Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

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

1. Whereas many studies have detailed the effects of exogenous atrial natriuretic peptide (ANP) infusions in heart failure, and a limited number have examined the effects of brain natriuretic peptide (BNP), none have directly compared the bioactivity of similar doses of ANP and BNP under standard conditions of impaired cardiac function. We compared the hormonal, haemodynamic and renal effects of 3 h infusions of ANP, BNP and a vehicle control in eight sheep with pacing-induced heart failure (225 beats/min for 8-12 days). 2. Infusion of ANP and BNP increased plasma ANP (P < 0.001) (276 +/- 27 versus control 142 +/- 26 pmol/l) and BNP (P < 0.001) (257 +/- 34 versus control 45 +/- 5 pmol/l) respectively, in association with increased cyclic 3',5'-guanosine monophosphate [control, 40 +/- 6; ANP, 53 +/- 6 (P < 0.05); BNP, 57 +/- 7 nmol/l (P < 0.001)]. Metabolic clearance rate and half-life were similar for both peptides. Infusion of ANP and BNP similarly reduced mean arterial pressure [control, 73.0 +/- 1.6; ANP, 67.6 +/- 1.2 (P < 0.01); BNP, 65.7 +/- 1.7 mmHg (P < 0.001)], left atrial pressure (both P < 0.05) (control, 22.0 +/- 0.7; ANP, 19.9 +/- 1.0; BNP, 19.8 +/- 0.9 mmHg) and peripheral resistance [control, 50.3 +/- 4.1 mmHg l-1 min-1; ANP, 46.0 +/- 2.8 (P < 0.05); BNP, 43.8 +/- 4.5 (P < 0.01)], and increased urine volume (2-3-fold, both P < 0.05), sodium excretion (> 10-fold, both P < 0.01) and haematocrit levels relative to control (both P < 0.05). Infused BNP tended to raise plasma ANP levels (by 28 pmol/l), while ANP increased plasma BNP (by 18 pmol/l). Plasma aldosterone was reduced by approximately 40% by both peptides (both P < 0.05). 3. In conclusion, ANP and BNP are both powerfully, natriuretic, similarly suppress aldosterone and appear equipotent in reducing preload and afterload in this model of pacing-induced heart failure.
...
PMID:Comparative bioactivity of atrial and brain natriuretic peptides in an ovine model of heart failure. 905 17

Cardiac index is widely used as a parameter of cardiac function for cardiovascular patients, but its value is limited when measured in the resting supine position, because it never demonstrates the maximal cardiac index performance. The incremental increase in cardiac index (delta CI) was evaluated during incremental exercise (delta work rate: delta WR), delta CI/delta WR, in patients with chronic congestive heart failure, and compared to brain natriuretic peptide (BNP), which is known to be increased in patients with chronic left ventricular dysfunction. The subjects were 18 heart failure patients (16 males and 2 females, mean age [+/-SD] 63.8 +/- 8.9 years). Symptom-limited cardiopulmonary exercise test using cycle ergometer was performed. Cardiac index was calculated with the Benchmark Exercise Test device using oxygen uptake, carbon dioxide output and respired flow. Blood samples were taken in the resting state before the exercise test. A positive correlation was obtained between delta CI/delta WR and peak oxygen uptake (peak VO2) (r = 0.71, p < 0.01), and delta CI/delta WR and peak oxygen pulse (r = 0.66, p < 0.01). A negative correlation was obtained between delta CI/delta WR and BNP (r = 0.45) in the resting state. Peak VO2 (20.9 +/- 7.5 vs 13.9 +/- 2.7 ml/min/kg, p < 0.05), peak cardiac index (7.2 +/- 1.7 vs 5.5 +/- 0.9 l/min/m2, p < 0.05), and delta CI/delta WR (20.1 +/- 8.1 vs 12.4 +/- 2.5 ml/m2/W, p < 0.05) were significantly higher in the group with normal BNP (mean [+/-SD] 11.0 +/- 3.2 pg/ml) than in the group with high BNP (40.7 +/- 22.7 pg/ml). Delta CI/delta WR reflects the grade of exercise tolerance and may be useful for evaluating exercise capacity in patients with congestive heart failure.
...
PMID:[Efficacy of increase of cardiac index during exercise in the chronic phase of various cardiovascular diseases: evaluation by exercise tolerance and brain natriuretic peptide]. 909 45

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are known to be elevated in patients with chronic heart failure at rest. While it is known that during exercise the circulating level of ANP increases in patients with heart failure, the response of BNP to exercise in these patients relative to control subjects is unclear. Ten patients with stable chronic heart failure and 10 normal control subjects performed symptom-limited exercise with respired gas analysis. All patients had depressed left ventricular ejection fractions (LVEF). Patients had lower peak oxygen consumption PVo2) than the control group [median (range) 1.18 (0.98-1.76) vs. 1.94 (1.53-2.31) L min-1; P < 0.001]. Circulating plasma levels of ANP and BNP were higher at rest in patients than in control subjects [ANP 335 (140-700) vs. 90 (25-500) pg mL-1; BNP 42 (25-50) vs. 20 (10-20) pg mL-1], and at peak exercise [ANP 400 (200-1000) vs. 130 (10-590); BNP 46 (40-51) vs. 20 (10-30)]. The rise in ANP at peak exercise was significant in patients compared with the resting level, but not in control subjects. For BNP, there was a significant rise in patients but no change in control subjects. The circulating plasma levels of both peptides showed a strong negative correlation with LVEF (ANP, P < 0.005; BNP, P < 0.0001) and, to a less extent, with RVEF. It is possible that BNP may give a better indication of cardiac function.
...
PMID:Responses of atrial natriuretic peptide and brain natriuretic peptide to exercise in patients with chronic heart failure and normal control subjects. 913 74

The level of plasma brain natriuretic peptide (BNP) was elevated in 8 of 15 female gene carriers of Duchenne muscular dystrophy (DMD), and the level correlated with indices of cardiac function. In one of these carriers, whose clinical course was followed for one year, the plasma BNP level was elevated before the development of cardiac symptoms, further increased with the evolution of cardiac symptoms, and then decreased after treatment for cardiac failure. These results suggest that the plasma BNP level may be useful for the early detection of cardiac dysfunction and for evaluating the efficacy of cardiac treatment in female DMD carriers.
...
PMID:Plasma levels of brain natriuretic peptide as an index for evaluation of cardiac function in female gene carriers of Duchenne muscular dystrophy. 924 May

Various alterations in the natriuretic peptide system have been observed in heart and plasma in humans and animals with heart failure. However, there is limited information about these hormones in hamster lung especially in those with genetic cardiomyopathy, a model of human congestive heart failure. Therefore, the aim of the present study was to investigate the content of the three natriuretic peptides (atrial natriuretic peptide (ANP); brain natriuretic peptide (BNP); C-type natriuretic peptide (CNP) and their gene expression in lungs of normal and cardiomyopathic hamsters. The presence of mRNA coding for ANP and BNP in lungs and heart was investigated by Northern blot and confirmed by reverse transcription polymerase chain reaction (RT-PCR). The peptide contents and plasma concentrations were determined by specific radioimmunoassays. Plasma ANP increased in hamsters with moderate to severe cardiomyopathy (aged 230 days) from control levels of 71.8+/-15.8 to 243.1+/-44.0 pg/ml (P < 0.01). Plasma BNP also increased from 79.7+/-23.5 to 227.9+/-51.6 pg/ml (P < 0.01). The levels of the three peptides in lungs of 30- and 120-day-old cardiomyopathic (CMO) hamsters were not different from their corresponding age-matched controls. However, lung ANP increased in 230-day-old CMO from 589+/-63 to 1624+/-219 pg/mg protein (P < 0.01). Lung BNP and CNP also increased from 332+/-35 to 531+/-55 pg/mg protein (P < 0.01) and from 118+/-21 to 224+/-29 pg/mg protein (P < 0.01), respectively. Lung ANP mRNA and BNP mRNA were significantly (P < 0.05) higher in 230-day-old hamsters than those detected in age-matched normal controls. Our data demonstrate that the hamster lungs produce ANP, BNP and CNP, and that this production is enhanced in moderate to severe cardiomyopathy. These findings imply that the lung natriuretic peptide system may participate in pulmonary function especially during cardiac dysfunction.
...
PMID:Elevated levels of natriuretic peptides in lungs of hamsters with genetic cardiomyopathy. 925 May 83

The level of tumor necrosis factor alpha (TNF-alpha) is increased in patients with congestive heart failure and may play an important role in the development and progression of heart failure. Two types of TNF receptor (TNF-RI and TNF-RII) are expressed in virtually every cell and have different biologic roles. Soluble forms of the two receptors (sTNF-RI and sTNF-RII) have been identified as extracellular domain fragments. Serum levels of TNF-alpha, sTNF-RI and sTNF-RII were measured in 66 patients with heart failure and 27 control subjects using an enzyme-linked immunosorbent assay (ELISA). Hemodynamic variables, norepinephrine, atrial natriuretic peptide (ANP), and brain natriuretic peptide (BNP) were evaluated. TNF-alpha was significantly higher in patients with heart failure than in controls subjects (9.4 +/- 1.4 vs 4.8 +/- 0.8 pg/ml; p < 0.05). sTNF-RI and -RII were significantly increased in relation to the severity of heart failure (control subjects, 0.66 +/- 0.04 and 1.97 +/- 0.15 ng/ml; NYHA class II, 1.10 +/- 0.08 and 2.28 +/- 0.12 ng/ml; NYHA class III, 1.63 +/- 0.22 and 3.00 +/- 0.24 ng/ml; NYHA class IV, 2.78 +/- 0.46 and 4.52 +/- 0.62 ng/ml, respectively). In 9 patients whose clinical symptoms improved after treatment, the levels of sTNF-RI and -RII decreased by 17.3 +/- 5.7% (p < 0.05) and 22.1 +/- 6.9% (p < 0.05), respectively. There were significant positive correlations between sTNF-RI and -RII and mean pulmonary pressure (r = 0.69 and r = 0.61; p < 0.001) and mean capillary wedge pressure (r = 0.65 and r = 0.54; p < 0.001 and p < 0.01, respectively), but not with left ventricular end-diastolic volume or ejection fraction (NS). sTNF-RI and -RII were also significantly positively correlated with plasma levels of norepinephrine (r = 0.75 and r = 0.50; p < 0.001 and p < 0.05), ANP (r = 0.72 and r = 0.70; p < 0.001), and BNP (r = 0.60 and r = 0.60; p < 0.001). In conclusion, soluble TNF receptors are increased in proportion to the severity of congestive heart failure and may reflect the current status of congestive heart failure rather than the level of left ventricular dysfunction.
...
PMID:Soluble tumor necrosis factor receptors are elevated in relation to severity of congestive heart failure. 927 70

Natriuretic peptide system consists of three endogenous ligands, ANP (atrial natriuretic peptide), BNP (brain natriuretic peptide) and CNP (C-type natriuretic peptide), and three receptor subtypes, natriuretic peptide receptor (NPR)-A or guanylate cyclase (GC)-A and NPR-B or GC-B and C receptor (NPR-C). ANP and BNP are mainly secreted from the atrium and ventricle of the heart respectively to act as cardiac hormones whereas CNP is secreted from the endothelium to act as an endothelium-derived relaxing peptide. ANP and BNP regulate body fluid and blood pressure to reduce cardiac pre- and after-load. Recent molecular biology and developmental biotechnology demonstrated the physiological role of ANP and BNP for the determination of basal blood pressure. CNP can modulate the phenotype of vascular smooth muscle cells to regulate vascular remodeling. Therefore, natriuretic peptide system is implicated in the pathophysiology of hypertension, congestive heart failure atherosclerosis and renal diseases. Clinical application of natriuretic peptide system is actively going on progress. Determination of plasma ANP and BNP levels are useful for the evaluation of congestive heart failure, cardiac hypertrophy and acute myocardial infarction. Infusion of ANP improves acute heart failure. Application of NEP (neutral endopeptidase) inhibitor for the treatment of congestive heart failure and hypertension is under clinical trial.
...
PMID:[Natriuretic peptide system]. 928 3

Plasma levels of brain natriuretic peptide (BNP) are raised in patients with left ventricular impairment and may play a role in the adaptation to left ventricular impairment. Manipulation of BNP levels may have therapeutic potential. The effects of BNP have not been well studied in patients with left ventricular impairment. We studied the effects of low-dose BNP infusion, reproducing the increment in plasma BNP seen with progression from mild to severe heart failure in patients with impaired left ventricular systolic function. BNP was infused in a placebo-controlled, single-blind, crossover design at a rate of 3.3 pmol x kg(-1) x min(-1) over 4 hours to 8 patients with a history of congestive heart failure and persistent impairment of left ventricular systolic function (left ventricular ejection fraction <35%). Endocrine, renal, and hemodynamic effects were measured. Compared with time-matched placebo-control, BNP infusion decreased mean systemic arterial pressure (peak decrease, 17.1 mm Hg; P=.04), mean pulmonary artery pressure (peak decrease, 6.1 mm Hg; P=.007), mean pulmonary capillary wedge pressure (peak decrease, 5.5 mm Hg; P=.04), and systemic vascular resistance (peak decrease, 1400 dyne s(-1) cm(-5); P=.015), but cardiac output and heart rate were unchanged. Urinary volume and urinary excretion of sodium and potassium were not altered. BNP infusion increased plasma cGMP (2.3-fold change, P=.002). Plasma atrial natriuretic peptide levels were increased for the first hour of BNP infusion (peak increase, 11.5 pmol/L; P=.005). Plasma aldosterone levels were unchanged during but increased over time-matched control levels after the end of the BNP infusion (peak increase, 90 pmol/L; P=.02). Plasma renin activity and cortisol and catecholamine levels were unchanged. Low-dose infusion of BNP causes favorable hemodynamic changes and relative neurohormonal suppression but has attenuated renal effects in patients with impaired left ventricular systolic function.
...
PMID:The effects of pathophysiological increments in brain natriuretic peptide in left ventricular systolic dysfunction. 931 23

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are homeostatic hormones secreted from the human heart which protect both cardiac and the renal function. It is well known that these hormones increase in patients along with increases in the severity of congestive heart failure or acute myocardial infarction. However, as yet there are no reports in the literature on changes of the secreted level of ANP or BNP in surgical patients undergoing cardiopulmonary bypass (CPB). We evaluated the relationship between ANP, BNP, and perioperative cardiac and renal functions in patients with heart failure caused by CPB. We selected 45 patients of elective open heart surgery. We measured plasma level of ANP in all 45 cases, and BNP in 18 cases at preoperation, postoperation, and postoperatively three days after, respectively. At the same time, the cardiac index (CI) was measured. These cases were divided into the following groups. Group A1 (n = 23): cases in which the preoperative ANP was less than 40 pg/ ml. Group A2 (n = 22): cases in which the preoperative ANP was more than 40. Group B1 (n = 8): cases in which the preoperative BNP is increased to the level of 5 times as mach as the normal level. Group B2 (n = 8): cases in which the preoperative BNP is increased to the level of 5 times as much as the normal level. Group B2 (n = 10): cases in which the preoperative BNP was more than that of 10 times as mach as normal level. We then carried out a comparative study of the perioperative cardiac and renal functions in group A1 and A2, and group B1 and B2, respectively. In the terms of preoperative cardiac and renal function, there were no significant differences between groups A1 and A2, and there were no significant differences in urinary volume during CPB or post operative CI. However, the urinary volume during CPB of group B1 was significantly more than that of B2. Furthermore, the incidence of postoperative CI in group B1. Furthermore, the incidence of postoperative CI in group B1 was significantly higher than in B2. The preoperative and post operative third day BNP level had significant negative correlations with postoperative CI and postoperative third day CI, respectively (r = -0.641, -0.514, p = 0.008, 0.012). The postoperative ANP and BNP levels tend to a mean level roughly similar to one another because of the easing of cardiac stress by surgery and postoperative management. According to these results and several instances in the literature, a preoperative high BNP is considered to suggest a potential perioperative risk for cardiac and renal function. We conclude that determination of the plasma BNP level can be helpful for decisions related to CPB flow and measures taken to enhance cardiac and renal protection during surgery, and therefore is a useful reference for perioperative management.
...
PMID:[A correlation between atrial natriuretic peptide, brain natriuretic peptide, and perioperative cardiac and renal functions in open heart surgery]. 943 Sep 55

We examined for the first time the specific roles of angiotensin II and the natriuretic peptides during inhibition of angiotensin-converting enzyme (captopril, 25 mg bolus + 6 mg/3 h infusion) and endopeptidase 24.11 (SCH32615, 5 mg/kg bolus + 3 mg/kg/3 h infusion), both separately and in combination, in eight sheep with pacing-induced heart failure. Plasma atrial and brain natriuretic peptide levels were similarly increased by SCH32615 and to a lesser extent during combined inhibition but decreased with captopril. Captopril and combined inhibition induced identical increases in plasma renin activity and reductions in angiotensin II, whereas neither was changed by SCH32615 alone. Mean arterial pressure and peripheral resistance decreased during SCH32615 and further still during captopril and combined treatment. Left atrial pressure was reduced to a similar extent by SCH32615 and captopril alone and reduced further by combined inhibition. Cardiac output increased during all treatments. Urine volume and sodium excretion were significantly increased during SCH32615 and combined inhibition. Creatinine clearance increased during SCH32615, decreased during captopril, and was maintained during combined treatment. In conclusion, compared with captopril alone, cotreatment with an endopeptidase 24.11 inhibitor further improved filling pressures and induced a diuresis and natriuresis with preservation of renal glomerular filtration.
...
PMID:Combined neutral endopeptidase and angiotensin-converting enzyme inhibition in heart failure: role of natriuretic peptides and angiotensin II. 945 86


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---