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)

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

The efficiency of the developed scheme for a drug prophylaxis of chronic cardiac insufficiency (CCI) in patients with diabetes mellitus I (DM I) of autoimmune genesis (subtype B) was evaluated; such scheme comprised the inhibitors of angiotensin converting enzyme (ACE) of different chemical structures and a biological response modifier (BRM)--glutoxime, which were prescribed with regard for a changed biological rhythm of hemodynamic as well as of metabolic and immune profiles of patients. The following parameters were examined: cardiohaemodynamics, the content of cortisol, insulin, ACTH, TTH and thyroxin in blood, of transport proteins and of the concentration of IL-1 and TNF-alpha in blood. It was established that the use of ramipril and fosinopril combined with the glutoxime BRM within the scheme of drug prophylaxis of CCI concomitant with DM I was accompanied by an effective removal of desynchronosis of the immune-endocrine system in the discussed category of patients.
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PMID:[Chronopharmacological approaches to the therapeutic prophylaxis of chronic cardiac insufficiency in type I diabetes mellitus]. 1274 55

From experience in six cases the anabolic steroid hormones, especially long-acting testosterone and estrogen preparations, are the treatment of choice in Paget's disease, as in postmenopausal osteoporosis. Details of the management of three patients over a period of four years are presented. Roughly 4 per cent of the population, mostly persons over 40, show some evidence of Paget's disease. Only a small number of them, however, have severe manifestations requiring treatment, such as pain, howing or fracture of the bones, pressure on nerves or heart failure. In rare cases malignant changes occur in the involved bone. Since the cause of Paget's disease is not known, treatment in the past has been largely empirical. Reifenstein and Albright had advocated the therapeutic use of calcium, vitamin D and ascorbic acid, and, in postmenopausal women, administration of estrogens; but with fractures or immobilization, intake of calcium-containing foods, such as milk, must be restricted to avoid dangerous piling up of calcium and kidney stones, and fluids must be forced. In recent years anabolic steroid hormones, principally oral androgens and estrogens, have been employed by Gordan and others to promote bone repair, lessen bone pain and decrease urinary excretion of calcium. While these hormones probably do not arrest the disease, they seem to stabilize it and bring relief of symptoms. More recently, Albright and Henneman demonstrated that very large doses of corticotropin (ACTH) or cortisone resulted in immediate cessation of bone pain, decrease in urinary excretion of calcium and histologic evidence of regression of the disease process. The large doses required, however, also produce dangerous side effects, such as psychosis and osteoporosis, indicating that such treatment probably should not be continued over long periods.
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PMID:Paget's disease; changes occurring following treatment with newer hormonal agents. 1441 Jun 71

Co-localization of urocortin (Ucn) and its putative receptor (CRF-R2beta) in peripheral tissues, including the heart and vasculature, suggests an important role for the peptide as a regulator of cardiovascular function. Indeed, Ucn gene expression and/or immunoreactivity are increased in the ventricles of patients with failing hearts. Hemodynamic effects of Ucn include vasodilation and increases in cardiac contractility, coronary blood flow and conductance, cardiac output and heart rate. Due to the likely benefit of such actions in states of cardiac compromise, our laboratory has recently reported the first study examining the effects of Ucn in ovine experimental heart failure. We observed profound and sustained cardiovascular (reduced cardiac preload and afterload and increased cardiac output), hormonal (inhibition of vasopressin, endothelin and renin-angiotensin-aldosterone axis) and renal effects (natriuresis, diuresis and augmented creatinine clearance). Such effects incorporate many of the therapeutic goals of heart failure management. Recently, two further members of the CRF peptide family have been identified. In contrast to Ucn, Ucn II and III are reported to be highly selective for the CRF-R2beta, displaying negligible affinity for CRF-R1. As such, one could speculate that these new peptides might produce the salutary effects in heart failure as seen with Ucn, without concomitant activation of the stress-related hormone ACTH (mediated via CRF-R1). Clearly, further study is essential to confirm whether manipulation of this new family of peptides (especially Ucn II and Ucn III) offers benefit to the syndrome of heart failure with potential clinical applications in humans.
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PMID:Urocortins: putative role in cardiovascular disease. 1532 Aug 6

Edema develops as one of symptoms and signs in several endocrine disorders, and sometimes can be important clue in detecting the basal endocrine disorder. In patients with long-standing hypothyroidism, characteristic edematous skin changes develop and be called myxedema. In hyperthyroid patients with Graves' disease, peripheral edema sometimes develop with or without heart failure. Severe eyelid puffiness composing Graves' ophthalmopathy and 'circumscribing myxedema', mostly in the pretibial regions, are also highly disease-specific disorders. In Cushing's syndrome, both adrenal and ACTH-dependent, peripheral edema is sometimes important sign leading suspicion of this syndrome. In diabetic patients, attention should be paid to edema constantly especially with nephropathy and hypertension. In diabetic nephropathy stage 3B, aggravation of renal function is often progressive. Recently the range of therapeutic options of glycemic controls has been extended with introduction of thiazolidinediones (TZDs). Weight gain and peripheral edema are recognized side effects of these drugs, particularly when used in combination with insulin. The potential risk of worsened heart failure should be taken into consideration when TZDs are used in patients with diabetes and heart diseases.
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PMID:[Edema in endocrine and metabolic diseases]. 1567 23

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

Aldosterone synthase (CYP11B2) and 11beta-hydroxylase (CYP11B1) catalyze the production of aldosterone and corticosterone, respectively, in the rat adrenal cortex. Recently, there has been some debate as to whether these corticosteroids are also produced in the hearts of rodents and humans, possibly contributing to the development of hypertrophy and myocardial fibrosis. To investigate this, we have used our established, highly sensitive real-time quantitative RT-PCR method to measure CYP11B1 and CYP11B2 mRNA levels in adrenal and cardiac tissue from several rat models of cardiovascular pathology. We have also studied isolated adult rat ventricular myocytes treated with angiotensin II and ACTH. Total RNA was isolated from the adrenal and cardiac tissue of 1) male Wistar rats with heart failure induced by coronary artery ligation and sham-operated controls; 2) stroke-prone spontaneously hypertensive rats and Wistar Kyoto rats as controls; 3) cyp1a1Ren-2 transgenic rats and Fischer controls; 4) isolated adult Sprague-Dawley ventricular myocytes incubated with 11-deoxycorticosterone (DOC), DOC plus angiotensin II, or DOC plus ACTH. Adrenal CYP11B2 expression was significantly increased in transgenic rats compared with Fischer controls (1.3 x 10(9)+/- 1.2 x 10(9) vs. 2.1 x 10(7) +/- 7.0 x 10(6) copies/microg RNA; P < 0.05). There were no other significant differences in adrenal CYP11B2 or CYP11B1 expression between the model animals and their respective controls. Cardiac CYP11B1 and CYP11B2 mRNA transcript levels from all in vivo and in vitro groups were never greater than 100 copies per microgram total RNA and therefore too low to be detected reproducibly. This suggests that cardiac corticosteroid production is unlikely to be of any physiological or pathological significance.
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PMID:The aldosterone synthase (CYP11B2) and 11beta-hydroxylase (CYP11B1) genes are not expressed in the rat heart. 1617 17

Semax, a member of ACTH-derived peptides family, was used in treatment of ischemic stroke in patients. It decreased neurological deficiency and reduced NO hyperproduction in the rat brain caused by acute cerebral hypoperfusion. We suggest that semax is also capable of protecting the rat heart from ischemic damage 28 days after myocardial infarction (MI) induced by left descendent coronary artery occlusion. Semax (150 microg/kg) was given i. p. in the operating day twice: 15 min and 2 hours after coronary occlusion, and once a day for the following 6 days. In 28 days after infarction, the MI group developed cardiac hypertrophy, cell growth was caused mainly by the increase of contractile filaments not supported by the appropriate mitochondrial growth that indicated an impaired energy supply of the cells. Moreover, cardiac hypertrophy was accompanied by decreased mean arterial blood pressure and cardiac contractile function and increased left ventricular end-diastolic pressure. Pharmacological change of cardiac afterload revealed that, in 28 days after MI, the rat heart was not able to change its contractile performance in response to either increase or decrease of systemic blood pressure, and as a result could not maintain its diastolic pressure. All these changes obviously reflect development of heart failure. Semax did not affect cardiac work but partially prevented end-diastolic pressure growth in left ventricle as well as ameliorated cardiomyocyte hypertrophy and disproportionate growth of contractile and mitochondrial apparatus, thus exerting beneficial effect on the left ventricular remodeling and heart failure development late after myocardial infarction.
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PMID:[Protective effect of peptide semax (ACTH(4-7)Pro-Gly-Pro) on the rat heart rate after myocardial infarction]. 1738 23

Cushing's Syndrome (CS) may sometimes lead to dilated cardiomyopathy, even though this condition can be partially or completely reversed after treatment. In this article we report the case of a 28-yr-old woman with CS secondary to adrenal adenoma who exhibited congestive heart failure as an initial symptom. Two weeks before being admitted to our hospital, the patient started complaining of shortness of breath, orthopnea, paroxysmal nocturnal dyspnea and generalized edema. A physical examination did not reveal signs of hypercortisolism. Chest auscultation revealed bilateral diffused crepitation; blood pressure was 180/120 mmHg with heart rate of 90 beats/min. A chest X-ray showed a cardiac shade enlargement due to congestive heart failure. Transthoracic echocardiography demonstrated a dilated left ventricle and an impaired left ventricular systolic function. The patient's urinary cortisol excretion was elevated and circadian rhythm of cortisol was absent. ACTH level was low. In addition, plasma cortisol failed to decrease after administration of dexamethasone. An abdominal magnetic resonance imaging scan showed a 7-cm right adrenal mass. The patient was administered oxygen, spironolactone, ACE-inhibitor and the signs and symptoms of heart failure gradually improved. A laparoscopic right adrenalectomy was performed and pathological examination of the gland showed a benign adrenocortical adenoma. After the adrenalectomy the patient was started on hydrocortisone therapy and 5 months later the wall thickness of the left ventricle was within normal range and the patient's blood pressure was 130/80 mmHg. In conclusion we report the case of heart failure as the main clinical symptom in CS secondary to adrenal adenoma.
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PMID:Cushing's syndrome patient who exhibited congestive heart failure. 1764 30

Vasopressin plays a physiological role in regulation of blood pressure, fluid volume, and serum osmolality. In heart failure inadequate release of vasopressin may result in excess fluid retention and hyponatremia. Vasopressin receptor antagonists are a new class of orally active drugs targeted to inhibit one or more of three distinct vasopressin receptors, namely V1a- (-->vasoconstriction), V1b- (-->release of ACTH) und V2-receptors (-->inhibition of free water reabsorption in the kidney). In cardiac decompensation with fluid overload selective V2- (Lixivaptan, satavaptan and tolvaptan) and non-selective V1a/V2-receptor blockers (Conivaptan) have been shown to be superior to standard therapy, as they allow for a faster weight loss and a more rapid symptomatic improvement (i.e. reduction in dyspnea). Inhibiting free water reabsorption without affecting renal sodium excretion vasopressin receptor antagonists allow for a controlled normalisation of serum natrium in euvolemic and hypervolemic hyponatremia. Vasopressin antagonists are well tolerated and have--in contrast to diuretics--no negative influence on renal function and serum potassium. Heart rate and blood pressure are not affected by vasopressin receptor antagonists. However, despite its excellent acute clinical effects long-term treatment with tolvaptan did not result in a reduced mortality and morbidity in heart failure patients over a mean follow-up of 9.9 months in the EVEREST trial.
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PMID:[Vasopressin receptor antagonists and heart failure]. 1988 90


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