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)

In rats with unilateral renal artery stenosis, the malignant phase of hypertension is characterized by: systolic blood pressure above 180-190 mm Hg; sodium and water loss; polyuria and polydipsia; markedly activated renin-angiotensin-aldosterone system; impairment of renal function and malignant nephrosclerosis in the contralateral kidney; some rats exhibit signs of cerebral hemorrhage, heart failure, acute renal failure, and some rats die. After such a phase of malignant hypertension, a period of remission may occur, which is followed by another malignant phase, etc. When malignant hypertensive rats are offered, in addition to water, saline as drinking fluid, they compulsively drink the saline, BP falls transiently, and all signs of malignant hypertension nearly or completely disappear. These observations indicate that, at a critically high BP level, it is salt and water loss which, by activating the renin-angiotensin system, trigger the vicious circle of malignant renal hypertension in rats.
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PMID:Pathogenesis of malignant hypertension: experimental evidence from the renal hypertensive rat. 119 18

We have attempted to define a normal range for blood urea and creatinine for elderly inpatients and to determine the relative importance of pre-renal, renal and post-renal pathology in those with renal impairment. A total of 118 admissions to an acute geriatric unit and 67 separate post mortems in patients over 67 years of age were studied prospectively. Up to 123 items of data were coded and analysed including blood urea and creatinine, clinical or pathological changes associated with renal disease, clinical outcome and post mortem findings. We determined our own 'normal' hospital ranges for urea (1.4-13.2 mmol/l) and creatinine (48-141 mumol/l) from plasma values in 76 patients with no evidence of renal impairment, either on admission or in the past. Using these values 41% of post mortem cases and 25% of clinical admissions had a raised blood urea. Pre-renal conditions such as cardiac failure, dehydration and gastrointestinal haemorrhage, either alone or in combination, were present in 56% of these patients. Urea and creatinine values were substantially higher in patients who died in hospital as opposed to those who were discharged or transferred. Creatinine values were greater in those with intrinsic renal disease or post-renal obstruction as compared to patients with pre-renal causes of renal impairment. Patients with histological evidence of extensive glomerulosclerosis or nephrosclerosis had higher urea and creatinine levels than those with only minor ageing changes.
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PMID:Raised blood urea in the elderly: a clinical and pathological study. 158 74

The association between proteinuria and congestive cardiac failure was investigated in patients with hypertensive heart disease, cardiomyopathy, rheumatic heart disease and cor pulmonale. In 33 such patients, proteinuria occurred before and after successful treatment of the cardiac failure. Overall there was a wide variation in the degree of proteinuria amongst the various groups and statistical analysis showed that the distribution of levels of proteinuria and the mean levels of proteinuria were statistically different between any two groups of patients, P = 0.05. Biopsy proven hypertensive nephrosclerosis was found to be a cause of heavy proteinuria which was in the nephrotic range in two such patients. Congestive cardiac failure due to hypertensive heart disease should be included in the differential diagnosis of massive proteinuria even in the absence of renal insufficiency.
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PMID:The pattern of proteinuria in congestive cardiac failure due to common heart diseases. 206 87

The rationale for the use of new drugs in the treatment of mild to moderate hypertension is based on the knowledge that these drugs can both achieve the same goals as old drugs and offer additional advantages. Available data indicate that angiotensin-converting enzyme inhibitors (ACEIs) are as effective in reducing blood pressure as thiazide diuretics and beta-blockers, and that they maintain their effect without the development of tolerance. Therefore they may be expected to achieve at least the same prevention of target organ damage (heart failure, cerebral strokes, and arterial nephrosclerosis) as achieved by previous drugs and also to be effective when target organs have already been damaged. Moreover ACEIs seem to offer two possible advantages: cardioprotection and a favorable influence on the quality of life. Many experimental but indeed few clinical data suggest that these drugs can exert primary cardioprotection and that they might exert a beneficial therapeutic effect in hypertensives with coronary heart disease. Owing to the quality of their hypotensive effect, to the lack of detrimental effects on physical, psychical, and sexual activity, and to the positive influence on the sense of well-being, ACEIs seem to be better tolerated than previous drugs. However, although available data suggest that ACEIs can be considered a further advance in the treatment of hypertension, more extensive information is needed to confirm these promising results.
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PMID:Angiotensin-converting enzyme inhibitors in the treatment of mild to moderate essential hypertension. 256 45

The fawn-hooded (FH) rat develops hypertension spontaneously. Systolic blood pressure is already elevated at 5 weeks of age, increases with age, and the final range is 180-240 mmHg at the age of 1 year. Concomitantly with the rise in blood pressure proteinuria occurs and increases with age. Fawn-hooded rats reaching the accelerated phase of the hypertension are characterized by blood pressure values exceeding 220 mmHg, heavy proteinuria and increased heart, kidney, liver, adrenal and spleen weights. Those prone to malignant hypertensive disease show a period of increased water turnover for several weeks after weaning; during this period, they do not show the pronounced decrease in water intake upon fasting for 24 h as observed in FH rats of the same age prone to a milder form of hypertension, i.e. diuresis and drinking continue even when no food is consumed. The major cause of death for FH rats is malignant nephrosclerosis with the nephrotic syndrome and/or cardiac failure with chronic pulmonary congestion. Some animals die of bleeding from mesenteric vessels with periarteritis nodosa. In FH rats with malignant hypertension, heart, kidney, liver and spleen weights are significantly increased compared with FH rats of the same age with mild hypertension. Histopathology shows myocardial fibrosis and myocardial infarctions. Generalized arteriolosclerosis is common, sometimes accompanied with local fibrinoid degeneration and (peri)arteritis. Some major arteries show intimal proliferation. It is concluded that the FH rat provides an interesting model for the study of hypertension and its consequences.
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PMID:Spontaneous hypertension in the fawn-hooded rat: a cardiovascular disease model. 346 7

Spontaneous cardiac and renal lesions in APA hamsters were examined histopathologically. Myocardial degeneration, valvular thickening, coronary arterial degeneration and increase in heart weight were common in old hamsters. These changes, which suggest cardiac failure, seem to be related to cardiac thrombosis which predominantly affected the left atrium and was found in over 40% of each sex over 16 months of age. Neither glomerular amyloidosis nor arteriolar nephrosclerosis was detected. In general the histopathology of renal lesions in APA hamsters resembled that of the condition known as glomerulonephrosis in rats. Renal lesions occurred more frequently and more severely and developed more rapidly in females than in males. There was no apparent correlation between cardiac thrombosis and renal disease.
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PMID:Age-related non-neoplastic lesions in the heart and kidneys of Syrian hamsters of the APA strain. 362 72

It is well known that blood access is essential for long-term hemodialysis treatment. Arteriovenouos fistula (AVF) is the most widely used method. However, this method of access frequently fails (access failure) as a result of stenosis. We attempt simple femoral vein puncture (FV-method) instead of AVF in such patients and have experienced 12 patients who were undergoing hemodialysis treatment using the FV-method, three times a week for more than one year. We devised special needles (18- and 19-gauge) for the FV-method. Generally, we use a 19-gauge needle with 4 side holes. We discuss here the results of 12 patients consisting of 4 males and 8 females with a mean age of 57.9 years, a mean duration of dialysis of 10.0 years, and a mean duration of FV-method of 3.5 years. Their underlying diseases were chronic glomerulonephritis (9 patients), diabetic nephropathy (2 patients) and nephrosclerosis (1 patient). Before the use of the FV-method, AVFs were attempted a man of 3.8 times and an artificial graft, 4 times in 3 patients. Ten patients were outpatients and 2 were inpatients. As for the indications of the FV-method, 11 patients had access failure and another had suffered from heart failure resulting from an over flow of blood through AVF. KT/V, PCR and TACBUN were measured monthly and were within the normal range in almost all of the patients. Concerning complications of the FV-method, hematoma formation after detachment of the needle at the end of dialysis and pain at needle puncture were sometimes noted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Long-term hemodialysis treatment using femoral vein puncture method (FV-method) as blood access in 12 patients]. 747 9

The study of the current status of renal replacement therapy in Japan is based on the analysis of data from the registry reports for regular dialysis therapy and kidney transplantation. The total number of patients receiving regular dialysis therapy was 123,926 at the end of 1992: 117,809 (95.1%) on hemodialysis and 6,117 (4.9%) on peritoneal dialysis. The primary diseases of newly accepted patients were chronic glomerulonephritis (42.2%), diabetic nephropathy (28.4%), nephrosclerosis (5.9%), polycystic kidney disease (2.7%), chronic pyelonephritis (1.6%), and others. The number of kidney transplant patients in Japan was 8,384 at the end of 1991: 6,154 (73.4%) received a living donor transplantation and 2,230 (26.9%) received a cadaver donor transplantation. Overall 5-year survival rates of dialysis patients were 60.4%: 69.7% for chronic glomerulonephritis, 41.7% for diabetic nephropathy, 39.6% for nephrosclerosis, 73.6% for diffuse polycystic kidney disease, and 66.6% for chronic pyelonephritis. The causes of death of dialysis patients were heart failure (31.1%), cerebrovascular accident (13.6%), infectious diseases (11.3%), malignancies (7.1%), cachexia/uremia (6.7%), myocardial infarction (5.8%), and others. The gross mortality rate of dialysis patients was increased in cases of less than 4 hours of the average length of each dialysis session, less than 4% and more than 9% of the average weight loss during each dialysis session, less than 1.0 of Kt/V, and less than 0.9 and more than 1.7 g/kg/d of protein catabolic rate. Overall 5-year patient and graft survival rates of kidney transplant patients since 1964 were 82.7% and 60.3%: 84.4% and 65.0% in living donor cases, and 77.4% and 46.2% in cadaver donor case, respectively. Those since 1983 were 90.1% and 68.2%: 91.3% and 72.6% in living donor cases, and 87.8% and 59.3%, respectively. Graft survival rates were superior in cases treated with combined steroid, cyclosporine and azathioprine or mizoribine, to those treated with other immuno-suppressive regimens, and they decreased as the number of HLA-A, -B and -DR increased.
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PMID:Current status of renal replacement therapy in Japan. 781 May 20

Aldosterone, the final product of the renin-angiotensin-aldosterone system (RAAS), is a mineralocorticoid hormone that classically acts, via the mineralocorticoid (aldosterone) receptor, on epithelia of the kidneys, colon, and sweat glands to maintain electrolyte homeostasis. Aldosterone has also been shown to act at nonepithelial sites where it can contribute to cardiovascular disease such as hypertension, stroke, malignant nephrosclerosis, cardiac fibrosis, ventricular hypertrophy, and myocardial necrosis. Although angiotensin-converting enzyme (ACE) inhibitors and angiotensin type 1 (AT(1)) receptor antagonists act to suppress the RAAS, these agents do not adequately control plasma aldosterone levels--a phenomenon termed "aldosterone synthesis escape." Spironolactone, a nonselective aldosterone receptor antagonist, is an effective agent to suppress the actions of aldosterone; its use is, however, associated with progestational and antiandrogenic side effects due to its promiscuous binding to other steroid receptors. For these reasons, eplerenone--the first agent of a new class of drugs known as the selective aldosterone receptor antagonists (SARAs)--is under development. In rodent models, eplerenone provides marked protection against vascular injury in the kidney and heart. In phase II clinical trials, eplerenone demonstrates 24-h control of blood pressure with once or twice daily dosing, and is safe and well tolerated in patients with heart failure when given with standard of care agents. Pharmacokinetic studies reveal that eplerenone has good bioavailability with low protein binding, good plasma exposure, and is highly metabolized to inactive metabolites and excreted principally in the bile. Eplerenone is well tolerated in acute and chronic safety pharmacology studies. Ongoing phase III trials of eplerenone in the treatment of hypertension and heart failure are underway. These studies will extend our understanding of selective aldosterone receptor antagonism in the treatment of chronic cardiovascular disease.
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PMID:Eplerenone: a selective aldosterone receptor antagonist (SARA). 1160 37

Adrenomedullin (AM), identified from pheochromocytoma and having 52 amino acids, elicits a long-lasting vasodilatation and diuresis. AM is mainly mediated by the intracellular adenylate cyclase coupled with cyclic adenosine monophosphate (cAMP) and nitric oxide (NO) -cyclic guanosine monophosphate (cGMP) pathway through its specific receptor. The calcitonin receptor-like receptor (CLCR) and receptor-activity modifying protein (RAMP) 2 or RAMP3 models have been proposed as the candidate receptor. AM is produced mainly in cardiovascular tissues in response to stimuli such as shear stress and stretch, hormonal factors and cytokines. Recently established AM knockout mice lines revealed that AM is essential for development of vitelline vessels of embryo. Plasma AM levels elevate in cardiovascular diseases such as heart failure, hypertension and septic shock, where AM may play protective roles through its characteristic biological activities. Human AM gene delivery improves hypertension, renal function, cardiac hypertrophy and nephrosclerosis in the hypertensive rats. AM decreases cardiac preload and afterload and improves cardiac contractility and diuresis in patients with heart failure and hypertension. Advances in gene engineering and receptor studies may contribute to further understandings of biological implication and therapeutic availability of AM.
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PMID:A review of the biological properties and clinical implications of adrenomedullin and proadrenomedullin N-terminal 20 peptide (PAMP), hypotensive and vasodilating peptides. 1175 55


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