Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DIURETICS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources

Effect of diuretics on cardiopulmonary performance in severe chronic airflow obstruction. A controlled clinical trial.

In a randomized, controlled trial, ten patients with pulmonary heart disease due to severe chronic airflow obstruction were stratified into two groups: group 1 had clinical features of congestive heart failure during respiratory failure and were regularly receiving diuretics; group 2 had no such clinical features and were not receiving diuretics. In group 1, when placebo was substituted for diuretics, pulmonary edema developed in three patients; exercise performance and ventricular function of the remaining two patients deteriorated. In group 2, there was no difference in exercise tolerance or ventricular function between placebo and diuretic therapy. The clinical deterioration in group 1 was related to abnormal left ventricular function. Thus, diuretics benefit only patients who have clinical features of congestive heart failure. In patients with isolated abnormal right ventricular function, diuretics may be harmful.

Aged↗

Diuretic induced hypokalemia in the elderly.

The effects of four commonly prescribed diuretics on serum potassium were assessed. One hundred sixteen elderly clinic patients, independently living, (mean age 74.3 years, range 60 to 99 years) were taking hydrochlorothiazide (HCTZ) (n = 40; mean daily dose, 53.9 mg), a combination of hydrochlorothiazide-triamterene (HCTZ-TMTR) (n = 38; mean daily dose, 1.28 capsules), furosemide (n = 20; mean daily dose, 38.0 mg), or chlorthalidone (n = 18; mean daily dose, 55.6 mg). Patients did not take more than one diuretic. No patients received potassium supplementation or had diseases affecting potassium balance. The study design was a nonblinded, noncrossover retrospective chart audit with chi-square analysis. All patients were counseled about reducing excessive sodium intake and using potassium-rich foods and salt substitutes, although compliance concerning these dietary factors was not assessed. Even though some comparisons of diuretics showed statistical significance, these differences probably are not clinically significant because all serum potassium values were above 3.0 mEq/L and no patient was symptomatic. This study supports the use of HCTZ as an initial antihypertensive diuretic; it is as efficacious as the other diuretics in this study, is less expensive, and usually does not cause clinically significant hypokalemia more often than do the other diuretics.

Aged↗

Influence of diuretics on urinary general base catalytic activity and cyclophosphamide-induced bladder toxicity.

The influence of diuretics on the induction of bladder toxicity by cyclophosphamide was investigated in rats. Following ip administration, about 3.5% of the cyclophosphamide was excreted as 4-hydroxycyclophosphamide. This amount was found to be compatible with the view that the urotoxic effects of cyclophosphamide are caused by the acrolein generated in the urine from 4-hydroxycyclophosphamide, the primary metabolite of cyclophosphamide. In situ, acrolein was more potent than 4-hydroperoxycyclophosphamide with regard to producing an increase in bladder weight; phosphoramide mustard was essentially without urotoxic activity. The urotoxic potency of 4-hydroperoxycyclophosphamide, but not that of acrolein, increased as the pH and/or the phosphate concentration of the infusion medium increased. This was as expected in view of the knowledge that release of acrolein from 4-hydroxycyclophosphamide or 4-hydroperoxycyclophosphamide is facilitated by the presence of general base catalysts, eg, phosphate and bicarbonate, and that the rate at which this reaction proceeds in the presence of these catalysts increases as their concentration and the pH increases. In vivo, diuretics that acidified the urine, eg, ammonium chloride and furosemide, prevented the increase in bladder weight ordinarily elicited by the dose of cyclophosphamide used in these experiments. In contrast, a diuretic, acetazolamide, that markedly increased urinary bicarbonate concentration and alkalinized the urine, did not. None of the diuretics altered the systemic metabolism and urinary excretion of cyclophosphamide nor did they alter the systemic action, as judged by spleen weight, of cyclophosphamide. These observations demonstrate that the pH of the urine and the urinary concentration of general base catalysts greatly influence the urotoxic potential of oxazaphosphorines such as cyclophosphamide. They indicate that while the use of acidifying diuretics is likely to be beneficial in minimizing oxazaphosphorine-induced bladder toxicity, the use of alkalinizing diuretics may not be helpful.

Acrolein↗

Moderate sodium restriction and various diuretics in the treatment of hypertension.

Changes in total body potassium level and blood pressure (BP) were determined in multiple studies on 12 hypertensive subjects ingesting a diet either moderately restricted or higher in sodium. On both diets, the following diuretics were randomly given for four-week intervals: chlorthalidone, hydrochlorothiazide, or furosemide. Total body exchangeable potassium level fell 225 mEq with lower sodium intake and 455 mEq with higher intake, combining all diuretics. Chlorthalidone caused more potassium wastage than the other diuretics. The average falls in mean BP were 13.9 mm Hg with the lower sodium diet and 9.1 with the higher sodium diet, combinging all diuretics. Combining both diets, chlorthalidone produced the greatest fall and furosemide produced the slightest. These data suggest that if a diuretic is used to treat hypertension, a diet moderately restricted in sodium and a single morning dose of a diuretic of intermediate duration of action offer the best balance of efficacy and safety for most patient.

Adult↗

Diuretic and uricosuric activity of 6,7-dichloro-2,3-dihydro-5-(2-thienylcarbonyl)benzofuran-2-carboxylic acid and stereoisomers in chimpanzee, dog and rat.

The racemate and the d-isomer of 6,7-dichloro-2,3-dihydro-5-(2-thienylcarbonyl)benzofuran-2-carboxylic acid exhibited diuretic activity in the chimpanzee, dog and rat. In the chimpanzee, the diuresis and natriuresis presumably resulted from a site of action in the thick ascending limb of Henle's loop. The l-isomer was uricosuric but devoid of any diuretic action in the chimpanzee and similarly was not diuretic in the dog and rat. Various proportions of the two isomers were tested in the chimpanzee in an attempt to produce an optimal diuretic and uricosuric profile. It was concluded that the racemic mixture, under these experimental conditions, was responsible for the most effective overall response. This is apparently the first time in which there is a distinct separation of diuretic and uricosuric actions in the enantiomers of a racemic diuretic uricosuric agent.

Animals↗

[Diuretics and beta-blockers as the first option in the treatment of arterial hypertension].

Diuretics have increasingly come to be used for the treatment of arterial hypertension over the last few decades. Although their precise active mechanism is unknown, it is supposed that their usefulness as antihypertensive is a product mainly of their effect on the transport of ions across the cell wall, which reduces peripheral vascular resistance. The adverse metabolic effects of diuretics can be minimized by prescribing the lowest doses presently recommended, or by administering potassium salts or a potassium-retain diuretic. The antihypertensive action of beta blockers is similar to that of diuretics and other antihypertensive drugs, and again, their active mechanism is poorly understood. There are several contraindications for prescribing beta blockers, as well as side effects that must be considered before starting treatment. Well-controlled studies on large cohorts have demonstrated the usefulness of both diuretics and beta blockers in preventing the cardiovascular complications of hypertension. These studies have also allowed the medical profession to designate indications for using these drugs in various segments of the population defined by factors of age and race. Given the proved therapeutic efficacy of diuretics and beta blockers, as well as economic considerations, these drugs should be considered first-choice options for the arterial hypertension.

Adrenergic beta-Antagonists↗

The role of diuretics in the aetiology of idiopathic oedema.

The hypothesis that diuretic use and abuse and other purging behaviours cause idiopathic oedema was investigated in 102 patients. Of 91 symptomatic idiopathic oedema patients tested at referral, 16 (17.6%) had diuretic and four (4.4%) laxative in their urine. None had grossly disturbed serum urea and electrolytes. Examination of primary care records from 41 idiopathic oedema patients who denied current diuretic consumption, and denied or were uncertain about past consumption, showed that 20 had not been prescribed diuretics by their general practitioners at any time; a further 18 had not been prescribed diuretics for between seven months and 12 years before referral. The absence of evidence of plasma volume depletion (as judged by similar concentrations of mean serum urea, creatinine, total protein and albumin in patient and age-matched control groups) suggests that neither systematic diuretic and laxative use or abuse, nor episodic overeating and vomiting were responsible for symptoms of idiopathic oedema in our patients. Idiopathic oedema has a strong genetic basis, and correction of major and minor risk factors for this condition leads to substantial amelioration of symptoms in most cases.

Adult↗

[Diuretics in the treatment of heart failure].

Diuretics, together with other drugs and general measures, are of prime importance in the medical treatment of most heart failure patients, namely those with acute pulmonary oedema and overt congestive heart failure. Their beneficial effects result not only from preload and afterload reduction, but also because diuretics are able to improve responses to nitrates and ACE-inhibitors. The appropriate utilisation of diuretics in heart failure therapy frequently involves the use of efficient small doses and drug associations, namely between loop diuretics, thiazides, potassium sparing agents and spirolactone. Physicians must choose the drug carefully, its dosage, time and route of administration, according to the patient's characteristics: heart failure clinical syndrome, age, activity level, systolic or diastolic, left or right ventricular dysfunction, and associated diseases. The role of diuretics in the treatment asymptomatic systolic left ventricular dysfunction and oligosymptomatic diastolic ventricular dysfunction is unclear and should remain under investigation; diuretics may be of benefit in treating those patients with associated diseases, for example arterial hypertension and mild chronic renal failure.

Diuretics↗

[Indapamide--a substitute diuretic for hypertensives with hyperglycemia and/or dyslipidemia].

Diuretics are among the first drugs offered to the hypertensive patient. However, they can induce metabolic changes resulting in cardiovascular insult. Especially noteworthy are increased levels of glucose and lipids. Indapamide is a diuretic and vasodilator that does not raise blood glucose or lipid levels. We therefore investigated its use as a substitute diuretic in patients whose treatment had resulted in hyperglycemia and/or hyperlipidemia. In 24 hypertensives, Indapamide, 2.5 mg daily, replaced the diuretic therapy they were receiving. Blood pressure, blood glucose, hemoglobin A1C and lipid profile were measured before and every month during the 6 months of Indapamide treatment. Replacement of diuretics with Indapamide significantly reduced blood glucose from 148 +/- 53 mg/dl to 127 +/- 37, p = 0.05 HbA1C from 8.42 +/- 0.4 mg/dl to 7.7 +/- 2.0, p = 0.05; total cholesterol from 253 +/- 45 mg/dl to 228 +/- 43, p < 0.05; and triglycerides from 224 +/- 145 mg/dl to 176 +/- 91, p < 0.05. Blood pressure was better controlled with Indapamide than with previous medications. It was reduced from an average of 155 +/- 1 systolic and 89 +/- 8 diastolic (mm Hg), to 142 +/- 13 and 83 +/- 7, respectively, p < 0.05. We conclude that Indapamide is safe and effective in lowering blood pressure and contributes to better control of blood glucose and lipid levels in diabetic and dyslipidemic patients, compared to standard diuretics.

Antihypertensive Agents↗

[Effects of diuretic therapy on electrolyte and acid-base homeostasis].

The use of diuretics leads to a negative sodium and fluid balance without primary effects on serum sodium concentration. This parameter is regulated by the activity of the antidiuretic hormone (ADH) system. Secondary changes in other electrolyte systems and in acid base homeostasis also are induced by diuretic therapy. Especially diuretic induced hypokalemia is important as it is responsible for the excess mortality observed in patients with diuretic treated essential hypertension and cardiac abnormalities. All adverse metabolic effects of diuretic therapy are, in contrast to the antihypertensive action, dose dependent. Changes in fluid and electrolyte metabolism induced by diuretics occur within the first 2 or 3 weeks after initiation of medication. Counterregulatory mechanisms are activated and a new steady state is established. Serial laboratory determinations after this period are not necessary as long as this steady state is not affected by additional events (like a change in therapy or diet as well as the occurrence of vomiting or diarrhea).

Acid-Base Equilibrium↗

Effect of diuretic therapy on the electrocardiographic response to exercise.

For nearly 30 years clinicians have assumed that diuretic therapy, per se, even in the absence of clinical hypokalemia, can cause false-positive exercise ST-segment responses. The precept has stubbornly persisted in the literature and in the day-to-day interpretation of exercise tests in clinical settings. The assumption probably originated with very early studies of patients on diuretics, in which other causes of false-positive tests were not excluded. This study was undertaken to show that diuretic therapy alone is not sufficient to cause ST depression. Twenty healthy male volunteers, aged 18 to 35, with normal history and physical examinations, echocardiograms, electrocardiograms, serum electrolytes, renal function tests and exercise tests, took 50 mg of hydrochlorothiazide daily for four weeks. Exercise tests, serum electrolytes, and renal function tests were repeated at Weeks 2 and 4. The administration of the diuretic resulted in a statistically significant reduction in serum potassium (from 4.37 +/- 0.37 to 3.96 +/- 0.28, and 3.94 +/- 0.31 mEq/l at 2 and 4 weeks, respectively). There were no abnormal ST-segment shifts on any of the exercise tests. It is concluded that exercise-induced ST-segment shifts in otherwise healthy young male normokalemic subjects who are taking diuretics should not be ascribed to a false-positive response to diuretics.

Adolescent↗

Prescribing patterns for thiazide diuretics in a large health maintenance organization: relationship to participation as an ALLHAT clinical center.

The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) published its main findings in December, 2002. It recommended thiazide diuretics as a first-line treatment of hypertension. The current study describes the prescribing patterns of thiazide diuretics in four regions of Kaiser Permanente, a large national United States Health Maintenance Organization--two regions that had an ALLHAT clinical center and two that did not. We tested the hypothesis that participation in a clinical trial leads to quicker and greater adoption of study recommendations than non-participation in a trial. The relative percentage of filled outpatient prescriptions for the period 2 or 3 years before the ALLHAT main publication through December 31, 2004 was calculated by region for thiazide-type diuretics and for calcium channel blockers (CCBs), beta-blockers, central alpha-blockers, angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) and other antihypertensive diuretics. In the 2 years after publication of the ALLHAT trial findings, the percentage of all prescriptions for thiazide diuretics increased from 11.2% to 12.4% in the two regions with an ALLHAT clinical site and from 8.9% to 10.1% in the two regions without an ALLHAT clinical site (p > 0.05). The percentage of new prescriptions for thiazide diuretics increased from 13.7% to 16.6% in the two regions with an ALLHAT clinical site and from 10.8% to 13.0% in the two regions without an ALLHAT clinical site (p > 0.05). Participation in a clinical hypertension study does not appear to accelerate adoption of study recommendations.

Antihypertensive Agents↗

Oral theophylline and diuretics improve pulmonary mechanics in infants with bronchopulmonary dysplasia.

We studied the effects of orally administered theophylline and diuretics (chlorothiazide and spironolactone) on pulmonary mechanics in 16 infants with bronchopulmonary dysplasia. Their gestational age (mean +/- SD) was 28.5 +/- 3.4 weeks, and postnatal age at the time of study 19.5 +/- 10.7 weeks. The infants were randomized to two groups. Group 1 received successively placebo, theophylline, and theophylline plus diuretics; Group 2 received theophylline, placebo, and placebo plus diuretics on successive 4-day periods. Pulmonary function was measured before beginning the study (baseline) and at the end of each 4-day period. No significant changes in pulmonary function were noted after treatment with placebo. After treatment with theophylline, dynamic compliance (Cdyn) increased from baseline (mean +/- SD) 0.075 +/- 0.017 to 0.091 +/- 0.028 mL/cm H2O/cm (P less than 0.01), airway resistance (Raw) decreased from 67.19 +/- 36.71 to 41.44 +/- 22.50 cm H2O/L/sec (P less than 0.001), maximal expiratory flow at functional residual capacity (VmaxFRC) increased from 0.261 +/- 0.240 to 0.357 +/- 0.299 thoracic gas volume (TGV)/sec (P less than 0.01), and time constant decreased from 0.312 +/- 0.224 to 0.275 +/- 0.247 sec (P less than 0.02). After treatment with combined placebo and diuretics, Cdyn increased to 0.103 +/- 0.023 mL/cm H2O/cm (P less than 0.05), Raw decreased to 31.76 +/- 24.90 cm H2O/L/sec (P less than 0.001), VmaxFRC increased to 0.638 +/- 0.595 TGV/sec (P less than 0.02), and time constant decreased to 0.180 +/- 0.141 sec (P less than 0.05). After treatment with combined theophylline and diuretics, Cdyn increased to 0.118 +/- 0.017 mL/cm H2O/cm (P less than 0.001), Raw decreased to 35.98 +/- 25.85 cm H2O/L/sec (P less than 0.02), VmaxFRC increased to 0.479 +/- 0.377 TGV/sec (P less than 0.02), and time constant decreased to 0.180 +/- 0.137 sec (P less than 0.01). We conclude that theophylline and diuretics have additive effects on the improvement of pulmonary function in infants with bronchopulmonary dysplasia.

Administration, Oral↗

Diuretic Doppler sonography in postnatal hydronephrosis.

Renal resistive indexes were measured by Doppler sonography in 12 children undergoing other standard diagnostic studies to evaluate hydronephrosis. Measurement of renal resistive indexes was modified by prior placement of a bladder catheter, oral hydration and administration of 1 mg./kg. furosemide after baseline measurement. Renal resistive indexes were again measured at 10 and 30 minutes after diuretic. While diuretic administration had no measurable influence on 10 nonobstructed kidneys, the elevated 10-minute post-diuretic renal resistive indexes recorded in 10 obstructed kidneys differed significantly from the indexes recorded in the nonobstructed group (p less than 0.001). The highest elevations in renal resistive indexes were recorded in nonpaired kidneys, which included 7 of the 10 kidneys in the obstructed group. In the 3 unilaterally obstructed kidneys the 10-minute post-diuretic renal resistive indexes did not differ significantly. However, renal resistive indexes in these kidneys increased at least 15% over baseline readings after diuretic administration. Diuretic Doppler sonography appears to be another useful method for differentiating functionally significant hydronephrosis from nonobstructive hydronephrosis in children.

Child↗

Diuretic therapy of heart failure in infants and children.

Diuretics are the mainstay of traditional therapy for congestive heart failure. The syndrome of heart failure is now understood to involve complex interactions of neurohumoral substances released in response to poor cardiac function. Developmental changes during infancy and childhood will affect both the activation of systemic neurohumoral responses and the pharmacokinetic and pharmacodynamic actions of diuretics. Few human studies directly evaluate the efficacy of diuretic therapy in heart failure in adults. The pharmacodevelopmental aspects of diuretic therapy in infants and children are also incompletely studied. This review will describe the kidney's role in the pathogenesis of sodium and water retention in heart failure and the developmental changes in the kidney related to fluid retention. Known principles of diuretic therapy in congestive heart failure will be described. All these factors can then be used by the reader to evaluate the role of diuretic therapy in the complex syndrome of heart failure in infants and children.

Journal Article↗

Isolation and identification of a diuretic hormone from the mealworm Tenebrio molitor.

A diuretic hormone of unusual structure was isolated from extracts of whole heads of the mealworm Tenebrio molitor. The hormone is a 37-aa peptide of 4371 Da, with the sequence SPTISITAPIDVLRKTWEQERARKQMVKNREFLNSLN. This peptide increases cAMP production in Malpighian tubules of T. molitor. The amino acid sequence reveals that this peptide is a member of the family of sauvagine/corticotropin-releasing factor/urotensin I-related insect diuretic hormones. The C-terminal sequence of this peptide is quite different from other members of this family, which have a hydrophobic C terminus (isoleucinamide or valinamide). When aligned comparably, T. molitor diuretic hormone has a more hydrophilic C terminus, leucylasparagine (free acid). In contrast to all other known diuretic hormones of this family, this peptide has exceptionally low stimulatory activity on cAMP production in Malpighian tubules of Manduca sexta. However, at nanomolar concentrations it stimulates cAMP production in Malpighian tubules of T. molitor. Diuretic hormones of this family have been isolated previously from Lepidoptera, Orthoptera, Dictyoptera, and Diptera. This appears to be the first diuretic hormone isolated from a coleopteran insect.

Amino Acid Sequence↗

PST 2238: a new antihypertensive compound that modulates renal Na-K pump function without diuretic activity in Milan hypertensive rats.

PST 2238 is a new antihypertensive compound that is able to correct the molecular and functional alterations of the renal Na-K pump and the pressor effect associated with either alpha-adducin mutations or high circulating levels of endogenous ouabain (EO) in genetic and experimental rat models. Due to the close relationship between renal Na-K pump function and tubular Na reabsorption, PST 2238 was investigated to determine whether it is endowed with diuretic activity and consequently might trigger alterations of the renin-aldosterone system and the carbohydrate and lipid metabolism often associated with chronic diuretic therapy. In Milan hypertensive (MHS) rats, in which hypertension is genetically associated with alpha-adducin mutation, increased tubular Na reabsorption, and hyperactivation of the renal Na-K pump. PST 2238 reduced blood pressure and normalized the renal Na-K pump activity at oral doses of micro g/kg, but did not induce, either acutely or chronically, any diuretic activity or hormonal or metabolic alterations. In contrast, HCTZ, given to MHS rats orally at 40 mg/kg, although it displayed diuretic activity and reduced the renal Na-K pump activity, did not lower blood pressure and caused hyperactivation of the renin-aldosterone system, hypokaliemia, and hyperglycemia. The findings lead to the conclusion that PST 2238 is a new antihypertensive compound that normalizes the altered function of the renal Na-K pump associated with hypertension in rat models, but that it is devoid of diuretic activity and does not induce the diuretic-associated side effects.

Androstanols↗

Diuretics and the renal adenylate cyclase system.

1 The relationship between the diuretic effectiveness and the effect on the renal adenylate cyclase of three diuretics, acetazolamide, frusemide and ethacrynic acid, was examined. The hypothesis that acetazolamide and parathyroid hormone (PTH), inhibit renal carbonic anhydrase by a cyclic adenosine 3',5'-monophosphate (cyclic AMP)-dependent mechanism was also tested.2In vitro, acetazolamide, frusemide and ethacrynic acid at high concentrations (10(-3)M) all produced some inhibition of basal and stimulated rat kidney plasma membrane adenylate cyclase. The effect of acetazolamide was much less than that of frusemide and ethacrynic acid. These plasma membrane effects were reproduced in studies of cyclic AMP formation in isolated kidney tubules of rats.3 Intravenous injections of acetazolamide did not change the total cyclic AMP content of the kidneys of rats killed by microwave irradiation.4 Acetazolamide produced a diuresis in the rat and a slight inhibition of the antidiuretic effect of Pitressin. Frusemide produced a diuresis and greatly reduced the antidiuretic response to Pitressin. Ethacrynic acid was ineffective as a diuretic in the rat and actually enhanced the antidiuretic response to Pitressin.5 In investigating the possible influence of diuretics and PTH on the activity and state of phosphorylation of carbonic anhydrase it was found that: there was no correlation between the ability of diuretics to inhibit carbonic anhydrase activity and to inhibit carbonic anhydrase phosphorylation; neither PTH nor cyclic AMP (in the presence of adenosine triphosphate, Mg(2+), K(+) and incubation at 37 degrees C) inhibited rat cortex homogenate carbonic anhydrase activity.6 It seems unlikely that any of the tested diuretics exerts its pharmacological effect by means of changes in kidney cyclic AMP metabolism.

Acetazolamide↗