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

Long-lasting problem on the differentiation of adenohypophyseal cell, which prepares them for their specific tasks (somatotropic, lactotropic ect.), becomes elucidated after recognition of the differentiational effect of transcription factor Pit-1. Expression of that factor in somatotrops results in STH secretion, contrary to lactotrops producing prolactin. Subclinical hypothyreosis (increased TSH with normal T3 and T4) endangers vessel not because of hypercholesterolemia, but because of changes in the dynamics of the blood flow. The idea of cardiotropic effect of thyroidal hormones is supported by the finding that administration of trijodthyronine to children after the surgical correction of heart malformations (cardiopulmonary bypass) improves myocardial function--it elevates cardiac output and decreases requirements on the intensive care. Receptors for hormones in tissues are flexible, they can be "heterooligomers" for dopamine and somatostatin. Mutations of mineralocorticoid receptor may cause hypertension in pregnancy and progesterone receptors have several isoforms. Receptors can be also activated by short exposition to a hormone. Glucocorticoids have probably also membrane receptors. Diabetes mellitus "type I" needn't to be immunogenic and DM type II not only results from down-regulation of receptors and subsequent insulin resistance, but it can be also caused by defects in insulin secretion. Insulin has receptors in the brain and participates in the appetite regulation. The attempt to use "desensibilisation" by peroraly administered insulin in patients with immunogenic DM had no effect. Stress affects memory mechanisms, heavy emotional stress during gravidity can bring congenital malformations. The decrease of mental functions in aged women depends on the level of free estradiol (the fraction, which is not bound to plasma proteins). Activation of dopaminergic neurons can be achieved by neurotropic growth factors. Nesiritide is a recombinant brain natriuretic hormone successfully tested in heart failure. The role of leptin in the appetite regulation in man is still not clear, other signalling molecules may have also an effect, e.g., ghrelin, which primarily stimulates STH secretion and brings about weight gain. Sildenafil influences nitrergic neurons elsewhere than in penis, for example it has positive effects in patients with oesophageal achalasia.
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PMID:[Endocrinology 1999-2000]. 1128 21

Ghrelin is a novel GH-releasing peptide that may also induce vasodilation and a positive energy balance through GH-independent mechanisms. However, the hemodynamic, renal, and hormonal effects of ghrelin in patients with chronic heart failure (CHF) remain unknown. Accordingly, 12 patients with CHF were given an iv infusion of human ghrelin (0.1 microg/kg.min) or placebo. Ghrelin significantly decreased mean arterial pressure (-9 mm Hg, P < 0.05) without a significant change in heart rate. Ghrelin significantly increased cardiac index (+25%, P < 0.05) and stroke volume index (+30%, P < 0.05), although it did not significantly alter mean pulmonary arterial pressure or pulmonary capillary wedge pressure. Infusion of ghrelin induced a marked increase in serum GH level (15-fold), associated with slight increases in circulating epinephrine, ACTH, cortisol, and PRL. Infusion of ghrelin did not significantly alter urine volume, urinary sodium excretion, or creatinine clearance. These hemodynamic, renal and hormonal parameters remained unchanged during placebo infusion. In summary, iv infusion of ghrelin, a potent GH-releasing peptide, had beneficial hemodynamic effects in patients with CHF in the absence of renal effects.
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PMID:Hemodynamic, renal, and hormonal effects of ghrelin infusion in patients with chronic heart failure. 1173 51

Ghrelin is a novel growth-hormone-releasing peptide isolated from the stomach that has been identified as an endogenous ligand for the growth-hormone secretagogue receptor. This peptide results in a positive energy balance by stimulating food intake and inducing adiposity through growth-hormone-independent mechanisms. In addition, ghrelin has several cardiovascular effects, as indicated by the presence of its receptor in blood vessels and ventricles of the heart. Infusion of ghrelin decreases systemic vascular resistance and increases cardiac output in patients with heart failure. Furthermore, repeated administration of ghrelin improves cardiac structure and function, and attenuates the development of cardiac cachexia in rats with heart failure. These results suggest that ghrelin has therapeutic potential in the treatment of severe chronic heart failure.
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PMID:Ghrelin improves left ventricular dysfunction and cardiac cachexia in heart failure. 1268 Dec 36

Ghrelin is a novel growth hormone (GH)-releasing peptide, isolated from the stomach, which has been identified as an endogenous ligand for growth-hormone secretagogues receptor (GHS-R). This peptide also causes a positive energy balance by stimulating food intake and inducing adiposity through growth hormone-independent mechanisms. In addition, ghrelin has some cardiovascular effects, as indicated by the presence of its receptor in blood vessels and the cardiac ventricles. In vitro, ghrelin inhibits apoptosis of cardiomyocytes and endothelial cells. In humans, infusion of ghrelin decreases systemic vascular resistance and increases cardiac output in patients with heart failure. Repeated administration of ghrelin improves cardiac structure and function and attenuates the development of cardiac cachexia in rats with heart failure. These results suggest that ghrelin has cardiovascular effects and regulates energy metabolism through GH-dependent and -independent mechanisms. Thus, administration of ghrelin may be a new therapeutic strategy for the treatment of severe chronic heart failure (CHF).
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PMID:Ghrelin, a novel growth hormone-releasing peptide, in the treatment of chronic heart failure. 1283 93

We provide the first evidence for the existence in human plasma of peptides derived from the 66 carboxyl-terminal amino acids of pro-ghrelin (C-ghrelin). C-ghrelin immunoreactivity in plasma was higher than ghrelin, and did not significantly correlate with body mass index in normal health. In patients with myocardial infarction, plasma levels of both ghrelin and C-ghrelin were significantly decreased (approximately 30%, P<0.05), whereas in patients with heart failure, C-ghrelin levels were significantly elevated (approximately 32%, P<0.05) compared with controls. HPLC coupled with RIA showed circulating C-ghrelin to be primarily of low molecular weight (M(r) approximately 3500), but in chronic heart failure, a higher molecular weight form (M(r) approximately 7500) is also present. This is the first evidence for potential circulating hormones derived from the carboxyl terminus of pro-ghrelin and for their modulation in cardiovascular diseases.
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PMID:C-terminal pro-ghrelin peptides are present in the human circulation. 1452 48

Expression of cardiac and gastric ghrelin messenger (m) RNA, together with heart and body weights, were measured in leptin-deficient (ob) and leptin receptor-deficient (db) mice with heart failure induced by viral myocarditis. Significant elevations in cardiac ghrelin mRNA levels and heart weight were observed in ob and db mice 10 days after viral inoculation compared with baseline values. Expression of gastric ghrelin mRNA was not upregulated in ob and db mice on day 10. The elevated expression of cardiac ghrelin mRNA seems to compensate for the lack of upregulation in gastric ghrelin mRNA.
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PMID:Upregulation of cardiac ghrelin mRNA in leptin-deficient and leptin receptor-deficient mice with viral myocarditis. 1470 15

Leptin and ghrelin are novel peptide hormones which are counter-regulatory in the central control of appetite. More recently, it has become clear that these hormones have a range of effects on the cardiovascular system. Leptin increases sympathetic activity, producing a pressor effect when acting on the central nervous system. However, leptin produces vasodilation by an endothelium-dependent mechanism peripherally. Ghrelin decreases sympathetic activity and has a depressor effect when acting on the central nervous system. Peripherally, ghrelin produces vasodilation by an endothelium-independent mechanism. Ghrelin improves left ventricular function and cardiac cachexia in heart failure. Leptin may contribute to cardiac cachexia, and to obesity-related cardiomyopathy by a variety of mechanisms. Leptin has pro-inflammatory, proliferative and calcification promoting effects in the vasculature. Ghrelin has recently been shown to be anti-inflammatory in the vasculature. Leptin may also produce a pro-thrombotic state through stimulation of platelet aggregation and inhibition of coagulation and fibrinolysis. The evidence for and against these effects as well as their pathophysiological significance in obesity hypertension, heart failure, atherosclerosis and thrombosis are discussed.
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PMID:The emerging roles of leptin and ghrelin in cardiovascular physiology and pathophysiology. 1585 36

In sheep with HF (heart failure), Ucn 1 (urocortin 1) decreases total peripheral resistance and left atrial pressure, and increases cardiac output in association with attenuation of vasopressor hormone systems and enhancement of renal function. In a previous study, we demonstrated in the first human studies that infusion of Ucn 1 elevates corticotropin ('ACTH'), cortisol and ANP (atrial natriuretic peptide), and suppresses the hunger-inducing hormone ghrelin in normal subjects. In the present study, we examined the effects of Ucn 1 on pituitary, adrenal and cardiovascular systems in the first Ucn 1 infusion study in human HF. In human HF, it is proposed that Ucn 1 would augment corticotropin and cortisol release, suppress ghrelin and reproduce the cardiorenal effects seen in animals with HF. On day 3 of a controlled metabolic diet, we studied eight male volunteers with stable HF (ejection fraction <40%; New York Heart Association Class II-III) on two occasions, 2 weeks apart, receiving 50 microg of Ucn 1 or placebo intravenously over 1 h in a randomized time-matched cross-over design. Neurohormones, haemodynamics and urine indices were recorded. Ucn 1 infusion increased plasma Ucn 1, corticotropin (baseline, 5.9+/-0.9 pmol/l; and peak, 7.2+/-1.0 pmol/l) and cortisol (baseline, 285+/-42 pmol/l; and peak, 310+/-41 pmol/l) compared with controls (P<0.001, 0.008 and 0.047 respectively). The plasma Ucn 1 half-life was 54+/-3 min. ANP and ghrelin were unchanged, and no haemodynamic or renal effects were seen. In conclusion, a brief intravenous infusion of 50 microg of Ucn 1 stimulates corticotropin and cortisol in male volunteers with stable HF.
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PMID:Effect of urocortin 1 infusion in humans with stable congestive cardiac failure. 1588 44

Ischemic and nonischemic cardiomyopathies are associated with significant morbidity and mortality in industrialized countries. Cardiomyopathies of primary origin, and more specifically the dilated form of the disease, have been associated with a number of gene defects in cytoskeletal, membrane, and sarcomeric proteins. Cardiomyopathies of secondary origin such as ischemic cardiomyopathy remain the leading cause of left ventricular systolic dysfunction and heart failure. Among novel strategies to improve cardiac function in heart failure, treatment with growth hormone, insulin growth factor-1 (IGF-1), and natural and synthetic growth hormone-releasing peptides such as ghrelin and hexarelin have been explored. The present review focuses on the issues involved in the use of exogenous growth hormone and its releasing peptides in experimental animal models of chronic heart failure and in clinical studies on cardiomyopathic patients as potential releasing peptides for the treatment of chronic heart failure developing as a consequence of cardiomyopathy.
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PMID:Cardiac and peripheral actions of growth hormone and its releasing peptides: relevance for the treatment of cardiomyopathies. 1621 2

Cachexia in patients with chronic heart failure (CHF) has been recognized for a long time; however, it has not received much attention until recently. Cardiac cachexia, a common and serious complication of CHF, is associated with very poor prognosis. Several studies have demonstrated that increased neurohormonal and immune abnormalities may play a crucial role in the pathophysiology of cardiac cachexia. Hormonal and catabolic/anabolic imbalances of the body are likely to be responsible for the development of cachexia in CHF. Recently, ghrelin, a novel growth hormone-releasing peptide, has been widely noticed to have potential in the treatment of severe CHF and cardiac cachexia. However, further research will be necessary to identify the exact pathways involved and to find the best therapeutic strategies of using ghrelin to fight the wasting process.
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PMID:Cachexia in chronic heart failure: prognostic implications and novel therapeutic approaches. 1633 13


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