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PubMed1994

Diuretics for heart failure.

For over 25 years diuretics have provided the mainstay of treatment for patients with heart failure. They reduce symptoms in both acute and chronic failure, rarely need to be stopped because of unwanted effects and cost very little. The overall effect of diuretic therapy on long-term mortality is not known, but outlook is certainly improved when an ACE inhibitor is added. In this article we review the use of diuretics in the management of acute and chronic heart failure and consider how they should be integrated with ACE inhibition.

Acute Disease↗

PubMed2000

Social deprivation increases cardiac hospitalisations in chronic heart failure independent of disease severity and diuretic non-adherence.

OBJECTIVE: To examine whether social deprivation has any independent effect on emergency cardiac hospitalisations in patients with chronic heart failure (CHF). DESIGN: Cohort study of 478 patients with CHF who had been hospitalised before 1993 and who were followed up during 1993 and 1994. SETTING: Emergency admissions within Tayside acute hospitals. PATIENTS: 478 CHF patients who had a previous myocardial infarction, a previous CHF admission, and were on diuretic treatment. MAIN OUTCOME MEASURES: Emergency hospital admissions are divided into those for all causes and those for cardiac causes only. RESULTS: Social deprivation was significantly associated with an increase in the number of cardiac hospitalisations (p = 0.007). This effect was mainly caused by increasing the proportion of patients hospitalised in each deprivation category (26% in deprivation category 1-2 versus 40% in deprivation category 5-6, p = 0.03). This effect of deprivation was independent of disease severity, as judged by the dose of prescribed diuretic, the death rate, and the duration of each hospital stay. Non-adherence with diuretic treatment could not account for these findings either. CONCLUSIONS: Social deprivation increases the chance of a CHF patient being rehospitalised independently of disease severity. Possible explanations are that doctors who look after socially deprived patients have a lower threshold for cardiac hospitalisation of their patients, or that social deprivation alters the way a CHF patient accesses medical care during decompensation. Understanding how social deprivation influences both doctor and patient behaviour in the prehospital phase is now crucial in order to reduce the amplifying effect that social deprivation appears to have on cardiac hospitalisations.

Aged↗

PubMed1987

Untreated heart failure: clinical and neuroendocrine effects of introducing diuretics.

The clinical and neuroendocrine response to diuretic treatment was assessed at rest and on exercise in 12 patients with heart failure. Before treatment all patients were limited by breathlessness on exercise; one was oedematous. Plasma renin activity and aldosterone were normal but plasma noradrenaline was raised both at rest and on exercise. After one month's treatment with frusemide (40 mg) and amiloride (5 mg) weight was significantly reduced by a mean of 3.5 kg and exercise capacity had doubled. Plasma noradrenaline fell to normal at rest but remained abnormally raised on exercise. Plasma renin activity and aldosterone increased significantly both at rest and on exercise. Diuretics bring about a considerable clinical improvement in patients with chronic heart failure but they stimulate the renin-angiotensin system. Activation of the renin-angiotensin system in moderate heart failure occurs as a response to diuretic treatment rather than as a result of the disease process itself.

Adult↗

PubMed2004

Use of diuretics in cardiovascular diseases: (1) heart failure.

Diuretics are used extensively in hospitals and in community medical practice for the management of cardiovascular diseases. They are used frequently as the first line treatment for mild to moderate hypertension and are an integral part of the management of symptomatic heart failure. Although diuretics have been used for several decades, there is still some ambiguity and confusion regarding the optimal way of using these common drugs. In this paper, the classes and action of diuretics are reviewed, and the various indications, optimal doses, and recommendations on the effective use of these agents are discussed.

Chronic Disease↗

PubMed1978

Potassium depletion in heart failure and its relation to long-term treatment with diuretics: a review of the literature.

There have been many studies which suggest that patients with heart failure were potassium depleted. This depletion has been attributed to the use of potent diuretics, and these are now given with either potassium supplements or potassium-retaining diuretics. A detailed examination of the studies suggests that the reported decrease in body potassium compared with the results in healthy persons is not due to the diuretics. It can be partly explained by a failure to match patients and controls in terms of age, and the remaining difference can be explained by muscle wasting. There is therefore no evidence of a potassium depletion in these patients with heart failure.

Adult↗

PubMed1987

Idiopathic oedema and diuretics.

Diuretic abuse has been invoked as the cause of idiopathic oedema. In this study, eight patients with idiopathic oedema were studied. Symptoms and weight variation continued despite the proven absence of diuretics in seven of them as determined by urinary chromatograms. Idiopathic oedema cannot therefore be attributed to diuretic use alone.

Adult↗

PubMed1984

Effect of diuretics on the tubuloglomerular feedback response.

To study the influence of diuretics on the tubuloglomerular feedback mechanism, early proximal stop-flow pressure (SFP) was measured during loop exposure to different drug concentrations. SFP was recorded continuously during arrested flow and at a perfusion rate of 50 nL/min. The perfusate consisted of isotonic saline, to which varying amounts of furosemide. bumetanide, piretanide, or hydrochlorothiazide were added to obtain final concentrations between 10(-6) and 10(-4)M. The loop diuretics furosemide, bumetanide, and piretanide showed inhibition: an inverse log-linear relation between the luminal concentration and the respective feedback response. No differences between the dose-response curves of furosemide, bumetanide, or piretanide could be demonstrated. The effective concentration range was between 10(-6) and 10(-4)M, the mean effective dose (ED50) was close to 10(-5)M for each of them. In contrast, hydrochlorothiazide did not alter the feedback response. The effect of loop diuretics was rapidly and repeatedly reversible.

Animals↗

PubMed1997

Expression of the sodium-chloride cotransporter in osteoblast-like cells: effect of thiazide diuretics.

The use of thiazide diuretics is associated with increased bone mineral density and, in some studies with reduced incidence of fractures, suggesting a potential role for these drugs in the treatment of osteoporosis. Our objective was to examine the effects of thiazides on osteoblast-like cells using the rat UMR-106 osteosarcoma cell line. Treatment of UMR-106 cells with chlorothiazide caused membrane depolarization and a rise of intracellular calcium but had no effect on adenosine 3,5'-cyclic monophosphate accumulation. The rise of intracellular calcium was partially inhibited by nifedipine and removal of extracellular calcium, indicating calcium uptake from the extracellular media, as well as by thapsigargin or dantrolene, indicating contributions from calcium release from intracellular stores. Reverse transcriptase-polymerase chain reaction was used to isolate a partial cDNA clone for the thiazide-sensitive sodium-chloride cotransporter from UMR-106 cells that hybridized to 5.0- and 11.0-kilobase mRNAs when Northern blot analysis was conducted. Antisense oligonucleotides to the sodium-chloride cotransporter specifically inhibited the chlorothiazide-induced depolarization and rise of intracellular calcium and reduced immunofluorescence staining for the sodium-chloride cotransporter protein in UMR-106 cells. We conclude that thiazide diuretics inhibit sodium-chloride cotransporter activity in UMR-106 cells, thereby altering intracellular calcium regulation. These results provide evidence for direct effects of thiazide diuretics on bone cells.

Animals↗

PubMed2000

Prolonged exercise after diuretic-induced hypohydration: effects on substrate turnover and oxidation.

To determine the influence of a diuretic-induced reduction in plasma volume (PV) on substrate turnover and oxidation, 10 healthy young males were studied during 60 min of cycling exercise at 61% peak oxygen uptake on two separate occasions > or =1 wk apart. Exercise was performed under control conditions (CON; placebo), and after 4 days of diuretic administration (DIU; Novotriamazide; 100 mg triamterene and 50 mg hydrochlorothiazide). DIU resulted in a calculated reduction of PV by 14.6 +/- 3.3% (P < 0.05). Rates of glucose appearance (R(a)) and disappearance (R(d)) and glycerol R(a) were determined by using primed constant infusions of [6,6-(2)H]glucose and [(2)H(5)]glycerol, respectively. No differences in oxygen uptake during exercise were observed between trials. Main effects for condition (P < 0.05) were observed for plasma glucose and glycerol, such that the values observed for DIU were higher than for CON. No differences were observed in plasma lactate and serum free fatty acid concentrations either at rest or during exercise. Hypohydration led to lower (P < 0.05) glucose R(a) and R(d) at rest and at 15 and 30 min of exercise, but by 60 min, the effects were reversed (P < 0. 05). Hypohydration had no effect on rates of whole body lipolysis or total carbohydrate or fat oxidation. A main effect for condition (P < 0.05) was observed for plasma glucagon concentrations such that larger values were observed for DIU than for CON. A similar decline in plasma insulin occurred with exercise in both conditions. These results indicate that diuretic-induced reductions in PV decreases glucose kinetics during moderate-intensity dynamic exercise in the absence of changes in total carbohydrate and fat oxidation. The specific effect on glucose kinetics depends on the duration of the exercise.

Adult↗

PubMed1993

Regulation of renal hemodynamics after protein feeding: effects of proximal and distal diuretics.

The purpose of these studies was to compare the effects of proximally and distally acting diuretics on the renal hemodynamic response to protein feeding to determine the importance of the proximal tubule in postprandial renal vasodilation. In chronically instrumented conscious dogs, a meat meal (10 g/kg raw beef) caused glomerular filtration rate (GFR) to increase from 63 +/- 5 to 87 +/- 10 ml/min and effective renal plasma flow (ERPF) to increase from 189 +/- 20 to 249 +/- 20 ml/min, while plasma alpha-amino nitrogen levels rose from 4.0 +/- 0.1 to 6.8 +/- 0.4 mg/dl. Administration of amiloride (0.2 mg/kg + 0.003 mg.kg-1.min-1) or potassium canrenoate (1.76 mg/kg + 1.76 mg.kg-1.h-1), diuretics that act in the distal tubule, had no effect on the renal hemodynamic responses to a meat meal. However, the normal renal hemodynamic responses to protein feeding were abolished during administration of a diuretic that acts in the proximal tubule, acetazolamide (20 mg/kg + 20 mg.kg-1.h-1), although plasma alpha-amino nitrogen levels increased after the meat meal in all experiments. These data suggest that normal proximal tubular sodium reabsorptive function is necessary for acute protein-stimulated renal vasodilation and are consistent with the hypothesis that a tubuloglomerular feedback mechanism may mediate postprandial renal vasodilation.

Acetazolamide↗

PubMed1984

Stimulation of Na-K-ATPase in the rat collecting tubule by two diuretics: furosemide and amiloride.

To test whether sodium availability controls the concentration of renal Na-K-ATPase, we evaluated the effect of chronic alterations in apical membrane sodium permeability in specific nephron segments on the maximal activity of Na-K-ATPase. For this purpose Na-K-ATPase activity was determined in nephron segments microdissected from rats treated continuously for 3-8 days with either furosemide or amiloride, two diuretics known to lower the apical permeability to sodium in the thick ascending limb and the collecting tubule, respectively. Unexpectedly, Na-K-ATPase activity was decreased neither in the thick ascending limb nor in the collecting tubule after administration of either drug. In fact, both diuretics paradoxically increased the pump activity by 60-150% in the collecting tubule. This stimulation of Na-K-ATPase activity was accompanied with an enhancement of the collecting tubule diameter. Stimulation of Na-K-ATPase was identical in the collecting tubule of diuretic-treated rats receiving spironolactone. These results suggest that Na-K-ATPase maximal activity is not controlled by sodium availability or by aldosterone under these conditions and that chronic administration of furosemide or amiloride induces Na-K-ATPase activity in the collecting tubule. This effect appears to be independent of aldosterone.

Adenosine Triphosphatases↗

PubMed2001

Ultrafiltration in diuretic-resistant volume overload in nephrotic syndrome and patients with ascites due to chronic liver disease.

Patients with nephrotic syndrome and those with cirrhosis are predisposed to salt and water retention due to reduced renal sodium excretion. Despite the prescription of low-sodium diets and diuretics, some patients develop refractory oedema. When other medical treatments have been ineffective, isolated ultrafiltration and hemofiltration have been successfully used to treat refractory nephrotic patients. Following fluid removal, patients become responsive to diuretics. In cirrhotic patients, re-infusion of ascites and paracentesis with albumin infusion have been reported to be equally effective in managing ascites refractory to diuretic and other standard therapies. Although isolated ultrafiltration has not been successful in controlling ascitic fluid, hemofiltration has been shown to be beneficial, whereas standard intermittent hemodialysis has been reported to be ineffective.

Ascites↗

PubMed1993

ICI 206,970: a novel calcium channel blocker with eukalemic diuretic activity.

ICI 206,970 is a novel eukalemic diuretic from the aminomethylphenol pyrazine series which exhibited a calcium antagonist profile. The isolated rat aorta evaluation and dihydropyridine ligand [3H]-PN 200-110 binding studies demonstrated that ICI 206,970, like verapamil and nifedipine, inhibits vascular smooth muscle tone by inhibiting voltage-sensitive calcium channels. ICI 206,970 produced dose-related hypotensive, negative chronotropic, dromotropic, and coronary vasodilator responses after i.v. injection in anesthetized dogs. ICI 206,970, similar to calcium channel blockers and dissimilar to diuretics, produced an acute antihypertensive effect in spontaneously hypertensive rats (SHR), and significant protection against the development of myocardial hypertrophy in SHR after chronic oral treatment for 28 consecutive days. It is concluded that ICI 206,970 is a calcium channel blocker in addition to its novel eukalemic diuretic property.

Animals↗

PubMed1997

Saturable accumulation and diuretic activity of hydrochlorothiazide in the isolated perfused rat kidney.

The role of tubular accumulation in renal disposition and diuretic efficacy of hydrochlorothiazide was studied in the isolated perfused rat kidney. Hydrochlorothiazide resulted in a dose-dependent increase in the fractional excretion of sodium, chloride and potassium, and in urinary flow and pH. Renal clearance of the drug was low as a result of a low extraction ratio and extensive nonionic back-diffusion. Hydrochlorothiazide was subject to saturable tubular secretion, following Michaelis-Menten kinetics. Parameters obtained after nonlinear regression analysis were a maximum tubular transport velocity of 42 +/- 6 micrograms/min, a Michaelis-Menten constant of secretion of 38 +/- 11 micrograms/ml and a fraction of excreted drug reabsorbed passively of 0.49 +/- 0.03. The thiazide diuretic accumulated extensively in kidney tissue due to active cellular uptake (maximum capacity of renal accumulation of 500 +/- 270 micrograms/g; affinity constant of renal accumulation of 28 +/- 16 micrograms/ml) and passive diffusion. Plots were constructed of the sodium excretion rate versus hydrochlorothiazide perfusate concentration or the renal excretion rate. The perfusate plot could be described by the sigmoid Emax model, while a simplification of the model had to be used for the response curve in urine because a maximum effect was not observed. The apparent maximum effect resulting from the perfusate concentration-response curve and the discrepancy with the renal excretion rate-response curve indicates that the diuretic effect of hydrochlorothiazide is restricted by saturable accumulation and secretion.

Animals↗

PubMed1994

Pharmacological classification and renal actions of diuretics.

Diuretics may be classified according to their chemical structure, their mechanism and site of action within the nephron, and their diuretic potency. Those agents with primary action in the proximal nephron include the carbonic anhydrase inhibitors, e.g. acetazolamide, a sulfonamide derivative. Other drugs containing the sulfonamido grouping, e.g. furosemide, chlorothiazide and metolazone, also have secondary effects on the proximal nephron. Those drugs which have their major pharmacologic activity within the ascending limb of the loop of Henle, inhibiting the sodium/potassium/2 chloride electroneutral transport system, include the sulfonamide agents furosemide, bumetanide, piretanide and torasemide, and the phenoxyacetic acid derivative, ethacrynic acid. In the early portion of the distal convoluted tubule, sodium chloride reabsorption is impaired by the thiazide group, indapamide and metolazone, as their primary site of action. In the late reaches of the distal convolution and in the collecting duct, agents that inhibit the exchange of sodium for that of hydrogen and potassium have their major sites of activity. These agents, spironolactone, amiloride and triamterene, differ not only chemically but in their mechanisms of action. Diuretics may also be grouped according to potency. The loop of Henle agents are the most powerful, causing the excretion of 20-25% of filtered sodium load. The thiazide group and metolazone are moderately potent, resulting in the excretion of 5-8% of filtered sodium, and the 'potassium-sparing' drugs are only mildly potent, causing the excretion of only 2-3% of filtered sodium.

Diuretics↗

PubMed1994

Liver cirrhosis with ascites: pathogenesis of resistance to diuretics and long-term efficacy and safety of torasemide.

In a prospective randomized short-term study, the efficacy and safety of xipamide and a combination of spironolactone and furosemide were compared in the treatment of hepatic cirrhotic ascites. Twenty-two patients were randomized to either xipamide, 20 mg/day (group I), or spironolactone, 200 mg/day, combined with furosemide, 40 mg on alternate days (group II). During the first 4 days of treatment, adequate diuresis, measured as loss of body weight greater than 1.6 kg, occurred in 7 patients in group I and in 3 in group II. In the latter group, another 4 patients responded satisfactorily after a further 4 days of treatment. Four patients in group I who failed to respond to xipamide with an adequate loss of body weight were subsequently treated with the spironolactone-furosemide combination, but only one responded. Two patients in group II who failed to respond to the combination of spironolactone and furosemide also failed to respond to xipamide. In both groups, a positive diuretic response occurred only when the pretreatment fractional sodium excretion exceeded 0.2%. Diuretic resistance was overcome only by additional treatments which reduced proximal tubular sodium reabsorption. Xipamide commonly induced hypokalaemia; in contrast hyperkalaemia was seen following treatment with the spironolactone-furosemide combination. Renal function remained stable in all patients during both diuretic treatments. An open ongoing 6-month trial of torasemide, 10-40 mg/day, in combination with spironolactone, 50-400 mg/day, has also been undertaken in 117 patients with cirrhotic ascites who showed inadequate responses to salt and water restriction and spironolactone alone. Twenty-seven patients have been withdrawn from the study, 9 for the complications of hepatic coma, bleeding oesophageal varices, or hyponatraemia. Twenty-two patients are still being treated and 68 have completed the trial on a mean dose of torasemide, 15 mg/day. Body weight was reduced by a mean of 2.3 kg at 6 weeks, 2.6 kg at 14 weeks and 3.2 kg after 6 months. Loss of body weight was primarily associated with reduction of ascites and secondarily with reduction of peripheral oedema. There were no untoward adverse reactions with torasemide, and no significant changes in serum electrolytes, liver, renal, or haematological variables.

Ascites↗

PubMed1990

Torasemide, a new loop diuretic, in patients with chronic renal failure.

Torasemide, a new loop diuretic, was administered in 9 hospitalized patients with chronic renal failure to treat both arterial hypertension and peripheral edema. The urine of 5 patients was collected over 12-hour periods to assess the long-lasting diuretic activity of torasemide. Torasemide induced a significant decrease in blood pressure and reversion of peripheral edema in all patients without adverse effects. Torasemide is a high-ceiling loop diuretic, useful in correcting extracellular fluid volume expansion in patients with chronic renal failure.

Adult↗

PubMed1992

Effects of thiazide diuretics on the lipid profile of infants with bronchopulmonary dysplasia.

Hyperlipidemia has been reported in some infants with bronchopulmonary dysplasia (BPD) who received thiazides for extended periods. In this prospective, controlled trial, we studied 17 infants with BPD who received diuretic therapy and 26 control infants who did not receive diuretics. Plasma triglycerides, total cholesterol and high-density lipoprotein (HDL) cholesterol were measured enzymatically prior to onset of diuretic therapy in the study group of infants and on the day of recruitment into the study in control infants, and every 2 weeks thereafter. Plasma low-density lipoprotein cholesterol concentrations were calculated. At the end of 4 weeks, plasma lipid concentrations were comparable in both groups of infants except for significantly higher plasma HDL cholesterol concentrations observed in infants who received chlorothiazide (39 +/- 15 vs. 30 +/- 6 mg/dl, p less than 0.05). Short-term administration of chlorothiazide to infants with BPD is not associated with clinically significant changes in plasma lipid concentrations.

Analysis of Variance↗