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)

As many as 76 patients suffering from inactive rheumatic fever associated with different stages of heart failure were examined for uricemia, diurnal uricosuria, and xanthine oxidase activity in blood serum. It was established that in rheumatic fever, the activity of xanthine oxidase increased even at the early stages of heart failure. The presence in some of the patient of the enzyme activation combined with hyperuricosuria and normal content of uric acid in blood serum suggests "latent" hyperuricemia. In patients with severe heart decompensation, there was an appreciable activation of xanthine oxidase, which correlated, as a rule, with high hyperuricemia. Activation of xanthine oxidase in patients with rheumatic fever evidences hyperproduction of uric acid. It is advisable that in such cases the uricodepressive treatment may be indicated.
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PMID:[Changes in xanthine oxidase activity in patients with circulatory failure]. 278 95

Oral diuretics are amongst the most widely used drugs in clinical practice today. Their discovery close on thirty years ago remains a major milestone in therapeutic progress. Though originally designed for treating heart failure, diuretics are more commonly prescribed, worldwide, in hypertension than for relief of oedema. Since the introduction of chlorothiazide, diuretic development has passed through a series of distinct stages. The thiazide era was followed by the 'high-ceiling' diuretics, the antikaliuretics and, more recently, polyvalent agents that cause both saluresis and uricosuria. Alongside these synthetic achievements, major advances have occurred in the knowledge of nephron function and ion transport mechanisms. These have acted as stimulus to the design of novel categories of diuretics. The practising clinician thus has a wide range of available diuretics to choose from. The most appropriate choice of an agent aimed at the relief of symptoms with minimal adverse effects requires an understanding of where and how diuretics act within their primary target organ, the kidney. Whereas various procedures, ranging from micropuncture to the study of brush border membrane vesicles, have been utilised experimentally, investigation of the mode and sites of action of diuretics in man has largely depended on application of clearance methodology. Refinements in analytical chemistry have encouraged study of the pharmacokinetic and metabolic fate of diuretics. Taken together, available evidence shows that most diuretics exert their saluretic action from the intraluminal aspect of the renal tubules. The time-course of drug delivery, as well as total quantity of drug transported into the lumen determine the cumulative drug response. Exceptions are muzolimine and the aldosterone antagonists which act at the peritubular membrane. Distinctive stereospecific effects on luminal tubular ion transport occur with indacrinone and etozoline. The clinical use of diuretics often involves concurrent administration with other drugs. The mechanisms involved in a number of the resulting pharmacodynamic and pharmacokinetic interactions have considerable relevance in patient management. Notable examples of these interactions are the blunting of diuretic action by non-steroidal anti-inflammatory agents and the diuretic-induced diminution in the renal clearance of lithium salts.
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PMID:Diuretic drugs. Progress in clinical pharmacology. 352 89

Uric acid (UA) is the final product of purine catabolism in man, and it is excreted mainly by the kidneys when renal function is not impaired. Consequently, serum (S) UA increases as a function of purine intake, and it varies inversely to uricosuria. The latter variable diminishes in response to low-sodium intakes and vice versa. Insofar as the diet is not usually controlled in studies in which the response of SUA to drugs is evaluated, most reports are to be considered cautiously. Common diuretics elevate SUA in healthy subjects, hypertensives and patients with heart failure, apparently by elevating net UA reabsorption in the nephronal proximal tubule. This drug action, which becomes noticeable shortly after the institution of treatment and remains throughout it, starts at low doses (e.g., 12.5 mg hydrochlorothiazide or 1.25 mg bendrofluazide once daily in subjects with uncomplicated hypertension) and increases in dose-dependent fashion. Beta-blockers tend to elevate SUA. The angiotensin-converting enzyme (ACE) inhibitors captopril, enalapril and ramipril have been found to increase uricosuria mildly, likely by lowering the net reabsorption of UA in the proximal tubule. These three drugs and lisinopril can blunt the rise in SUA provoked by diuretics in hypertensives if used at sufficiently high doses relative to the dose of the diuretic. The angiotensin II antagonist losartan augments uricosuria mildly and thereby decreases SUA. The cardiovascular implications of the response of SUA to drugs remain speculative. Uric acid can scavenge various reactive oxygen species and thus reduce oxidative stress, which seems to contribute to the development and/or progress of various cardiovascular conditions, including hypertension, atherosclerosis and heart failure. Consequently, it may be theorised that the elevations in SUA induced by diuretics might contribute to the established favourable action of these agents on cardiovascular prognosis. Conversely, diuretic-induced increases in SUA are to be considered detrimental according to an old hypothesis that maintains that SUA is a cardiovascular risk factor; this construct is largely based upon the results of selected epidemiological undertakings. The cardiovascular implications of the effects of drugs on SUA, if any, should be elucidated through purposive research.
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PMID:Cardiovascular drugs and serum uric acid. 1510 95