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)

Synthetic human brain natriuretic peptide (sBNP) is a polypeptide with the same amino acid sequence as the naturally occurring hormone. Preclinical studies have demonstrated that BNP has potent hemodynamic, diuretic, and natriuretic effects that might be beneficial in treating patients with heart failure. This study was a randomized, double-blind, placebo-controlled, ascending-dose trial of sBNP administered as a single intravenous bolus in 27 heart failure patients. Six groups of patients received sequentially increasing doses of sBNP (0.3, 1, 3, 10, 15, and 20 micrograms/kg, respectively) as a single intravenous injection, and hemodynamics were assessed by pulmonary artery monitoring catheter. The 10 and 15 micrograms/kg doses of sBNP resulted in significant reductions in pulmonary capillary wedge pressure (-73%, p < 0.001), mean pulmonary artery pressure (-41%, p < 0.001), mean arterial blood pressure (-28%, p = 0.001), and systemic vascular resistance (-53%, p = 0.004). Significant increases occurred in cardiac index (68%, p < 0.001) and stroke volume index (72%, p < 0.001). The magnitude and duration of hemodynamic changes were dose dependent. There were no adverse effects. sBNP injected as a single intravenous bolus in heart failure patients improves hemodynamics in a dose-related fashion. Further clinical investigations to determine the use of sBNP in decompensated heart failure are clearly warranted.
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PMID:Hemodynamic effects of a single intravenous injection of synthetic human brain natriuretic peptide in patients with heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. 888 62

Xinshuaikang (XSK) granule mainly consisted of Radix Ginseng, Aconifum carmichaeli, Ligustici wallichii, Semen Lepidii seu Descurainiae, etc. Thirty-five white rabbits of Japanese strain with big ears were used and five groups were divided randomly. The models of chronic heart failure (CHF) was made by injection of adriamycin through the marginal vein of rabbit's ear. Only one group without adriamycin injection was taken as blank group. After the making of models, Xinbao (XB) was used to treat one group which was regarded as control group, XSK was used to treat two model groups, one used higher dose, the other one used lower dose. Fifteen days was taken as a course of treatment. The results were: the body weight of all model groups was heavier than that without adriamycin. After a course of treatment, the body weight of the groups treated by XSK or XB decreased rapidly, the general conditions of the three groups were improved; the two drugs could reduce heart rate and enhance heart function, at the same time they reduced the level of atrial natriuretic polypeptide (ANP) in plasma. The best results was obtained in XSK group with higher dose, the effect of XSK group with lower dose was equivalent to that of XB group. Hence, XSK granule could enhance the CHF rabbits' heart function, improve their heart endocrine activity, this drug had a reliable effect on CHF.
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PMID:[Effects of xinshuaikang granule on cardiac function and atrial natriuretic polypeptide levels in rabbits with experimental congestive heart failure]. 938 39

Increased peripheral vascular tone is a critical factor in the deterioration of clinical stage and symptoms in chronic congestive heart failure (CHF) because of increased cardiac afterload and decreased nutritive skeletal muscle blood flow. Endothelial function as represented by nitric oxide (NO) production shows significant attenuation with the progression of clinical severity of CHF as determined by New York Heart Association class and exercise capacity parameters. This endothelial dysfunction emerges in the early stages of CHF. In the advanced stage of the condition, both endothelium-dependent and endothelium-independent dilator mechanisms are impaired in limb resistance vessels. This occurs because vascular endothelial function, especially NO production, is an important factor in the regulation of vasodilatory function, as well as making an important contribution to vascular structure. Furthermore, although such vasodilatory circulating factors as natriuretic polypeptides and newly discovered adrenomedullin are increased in heart failure, the vasodilatory potency of these polypeptide hormones in the limb vascular bed is significantly blunted. These observations suggest that peripheral circulatory failure in CHF is caused not only by simple arterial muscle constriction, but also by structural and functional changes, including receptor and postreceptor levels in the vasculature. This vascular remodeling may be an important mechanism underlying vasodilatory failure in both limb conduit and intraskeletal muscle vessels and may contribute significantly to left ventricular dysfunction and exercise intolerance in patients with heart failure.
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PMID:Peripheral vascular remodeling in chronic heart failure: clinical relevance and new conceptualization of its mechanisms. 1040 52

Ten years ago brain natriuretic peptide (BNP), the second compound of a family of polypeptide hormones named natriuretic peptides was identified. This peptide has great pathophysiologic importance as a stress-induced cardiac hormone secreted from ventricles, and it rises in several cardiac diseases. It promotes natriuresis and diuresis, acts as a vasodilator, and antagonizes the vasoconstrictor effects of the renin-angiotensin-aldosterone system. The measurement of this peptide in blood by immunoassay has shown promise over the past decade in clinical diagnosis and prognosis. Because heart failure is a major health problem worldwide, BNP is proposed as a biochemical marker that might provide a useful screening test to select patients for further cardiac investigations. Such a hormone assay is inexpensive and available. The implications of BNP in diagnosis, prognosis, and therapy will be reviewed.
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PMID:Review of 10 years of the clinical use of brain natriuretic peptide in cardiology. 1056 Sep 35

Postnephrectomy renal arteriovenous fistula (AVF) with an aneurysmal lesion is a rare clinical entity that may cause high-output heart failure. In this report, we describe the case of a 68-year-old man who had undergone nephrectomy for renal tuberculosis 43 years previously, in whom an acquired large renal AVF presenting as an aneurysm caused congestive cardiac failure. We also discuss the hemodynamic, hormonogenic (human arterial natriuretic polypeptide; hANP), and radiographic findings before and after surgery for the AVF. The AVF with an aneurysmal lesion was clearly visualized by three-dimensional-computerized tomographic (CT) scanning, and proximal ligation of the renal artery was followed by an uneventful recovery. This procedure can produce good results when a fistula is too large to allow safe embolization and when excision would be hazardous due to inflammation surrounding the fistula.
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PMID:High-output heart failure caused by a huge renal arteriovenous fistula after nephrectomy: report of a case. 1138 17

The mechanism and treatment of hypertensive systolic heart failure are not well defined. We compared the effect of an angiotensin-converting enzyme inhibitor (cilazapril, 10 mg/kg), an angiotensin receptor blocker (candesartan, 3 mg/kg), a calcium channel blocker (benidipine, 1, 3 or 6 mg/kg), and the same calcium channel blocker combined with renin-angiotensin blockers on systolic heart failure in Dahl salt-sensitive (DS) rats. DS rats were fed an 8% Na diet from 6 weeks of age and then subjected to the above drug treatments. Benidipine (1 mg/kg), cilazapril, and candesartan had compatible hypotensive effects and similar beneficial effects on cardiac hypertrophy, gene expression, and survival rate. The combination of benidipine with cilazapril or candesartan was found to have no additional beneficial effects on the above parameters, with the exception of a reduction in atrial natriuretic polypeptide gene expression. On the other hand, candesartan normalized serum creatinine, but serum creatinine was unaffected by either benidipine at 1 or 3 mg/kg or cilazapril. Further, the combined use of benidipine and either candesartan or cilazapril resulted in an additional reduction of urinary albumin excretion in DS rats. Thus systolic heart failure in DS rats is mainly mediated by hypertension, while renal dysfunction of DS rats is due to both hypertension and the AT1 receptor itself. These findings suggest that the combination of a calcium channel blocker with an AT1 receptor blocker or ACE inhibitor may be more effective in treating the renal dysfunction associated with systolic heart failure than monotherapy with either agent alone. However, further studies will be needed before reaching any definitive conclusion on the efficacy of this combination therapy in patients with heart failure.
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PMID:Combination treatment with a calcium channel blocker and an angiotensin blocker in a rat systolic heart failure model with hypertension. 1213 27

IGF-I and IGF-II are single-chain polypeptide growth factors that regulate pleiotropic cellular responses. We have characterized the effect of recombinant IGF proteins, as well as third-generation adenoviral vectors encoding either IGF-I or IGF-II genes, on cardiomyocyte apoptosis and on angiogenesis. We found that endothelial cells cultured in the presence of the extracellular protein laminin exhibit a robust response to IGF-I and -II proteins via enhanced cell migration and angiogenic outgrowth. Furthermore, IGF vectors greatly enhanced neovascularization in an in vivo Matrigel model. Transduction of cardiomyocytes with the IGF adenoviral vectors resulted in a dose- and time-dependent increase in the expression of IGF-I or IGF-II protein. This correlated with abrogation of apoptosis induced by ischemia-reoxygenation, ceramide, or heat shock with optimal inhibition of approximately 80%. We conclude that gene transfer of IGF-I and IGF-II is a plausible strategy for the local delivery of IGFs to treat ischemic heart disease and heart failure by stimulating angiogenesis and protecting cardiomyocytes from cell death.
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PMID:Gene therapy vector-mediated expression of insulin-like growth factors protects cardiomyocytes from apoptosis and enhances neovascularization. 1250 77

Atrial natriuretic peptide (ANP) is a polypeptide hormone found in increased concentrations in the plasma of dogs with heart failure. However, problems arise in using ANP as a diagnostic marker for heart failure because of its short half-life in plasma, proteolysis post-collection and the necessity for a radioimmunoassay. The diagnostic utility of a proANP 31-67 ELISA for the detection of heart failure in dogs was evaluated using plasma collected from 31 dogs with clinical and radiographic signs of heart failure and control samples from 40 dogs considered to be free of cardiac disease. Log proANP 31-67 levels were significantly higher in the heart failure group (P < 0.001). In this population of dogs, using a cut-off value of 1,750 fmol/ml, the sensitivity and specificity of the assay were 83.9 per cent and 97.5 per cent, respectively. Using a cut-off of 1,350 fmol/ml, the sensitivity and specificity were 93.5 per cent and 72.5 per cent, respectively. It is concluded that a proANP 31-67 fragment ELISA should prove to be a useful diagnostic aid in naturally occurring canine heart failure.
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PMID:Clinical validation of a proANP 31-67 fragment ELISA in the diagnosis of heart failure in the dog. 1265 23

The omnipresent 6kDa polypeptide relaxin (RLX) is emerging as a multi-functional endocrine and paracrine factor, with a broad range of target tissues that includes the cardiovascular system. Humans and other higher primates have three RLX genes, designated H1, H2 and H3, of which H2 RLX is the major stored and circulating form. Rodents have only two RLX genes: relaxin-1 (equivalent to H2 RLX) and relaxin-3 (equivalent to H3 RLX). The recent cloning of the human RLX receptor (LGR7), a member of the leucine-rich repeat family of G-protein-coupled orphan receptors, and detection of LGR7 gene transcripts in the heart confirm this organ as a target for RLX (H2). However, evidence for production of the ligand within the cardiovascular system is limited, and few studies have clearly identified the physiological effects of RLX on cardiac function. To add to the controversy, serum concentrations and expression of RLX in the heart are elevated in chronic heart failure patients and animal models of cardiomyopathy, implying that RLX may only be a marker for pathological cardiovascular conditions, rather than normal physiology.
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PMID:Physiological or pathological--a role for relaxin in the cardiovascular system? 1268 Dec 37

Abstract B-natriuretic peptide (BNP) is a 32-amino acid polypeptide secreted from the cardiac ventricles in response to ventricular volume expansion and pressure overload. BNP levels are elevated in patients with symptomatic left ventricular dysfunction, and levels correlate with severity of symptoms and with prognosis. Numerous studies indicate that BNP may considerably improve the management of patients with heart failure and may become a routine serum parameter in clinical medicine. In this review, the utility of BNP in different clinical settings will be discussed.
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PMID:[B-type natriuretic peptide--current use in the diagnosis and management of heart failure]. 1292 36


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