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 hemodynamic and renal effects of anaritide (human atrial natriuretic peptide 102-126), a synthetic analog of atrial natriuretic peptide, were evaluated in 35 patients with chronic New York Heart Association class II to IV heart failure. There were 32 men and 3 women, aged 33 to 75 (mean +/- standard error of the mean 56 +/- 2) years. In the first phase of the study, right-sided heart catheterization was performed, and anaritide was administered as 1-hour infusions. The rate of the infusion varied among patients from 0.03 to 0.3 micrograms/kg/min. In response to anaritide, there were decreases in mean systemic arterial (94 +/- 2 to 87 +/- 2 mm Hg), right atrial (10 +/- 1 to 8 +/- 1 mm Hg), mean pulmonary arterial (33 +/- 2 to 28 +/- 2 mm Hg) and pulmonary artery wedge (22 +/- 2 to 15 +/- 2 mm Hg) pressures (all p less than 0.05). Cardiac index increased (2.39 +/- 0.15 to 2.62 +/- 0.15 liters/min/m2, p less than 0.05) and heart rate was unchanged. Systemic vascular resistance decreased significantly, but pulmonary vascular resistance was unchanged. There were increases in urine volume (1.6 +/- 0.2 to 2.3 +/- 0.4 ml/min), sodium excretion (47 +/- 13 to 74 +/- 20 muEq/min) and fractional excretion of sodium (0.41 +/- 0.11 to 0.59 +/- 0.14%, all p less than 0.05), while potassium excretion and creatinine clearance did not change. In the second phase of the study, patients received 2-hour infusions of anaritide (0.03 to 0.6 micrograms/kg/min) and placebo with noninvasive monitoring.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic and renal effects of atrial natriuretic peptide in congestive heart failure. 213 69

A possible role of the proopiomelanocortin derived peptide gamma 2-melanocyte stimulating hormone (gamma 2-MSH) has been studied in patients with various degrees of congestive heart failure (CHF). The profile of changes in circulating levels of gamma 2-MSH-like immunoreactivity (-LI) has been compared with those of atrial natriuretic peptide (ANP)-LI, arginine vasopressin (AVP)-LI and catecholamines in CHF. Patients with moderate CHF (New York Heart Association stages I-II) showed significantly higher levels of h-alpha ANP-LI and NA (P less than 0.05) compared to controls. Patients with severe CHF (stages III-IV) had significantly higher levels of all hormones measured compared to controls: noradrenaline, P less than 0.001; adrenaline, P less than 0.001; gamma 2-MSH-LI, P less than 0.001; h-alpha ANP-LI, P less than 0.05; AVP-LI, P less than 0.01. For the catecholamines and gamma 2-MSH-LI there was a significant increase from moderate to severe forms of CHF. A significant correlation was observed between gamma 2-MSH-LI and noradrenaline, and between h-alpha ANP-LI and noradrenaline in patients with CHF. The present results show that gamma 2-MSH-LI is increased only in severe forms of cardiac failure, and that this change is more closely related to the increase in circulating levels of noradrenaline than to increased levels of ANP-LI or AVP-LI.
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PMID:Gamma 2-MSH in congestive heart failure: relation to atrial natriuretic peptide, arginine vasopressin and catecholamines. 213 8

We investigated whether or not the extent of secretion of atrial natriuretic peptide (ANP) was altered during the chronic course of aortic regurgitation (AR) in rabbits. AR was induced by aortic valve perforation in 20 rabbits. Left ventricular end-diastolic pressure (LVEDP) was used as an index of the severity of heart failure. LVEDP and plasma immunoreactive(IR)-ANP were measured before and at 15 min, 1 week, and 4 weeks after induction of AR. In each period a correlation between LVEDP and plasma IR-ANP was observed, and the coefficients and covariances did not vary throughout the experiment. We conclude, therefore, that a chronic change in ANP secretion does not develop during the first 4 weeks after induction of AR in rabbits.
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PMID:Atrial natriuretic peptide secretion in rabbits with aortic regurgitation. 213 49

In previous studies, a pharmacological dose of human atrial natriuretic peptide (hANP) was found to increase serum insulin without influencing C-peptide levels. To examine whether blood glucose and insulin response to an oral or i.v. glucose load are influenced by raising hANP levels into the pathophysiological range, eight healthy, normal-weighted, male volunteers were studied. According to a randomized, double-blind study design, an oral glucose tolerance test (ogtt, 75 g) or an i.v. glucose tolerance test (ivgtt, 0.5 g/kg b.w.) were carried out. Beginning 30 minutes before glucose administration infusions of hANP 0.3 micrograms/min) or placebo were given for 180 minutes (ogtt) or 120 minutes (ivgtt). During the hANP-infusions maximal hANP levels were 72 +/- 11 pg/ml (normal less than 25 pg/ml). Responses of blood glucose and C-peptide levels to the glucose load remained unaffected by hANP in both studies. However, hANP increased mean insulin responses (given as area under the curve) by 11.5% in ogtt and by 15.9% in ivgtt (both p less than 0.05). Thus, elevated hANP levels within the pathophysiological range, as observed in chronic heart failure or in hypertension, lead to an increase in serum insulin. Unchanged C-peptide levels demonstrate that hANP does not interfere with insulin secretion, but exclusively inhibits insulin degradation in liver and/or kidney. Further studies are required to elucidate whether these findings play a part in the pathomechanisms of insulin resistance in patients with elevated hANP levels, e.g. in chronic heart failure or hypertension.
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PMID:[The effect of atrial natriuretic peptide on glucose tolerance and insulin level]. 213 3

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 less than 0.01) and BEC (20.6 +/- 3.45 pmol/l, n = 7, P less than 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 less than 0.01) higher compared with that in cattle with BEC. Plasma concentration of ANP correlated significantly with right atrial pressure (r = 0.95, P less than 0.01) and left ventricular end-diastolic pressure (r = 0.84, P less than 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 beta-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 less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bovine atrial natriuretic peptide in heart failure. 213 92

In heart failure, neurohumoral factors are activated, influencing ventricular performance by modulation of pre- and afterload. There is evidence from experimental models of congestive heart failure that in the early phase of the disease the sympathetic nervous system and atrial natriuretic peptide secretion are activated. Despite a reduction in cardiac output, decreased blood pressure and stimulated sympathetic nerve activity, atrial natriuretic peptide seems to be able to significantly suppress the renin-angiotensin-aldosterone system. In later phases of the disease, when more profound circulatory impairment develops, the renin system is activated and peripheral vascular resistance increases and renal blood flow decreases. In very severe heart failure, when dilutional hyponatraemia develops, plasma levels of vasopressin are inappropriately increased by nonosmolar stimuli. At the time the renin system is activated, there is an imbalance between vasodilator and vasoconstrictor mechanisms, favouring vasoconstriction which, completing the vicious circle, leads to deterioration of cardiac function.
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PMID:Interaction between atrial natriuretic peptide, renin system and vasopressin in heart failure. 214 83

The plasma concentration of atrial natriuretic peptide was measured in patients with muscular dystrophies to study its relationship with congestive heart failure. In patients with Duchenne muscular dystrophy, the plasma atrial natriuretic peptide concentration was 35.5 +/- 3.3 pg/mL (mean +/- SE), which was higher than that in age-matched normal subjects (9.8 +/- 0.6 pg/mL). It increased with progression of disability and showed significant correlations with the cardiothoracic ratio and the ratio of the preejection period to the left ventricular ejection time. In patients with other types of muscular dystrophy, the plasma atrial natriuretic peptide concentration showed no significant change. Immunohistochemical examination demonstrated many atrial natriuretic peptide-positive cells in atrial muscle of an autopsied patient, indicating preservation of the peptide until the end stage. These findings suggest that measurement of the plasma atrial natriuretic peptide concentration is useful for evaluating heart failure in patients with Duchenne muscular dystrophy.
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PMID:Secretion and clinical significance of atrial natriuretic peptide in patients with muscular dystrophy. 214 80

Hormonal, renal and blood pressure effects of SCH 39370, a selective inhibitor of neutral metalloendopeptidase (endopeptidase 24.11, NEP), were studied in a chronic, congestive heart failure (CHF) model produced by coronary artery ligation in the rat. Sham-operated control rats and rats with CHF were treated either with vehicle or SCH 39370, 30 mg/kg s.c. b.i.d. for 2.5 days. Plasma levels of atrial natriuretic peptide (ANP) and urinary excretion of cyclic GMP (cGMP) were clearly raised in rats with CHF as compared with controls during vehicle treatment. SCH 39370 caused a further increase in plasma ANP in CHF rats but not in control rats. Urinary excretion of immunoreactive ANP and cGMP increased during SCH 39370 treatment both in CHF rats and in controls. SCH 39370 treatment resulted in an initial increase in urine volume in rats with CHF whereas urine sodium excretion did not change significantly. No changes in renal function due to SCH 39370 treatment were seen in control rats. Systolic blood pressure, plasma renin activity and urine excretion of catecholamine metabolites (4-hydroxy-3-methoxyphenyl acetic acid and metanephrines) did not change during SCH 39370 treatment either in controls or in CHF rats. We conclude that the NEP-inhibitory compound SCH 39370 is capable of increasing plasma ANP concentration and urinary excretion of cGMP in rats with chronic CHF. In this severe heart failure model, the possible beneficial effects of additional ANP increments may be blunted, however. NEP inhibitors offer a novel approach to study the significance of ANP elevation in chronic CHF.
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PMID:Elevation of plasma atrial natriuretic peptide in rats with chronic heart failure by SCH 39370, a neutral metalloendopeptidase inhibitor. 214 36

The aim of the present study was to determine whether left atrial size--a likely indicator of atrial stretching--correlates with the plasma concentration of atrial natriuretic peptide and whether this relation is different in patients in sinus rhythm and in those with atrial fibrillation. Arterial plasma concentrations of immunoreactive atrial natriuretic peptide (ir-ANP), adrenaline, noradrenaline, aldosterone, and vasopressin were measured in 13 patients in sinus rhythm without apparent heart failure and in 13 patients in atrial fibrillation. The two groups were matched for left atrial diameter and the ratio of the left atrial diameter to the diameter of the aortic root (assessed by echocardiography). There were no significant differences in age, heart rate, blood pressure, or left ventricular end diastolic diameter between the two groups. Left atrial diameters varied from 33 to 60 mm. The mean (SD) plasma concentration of ir-ANP was significantly higher (35 (21) pmol/l) in the patients with atrial fibrillation than in those in sinus rhythm (12 (11) pmol/l). The concentration of plasma aldosterone was also higher in patients with atrial fibrillation (831 (366) v 523 (211) pmol/l). Concentrations of adrenaline, noradrenaline, and vasopressin were similar in both groups. None of the hormone concentrations correlated with left atrial dimensions. These results indicate that plasma concentrations of ir-ANP and aldosterone are highly sensitive indicators of changes in haemodynamic function during atrial fibrillation. They also underscore the difficulties of correlating echocardiographic assessment of patients with plasma concentrations of a vasoactive hormone.
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PMID:Raised plasma concentrations of atrial natriuretic peptide are independent of left atrial dimensions in patients with chronic atrial fibrillation. 214 16

Several reports have demonstrated a close correlation between plasma atrial natriuretic peptide (ANP) concentration and atrial pressure in stable heart diseases. However, few studies have investigated whether plasma ANP concentration is a noninvasive indicator of hemodynamic parameters during the treatment of heart failure. Thus, we have studied the relationship between peripheral plasma ANP concentration and concurrent hemodynamic variables during the treatment of heart failure, and, in order to determine whether secretion of ANP is stimulated in this disease condition, we compared the plasma ANP concentration in the pulmonary artery with that in the peripheral veins. Studies were performed in each of 9 patients with acute heart failure due to myocardial infarction (Group A) or chronic heart failure (Group B), who were matched as closely as possible for treatment, age, sex and cardiac output. In group A, no significant correlation was found between plasma ANP levels and any measured hemodynamic variables. In group B, peripheral plasma ANP concentrations were significantly correlated with left atrial pressure (r = 0.82, p less than 0.01), but not with right atrial pressure (r = 0.56, p greater than 0.05). Furthermore, in group B ANP levels in pulmonary arterial plasma were consistently higher than those in peripheral venous plasma, whereas in group A the opposite was observed in expired cases. These results suggest that measurement of peripheral plasma ANP is a useful noninvasive method for estimating left atrial pressure during the treatment of chronic heart failure. However, plasma ANP concentration may not be a valid means of estimating hemodynamic parameters in acute heart failure due to myocardial infarction. In such cases, the increased secretion of ANP was not obvious, and there may be other factors, in addition to atrial pressure, that regulate cardiac secretion of ANP.
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PMID:Relationship between plasma atrial natriuretic peptide concentration and atrial pressure in acute and chronic heart failure. 214 22


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