and changes of the heart rate were insignificant. During 2 h after drug ingestion urinary flow was raised from 124 +/- 81 to 227 +/- 166 ml/2 h in the ibopamine group (p less than 0.05), while the application of furosemide (with or without ibopamine) resulted in several fold increases of urinary flow. After ibopamine, the 2-h-creatinine-clearance rose from 123 +/- 73 to 130 +/- 85 ml/min (not significant). Sodium excretion remained unchanged by ibopamine, potassium excretion was increased from 2.9 +/- 1.7 to 4.0 +/- 3.3 mmol/h (p less than 0.05), while effects of furosemide were several fold of those of ibopamine. Atrial natriuretic factor concentrations in plasma increased significantly after ibopamine and after ibopamine plus furosemide (p less than 0.01), but remained constant after furosemide alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Renal effects of ibopamine in comparison with furosemide in patients with mild heart failure]. 215 13

Thirty-seven patients with volume-retaining disorders (liver cirrhosis with ascites, n = 8; heart failure NYHA III-IV, n = 12; endstage renal failure, n = 17) and twelve healthy age-matched controls were given a small dose (33 micrograms) of hANF (human atrial natriuretic factor). We tested the resulting hemodynamic and renal effects as well as the effect on plasma cyclic GMP levels and compared them with the properties of platelet ANF receptors. The ANF injection evoked an increase in cyclic GMP plasma levels of 19.3 +/- 2.2 nM in healthy controls. This increase tended to be smaller in the cirrhosis group (15.5 +/- 3.3 nM) and in the heart failure group (16.8 +/- 2.3 nM) than in the dialysis group (20.5 +/- 2.5 nM). The invasion rates of cyclic GMP were comparable in all groups, but the evasion rates increased more in the heart failure and endstage renal failure groups (27.9 +/- 7.7 min and 26.1 +/- 3.4 min, respectively) than in the cirrhosis and control groups (14.9 +/- 1.9 min and 14.2 +/- 1.9 min, respectively). Patients with endstage renal failure and congestive heart failure showed a smaller decrease in diastolic blood pressure than controls and patients with liver cirrhosis. Renal actions of ANF were diminished in cirrhosis and heart failure patients. Binding capacities of platelet ANF receptors were higher in the control group (12.2 +/- 1.5 receptors/cell) than in the patient groups (cirrhosis, 7.8 +/- 1.2; endstage renal failure, 8.0 +/- 0.9; heart insufficiency, 8.0 +/- 1.0 receptors/cell), with no differences among the patient groups. Binding affinities were not significantly different. Correlation analysis showed that the relationship between the actions of ANF and the increases in plasma cyclic GMP levels is loose and cannot predict the hemodynamic or renal effects of exogenous ANF in a given patient. Although the behavior of plasma cyclic GMP levels fails to predict the responsiveness of the body to ANF in a given patient, it does reflect the differences between the patient groups and the control group. In contrast, we found no correlation between the properties of platelet ANF receptors and ANF action.
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PMID:Effects of a small bolus dose of ANF in healthy volunteers and in patients with volume retaining disorders. 216 5

STUDY OBJECTIVE--The aim was to investigate the relationship between urinary cyclic guanosine monophosphate (GMP) excretion and activation of the heart endocrine function in two rat models of cardiac failure. DESIGN--Left ventricular infarction and aging in spontaneously hypertensive rats (SHR) are two models that could lead to congestive heart failure. In the first the degree of failure depends on the length of the infarcted area. In the second the degree of failure depends on time. Urinary cyclic GMP, plasma atrial natriuretic factor (ANF), and degree of congestive heart failure were evaluated in both models. EXPERIMENTAL ANIMALS--31 male Wistar rats were used for myocardial infarction and sham operated controls. Spontaneously hypertensive (SHR) rats (2, 6, 12 and 24 months old, n = 10 per group) were used for the age overload studies. MEASUREMENTS AND MAIN RESULTS--In myocardial infarction, the amount of left ventricular ANF mRNA, plasma ANF concentration, and urinary cyclic GMP excretion were correlated and were proportional to the degree of cardiac failure, as assessed by the increase in right ventricular mass and the decrease in blood pressure. In male SHR (aged 6-24 months), plasma ANF and urinary cyclic GMP were correlated, increased with age, and were proportional to the heart to body weight ratio. These correlations between plasma ANF, daily urinary cyclic GMP excretion, and left ventricular hypertrophy persisted in two year old SHR. The presence of pleural extravasation in these old animals was also characterised by significant increases in both plasma ANF and urinary cyclic GMP. The plasma ANF and the daily urinary cyclic GMP excretion were negative prognostic indicators of life expectancy in two year old SHR. CONCLUSIONS--Urinary cyclic GMP excretion, correlated with the plasma ANF level, is a non-invasive indicator of congestive heart failure in two models of overloaded left ventricle in rats.
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PMID:Urinary cyclic guanosine monophosphate as an indicator of experimental congestive heart failure in rats. 217 35

Hemodynamic and neurohumoral effects of intravenous captopril were studied in ten patients with severe chronic congestive heart failure (NYHA Functional Class III and IV). Incremental bolus doses of captopril, titrated to a maximum cumulative dose of 15 mg, were given at 10-minute intervals. Systemic arterial pressure, mean pulmonary capillary wedge pressure, systemic vascular resistance, mean pulmonary artery pressure, and heart rate decreased (P less than .05). Cardiac index and stroke volume index increased (P less than .05). Maximum hemodynamic effects occurred after cumulative doses of 7 mg and were seen within 30 minutes after initiation of therapy; responses persisted for 30-90 minutes after the last dose. Plasma renin activity increased, and plasma atrial natriuretic factor concentration decreased. No adverse effects were observed with the use of intravenous captopril. Thus, intravenous captopril produces rapid and favorable hemodynamic improvement in advanced heart failure patients.
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PMID:Intravenous captopril in congestive heart failure. 220 53

The increased neuroendocrine activity in patients with congestive heart failure appears to be a generalized attempt to maintain blood pressure at the expense of reduced cardiac performance and salt and water retention. It is likely that baroreceptor dysfunction contributes to increased sympathetic nervous system activity in patients with congestive heart failure. The usual tonic inhibitory messages emanating from baro- and mechanoreceptors in the great vessels and heart fail to adjust sympathetic traffic from the brain to the periphery, leading to uninhibited sympathetic tone. Arginine vasopressin and plasma renin activity may be increased secondarily; however, plasma renin activity activation could also be induced by a low-salt diet and diuretic use. Preliminary baseline data indicate that patients with left ventricular dysfunction (ejection fraction less than or equal to 35%) but no or very mild symptoms of heart failure have increased plasma levels of norepinephrine, atrial natriuretic factor and arginine vasopressin, while plasma renin activity is normal, suggesting that neuroendocrine activity contributes to the pathogenesis of congestive heart failure. Neurohormones such as angiotensin II may alter gene expression, leading to changes in the shape and size of the cell. Remodeling of the heart and blood vessels is associated with both heart failure and hypertension. Angiotensin-converting enzyme inhibitors have been demonstrated to retard or reverse the remodeling process under certain experimental conditions. Studies are currently under way to test this possibility in patients.
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PMID:Neuroendocrine activity in congestive heart failure. 222 Jun 3

There is a varying hormonal activation in heart failure. To be able to evaluate this activation and relate it to prognosis, we took blood samples at baseline and after 6 weeks from 239 patients with severe heart failure (all in New York Heart Association class IV) randomized to additional treatment with enalapril or placebo. In this study (CONSENSUS), which has previously been reported, there was a significant reduction in mortality among patients treated with enalapril. The present data show in the placebo group a significant positive relation between mortality and levels of angiotensin II (p less than 0.05), aldosterone (p = 0.003), noradrenaline (p less than 0.001), adrenaline (p = 0.001), and atrial natriuretic factor (p = 0.003). A similar relation was not observed among the patients treated with enalapril. Significant reductions in mortality in the groups of patients treated with enalapril were consistently found among patients with baseline hormone levels above median values. There were significant reductions in hormone levels from baseline to 6 weeks in the group of patients treated with enalapril for all hormones except adrenaline. There were no correlations between these changes in hormone levels. Summarily, there is a pronounced but variable neurohormonal activation in heart failure even in patients with similar clinical findings. This activation is reduced by enalapril therapy. The results suggest that the effect of enalapril on mortality is related to hormonal activation in general and the renin-angiotensin system in particular.
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PMID:Hormones regulating cardiovascular function in patients with severe congestive heart failure and their relation to mortality. CONSENSUS Trial Study Group. 222 74

The characteristics of norepinephrine and epinephrine as well as plasma renin activity, angiotensin II, aldosterone, vasopressin, and atrial natriuretic factor (ANF) were examined in 64 patients (mean age of 52 +/- 16 years) with dilated cardiomyopathy. The findings were grouped according to the NYHA classification and compared with a normal cohort of 38 patients (mean age of 42 +/- 10 years). Furthermore, the influence of different cardioactive substances used in the treatment of cardiac failure was analyzed in more detail. Patients in NYHA class II already demonstrated an increased activity of the sympathicoadrenal, renin-angiotensin-aldosterone system (RAAS), vasopressin, and ANF system. The highest values were found in patients of NYHA class IV. In these patients, norepinephrine was enhanced by a factor of 7, epinephrine by a factor of 2, plasma renin activity by a factor of 7, angiotensin II by a factor of 2.5, aldosterone by a factor of 5, vasopressin by a factor of 1.5, and ANF by a factor of 4 compared with those in normal subjects. The highest correlation coefficient was found for norepinephrine (r = 0.84). The acute application of 1-2 mg/kg of body weight of enoximone in patients with dilated cardiomyopathy (n = 15) resulted only in a significant lowering of the atrial natriuretic factor as an indicator for drug-induced unloading effects (venous pooling). All the parameters showed only a tendency; in none could statistical significance be established. Application of 0.75 mg/kg of body weight of enoximone i.v. in patients with coronary artery disease (n = 17) has no direct influence either on the sympathoadrenal, the ANF, or the prostaglandin systems. It could be demonstrated that the mode of medical treatment influences the parameters of vasoconstrictor systems in different ways.
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PMID:The influence of various degrees of cardiac failure, chronic medical treatment, and acute additional enoximone application on the parameters of the vasopressor system. 248 Apr 85

Water, sodium, and potassium balance and urinary excretion of norepinephrine and aldosterone were investigated in rats with left ventricular failure due to left ventricular infarction, and measurements were obtained of plasma levels of atrial natriuretic factor (ANF). Increased plasma levels of ANF in relation to the size of the infarction and to the right atrial and left ventricular end-diastolic pressure were found. The augmented levels of ANF were not able to prevent an accumulation of sodium in the rats with myocardial infarction in which urinary excretion of norepinephrine and aldosterone was unchanged in comparison to control values. Plasma levels of ANF in the pulmonary artery, aorta, and renal vein of six conscious dogs were studied during the development of heart failure due to rapid right ventricular pacing. A threefold increase in ANF was found: ANF levels did not differ between the pulmonary artery and the aorta, but a reduction in ANF of about 30% was reported in the renal vein in comparison to the arteries. A close positive correlation between right atrial pressure and plasma levels of ANF was noted. No correlation could be demonstrated between mean pulmonary arterial pressure and ANF or between the stimulated plasma renin concentration and plasma ANF values.
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PMID:Atrial natriuretic factor in acute and chronic cardiac failure. 248 23


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