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PubMed1984

Potassium-sparing diuretics: interaction with digoxin in elderly men.

The effects of two potassium-sparing diuretic combination drugs, triamterene-hydrochlorothiazide and spironolactone-hydrochlorothiazide, were compared with those of two kaliuretic diuretics, hydrochlorothiazide and furosemide, in order to ascertain the effects of those diuretics on concentrations of serum digoxin, serum potassium, and erythrocyte potassium, and to determine whether any of these diuretics should be preferred for patients taking digoxin. It was concluded that in patients for whom potassium depletion may lead to digoxin toxicity, a potassium-sparing diuretic may safely be used in order to reduce potassium excretion and thereby reduce the risk of arrhythmias.

Aged↗
PubMed1984

The use of diuretics in modern antihypertensive therapy.

A review is made to sum up the indications when diuretics may be the drug of choice in the treatment of hypertension. Advantages from the combined treatment of thiazide diuretics and other antihypertensive agents are also emphasized. Adverse effects from diuretic treatment, i.e. hypokalemia, hyperuricemia, impaired glucose tolerance and risks associated with unfavourable serum lipoprotein patterns are discussed. It is concluded that from a hemodynamic point of view thiazide diuretics can be a good therapeutic alternative for most patients, excepting those with hyperkinetic circulation. It is recommended to use lower doses of thiazide diuretics than previously and the monitoring of S-potassium is necessary in all patients.

Adrenergic beta-Antagonists↗
PubMed1986

Loop-diuretic inhibition of adrenaline-stimulated Cl- secretion in a cultured epithelium of renal origin (MDCK).

Loop diuretics (furosemide, bumetanide, piretanide) inhibit the adrenaline-stimulated short-circuit current due to transepithelial Cl- secretion in cultured renal epithelial layers (MDCK). The inhibition of Cl- secretion by loop diuretics is consistent with the presence of basal-lateral 'cotransport' since inhibition is observed only with the basal applications of loop diuretics, is of high potency (half-maximal bumetanide inhibition being observed at 0.8 microM, bumetanide being more potent than furosemide) and is without effect upon the adrenaline-stimulated increase in tissue conductance. Loop diuretics are also shown to inhibit a component of K+ efflux across the basal-lateral surfaces. Cellular uptake of [3H]bumetanide across both apical and basal surfaces of intact epithelial layers was measured in order to localize the cotransport system. A component of cellular [3H]bumetanide uptake sensitive to competition by 0.1 mM unlabelled loop diuretic is only observed from the basal-lateral cell surfaces. There is no evidence for transepithelial bumetanide secretion as is seen in renal cortex.

Animals↗
PubMed1975

Effect of diuretics on urinary excretion of cephalothin in humans.

Diuretics and antibiotics are frequently used concomitantly. The possibility of drug interactions led us to study the effects of several diuretics on the renal elimination of cephalothin. Five healthy volunteers received a constant infusion of 500 mg of sodium cephalothin per h for 9 h on 4 consecutive days. Each day, after the third hour of infusion, the subjects were given one of the following in varying order: (i) furosemide (1 mg/kg, intravenous), (ii) mercaptomerin (250 mg, intramuscular), (iii) mannitol (25 g, intravenous), or (iv) no diuretic (control day). Fluid losses were replaced hourly. Serum and complete urine collections were obtained each hour and assayed for creatinine and cephalothin (bioassay). Clearances (milliliter per minute) and urinary excretions (milligram per hour) of cephalothin did not differ either when the diuretic day values were compared with control day, or when pre- and postdiuretic results on the same day were compared. Creatinine clearances were not affected by diuretics except for a transient rise after furosemide.

Adult↗
PubMed1980

Attenuation of hypotensive effect of propranolol and thiazide diuretics by indomethacin.

The effects of 100 mg indomethacin daily for three weeks on blood pressure and urinary excretion of prostaglandin F2 alpha were studied in a double-blind, placebo-controlled comparison of two groups of patients with essential hypertension, eight receiving propranolol and seven thiazide diuretics. Compared with placebo, adding indomethacin to the patients' established antihypertensive treatment increased blood pressure by 14/5 Hg supine and 16/9 mm Hg erect in the patients receiving propranolol, and by 13/9 mm Hg supine and 16/9 mm Hg erect in the patients receiving thiazide diuretics (all p less than or equal to 0.05). The excretion of the major urinary metabolite of prostaglandin F2 alpha was reduced by 67% in the propranolol-treated patients and by 57% in those receiving a thiazide diuretic. Body weight increased by 0 . 8 kg (propranolol) and 1 . 1 kg (thiazide diuretic) when indomethacin was given, but there were no significant changes in creatinine clearance, urinary sodium excretion, or packed cell volume in either treatment group. These results suggest that products formed by the arachidonic acid cyclo-oxygenase contribute to the regulation of blood pressure during treatment with both propranolol and thiazide diuretics. Inhibition of the cyclo-oxygenase with indomethacin partially antagonises the hypotensive effect of these drugs.

Adult↗
PubMed1988

Reduced concentrations of potassium, magnesium, and sodium-potassium pumps in human skeletal muscle during treatment with diuretics.

Animal studies have shown that potassium depletion induced by diuretics or potassium deficient fodder leads to a selective decrease in the concentrations of potassium and in the concentration of sodium-potassium pumps in skeletal muscle. In 25 patients who had received diuretics for 2-14 years the mean concentrations of potassium, magnesium, and sodium-potassium pumps were measured in skeletal muscle biopsy specimens and were significantly lower than in those from a group of age matched controls. The reductions in all three variables were significant in those patients receiving diuretics for arterial hypertension as well as in those being treated for congestive heart failure. In 14 patients the mean muscle potassium concentration was below the control range, but only one of those was hypokalaemic (3.4 mmol/l), and 13 were receiving potassium supplements. In 15 patients the mean muscle magnesium concentration was below normal, and the mean muscle potassium and magnesium concentrations showed a linear correlation. In 12 patients in whom the mean muscle potassium concentration was below 80 mumol/g wet weight there was a linear correlation between the cellular potassium:sodium ratio and the concentration of 3H-ouabain binding sites indicating that potassium deficiency also leads to a down regulation of sodium-potassium pumps in human skeletal muscle. In spite of potassium supplements long term treatment with diuretics may lead to potassium and magnesium deficiencies, which are not detectable using the standard methods of serum analysis. The changes in concentrations of electrolytes and sodium-potassium pumps associated with treatment with diuretics may impair muscle function and potassium homoeostasis and interfere with the distribution of digitalis glycosides.

Adult↗
PubMed1994

Effect of loop diuretics on cholinergic neurotransmission in human airways in vitro.

BACKGROUND: Frusemide can inhibit various indirectly acting bronchoconstrictor stimuli in asthmatic patients. Both frusemide and bumetanide also modulate airway neurotransmission in some species but there are no data on the effect of loop diuretics on neurotransmission in man. An in vitro study was performed in human airways to investigate the possible neuromodulatory action of two loop diuretics, frusemide and bumetanide, and to elucidate whether a cyclooxygenase inhibitor such as indomethacin could modulate the effect of frusemide. The effect of acetazolamide, a carbonic anhydrase inhibitor, was also investigated. METHODS: Electrical field stimulation (EFS; 40 V, 0.5 ms, 0.5-32 Hz for 15 seconds) in human airways with or without epithelium was used to induce a cholinergic contraction (n = 5 in all experiments). Indomethacin was present throughout. After obtaining a control frequency-response curve, different concentrations of diuretic were added to the organ bath and another frequency-response curve was constructed. To determine whether the effect of the diuretic was prejunctional or postjunctional a cumulative concentration-response curve to exogenous acetylcholine (Ach, 0.3 mumol/l to 10 mmol/l) was constructed in the presence of a diuretic (frusemide 1 mmol/l or bumetanide 0.1 mmol/l) or its vehicle. In some experiments indomethacin was omitted from the organ bath to investigate the possible involvement of cyclooxygenase products. RESULTS: Both frusemide (10 mumol/l to 1 mmol/l) and bumetanide (1 mumol/l to 0.1 mmol/l) produced a concentration-dependent inhibition of the EFS-induced cholinergic contraction in human airways in vitro but only in epithelium denuded tissues. Frusemide (1 mmol/l) produced a maximum inhibition of 46.3% (SE 9.9%) at 0.5 Hz and bumetanide (0.1 mmol/l 39.6 (6.2)% at 0.5 Hz. Without indomethacin in the organ bath the frusemide-induced inhibition was enhanced at 4, 8, and 16 Hz, but bumetanide-induced inhibition was not enhanced at any frequency when indomethacin was omitted. Frusemide (1 mmol/l) and bumetanide (0.1 mmol/l) had no effect on the cumulative concentration-response curve to exogenous Ach (0.3 mumol/l to 10 mmol/l). Acetazolamide (100 mumol/l) had no effect on the EFS-induced cholinergic contraction in tissues with or without epithelium. CONCLUSIONS: In human airways in vitro both frusemide and bumetanide produced a concentration-dependent inhibition of the EFS-induced cholinergic contraction. This inhibition is mediated through a prejunctional mechanism. Epithelium removal was necessary to achieve this effect. The mechanism of action of frusemide and bumetanide on airway nerves remains unclear: inhibition of the Na-K-Cl cotransporter is a possibility and, for frusemide, release of endogenous cyclooxygenase products may be involved. Carbonic anhydrase inhibition, on the other hand, is unlikely to be a factor.

Acetazolamide↗
PubMed1993

Diuretic-enhanced I-131 clearance after ablation therapy for differentiated thyroid cancer.

The authors assessed whether the whole-body radiation burden can be reduced with diuretic enhancement of iodine-131 excretion in patients with thyroid cancer and slow clearance. Whole-body imaging and quantitative I-131 clearance data obtained before and after ablation therapy were evaluated in 56 patients. Fourteen patients with slow pre-ablation therapy clearance (> 50% retention at 24 hours) received oral diuretics after I-131 therapy. Nine patients began taking furosemide 24 hours after I-131 treatment. Five patients had been receiving thiazide diuretics and were continued on the same dose after treatment. The mean half-time of I-131 clearance for the patients treated with furosemide decreased by 12 hours (P < .05) but was not significantly decreased for those who received thiazides or for the patients who did not receive diuretics. Administration of diuretics can improve I-131 clearance in patients with thyroid cancer and slow clearance, reducing the radiation burden and shortening the hospital stay.

Adolescent↗
PubMed2002

Upregulation of Na+ transporter abundances in response to chronic thiazide or loop diuretic treatment in rats.

Furosemide and hydrochlorothiazide (HCTZ) exert their diuretic actions by binding to apical Na(+) transporters, viz., the Na(+)-K(+)-2Cl(-) cotransporter in the thick ascending limb and the Na(+)-Cl(-) cotransporter in the distal convoluted tubule, respectively. We carried out semiquantitative immunoblotting and immunohistochemistry of rat kidneys to investigate whether chronic administration of furosemide or HCTZ is associated with compensatory changes in the abundance of Na(+) transporters downstream from the primary site of action. Osmotic minipumps were implanted into Sprague-Dawley rats to deliver furosemide (12 mg/day) or HCTZ (3.75 mg/day) for 7 days. To prevent volume depletion, all animals were offered tap water and a solution containing 0.8% NaCl and 0.1% KCl as drinking fluid. The diuretic/natriuretic response was quantified in response to both agents by using quantitative urine collections. Semiquantitative immunoblotting revealed that the abundances of thick ascending limb Na(+)-K(+)-2Cl(-) cotransporter and all three subunits of the epithelial Na(+) channel (ENaC) were increased by furosemide infusion. HCTZ infusion increased the abundances of thiazide-sensitive Na(+)-Cl(-) cotransporter and beta-ENaC in the cortex and beta- and gamma-ENaC in the outer medulla. Consistent with these results, beta-ENaC immunohistochemistry showed a remarkable increase in immunoreactivity in the principal cells of collecting ducts with either diuretic treatment. These increases in the abundance of Na(+) transporters in response to chronic diuretic treatment may account for the generation of diuretic tolerance associated with long-term diuretic use.

Animals↗
PubMed1996

Loop diuretics attenuate bradykinin-induced increase in clearance of macromolecules in the oral mucosa.

The purpose of this study was to determine whether loop diuretics attenuate bradykinin-induced increase in clearance of macromolecules in the oral mucosa in situ and, if so, to start to determine the mechanisms that mediated these responses. By using intravital microscopy, we found that bradykinin induced a significant concentration-dependent increase in fluorescein isothiocyanate-labeled dextran (mol mass 70 kDa) leaky site formation in the hamster cheek pouch. These responses were significantly attenuated by topical application of two structurally distinct loop diuretics, furosemide and ethacrynic acid, onto the cheek pouch (P < 0.05). Hydrochlorothiazide, a nonloop diuretic, had no significant effects on bradykinin-induced responses. Furosemide had no significant effects on adenosine-induced leaky site formation. Application of bradykinin after furosemide, but not after hydrochlorothiazide, was associated with a significant concentration-dependent decrease in bradykinin-like immunoreactivity in the cheek pouch suffusate (P < 0.05). Prostaglandins and changes in vasomotor tone did not modulate the effects of furosemide on bradykinin-induced responses. These data indicate that loop diuretics attenuate bradykinin-induced increase in clearance of macromolecules in the oral mucosa in a specific fashion, probably by amplifying local bradykinin catabolism. We suggest that topical loop diuretics could be useful in the treatment of oral mucosa inflammation elicited by bradykinin.

Adenosine↗
PubMed1999

Pearls and pitfalls in the use and abuse of diuretics for chronic congestive heart failure.

The main purpose of using diuretics is usually lost sight of, i.e. it is for the relief of dyspnea by using the least amount of a diuretic. The production of a low output state and hypercoagulation in an attempt to achieve dry weight by lowering blood volume excessively are among the hazards of using more diuretic than is absolutely necessary to achieve the goal of relieving dyspnea. The use of jugular venous pressure measurement and the status of dyspnea should have precedence over body weight in determining diuretic dose adjustment. Often forgotten in using diuretics is that potassium without magnesium will not enter cells and that the almost universal preference for furosemide over thiazides threatens to increase the incidence of osteoporosis. Also, the tendency to ignore loss of the water-soluble vitamins thiamine and ascorbic acid may result in refractory edema and the inability to manage the stresses of congestive heart failure.

Animals↗
PubMed2003

Effects of forced diuresis achieved by oral hydration and oral diuretic administration on uroflowmetric parameters and clinical waiting time of patients with lower urinary tract symptoms.

INTRODUCTION: We studied the impact of diuresis forced by oral hydration or single-dose oral diuretic administration on uroflowmetric parameters and clinical waiting time of patients with lower urinary tract symptoms. PATIENTS AND METHODS: A total of 58 patients with a mean age of 59 (range 41-77) years who presented with lower urinary tract symptoms were included in the study. The patients were grouped with respect to their International Prostate Symptom Scores as having mild, moderate, or severe symptoms. The prostatic volumes of the patients were calculated using transrectal ultrasound. Uroflowmetric measurements were performed on 3 consecutive days. On the 1st day, the test was performed without diuretic stimulation; on the 2nd day, oral hydration was applied, and on the 3rd day, the patients received 20 mg of furosemide orally. Voiding time, maximum flow rate, voided volume, and the time elapsed in minutes until voiding (waiting time) were recorded. RESULTS: Diuretic stimulation did not significantly alter the uroflowmetric parameters in each symptom group, but the waiting time was significantly reduced. Forced diuresis caused acute urinary retention in 5 of 20 (25%) severely symptomatic patients. CONCLUSIONS: Forced diuresis with oral hydration or oral administration of diuretics improves patient comfort and test applicability by shortening clinical waiting time and reducing the number of attempts to reach the sufficient urine volume for reliable measurements and can be applied safely for mild and moderately symptomatic patients. On the other hand, the risk of 25% of acute urinary retentions should be reconsidered, and the decision about diuretic stimuli should be made carefully by the clinician in severely symptomatic patients.

Administration, Oral↗
PubMed1994

Comparative pharmacokinetics and pharmacodynamics of loop diuretics in renal failure.

Loop diuretics increase the fractional excretion of volume, sodium, potassium, chloride and calcium in all stages of renal failure, and their potency is directly correlated with these excretory activities. Tubular secretion of loop diuretics in renal failure is impaired both by reduced renal blood flow and by reduced activity of the tubular carrier system. For these reasons, high concentrations of diuretics in the peritubular capillaries are necessary to guarantee delivery of sufficient drug to their site of action in the ascending limb of the loop of Henle. Piretanide and furosemide have a constant extrarenal elimination and thus accumulate in renal failure. Decreased renal excretion of bumetanide is compensated by hepatic elimination and hence bumetanide does not accumulate. Elimination of torasemide is also independent of its renal excretion. Thus in renal failure, torasemide is the only loop diuretic in which the plasma concentration is strictly dose dependent. Loop diuretics follow a number of different metabolic pathways, but this may not be clinically relevant.

Diuretics↗
PubMed1988

Diuretic pharmacokinetics and pharmacodynamics in infants from the analysis of urinary drug excretion data.

New equations are described that permit the determination of both drug disposition and diuretic response of luminally active diuretics from the analysis of urinary drug excretion data. The methods represent a convenient and logical approach for the clinical study of the disposition of renally excreted drugs that are described by a one-compartment open model and the response of luminally active diuretics that exhibit a linear diuretic excretion rate-response relationship. The validity of the approach is verified in a study of furosemide disposition and response in 10 infants. These methods will facilitate the studies of diuretics in newborn and young infants and other populations that are difficult to study by conventional methodology.

Child, Preschool↗
PubMedDate not supplied

Effects of withdrawing diuretic therapy on blood pressure in mild hypertension.

A 1-year double-blind placebo-controlled study on the effects of diuretic withdrawal was conducted on a group of 62 previously well-controlled, mildly hypertensive patients. Data were collected on blood pressure (BP), biochemical laboratory values, and subjective reports of side-effects. Twenty-six percent of placebo subjects and 3% of the active treatment subjects reached preset criteria for the return of hypertension (reverters). The average systolic and diastolic pressures of all placebo-treated patients who did not revert showed statistically significant increases. BP control was quickly reestablished in reverters by restarting diuretic therapy. No substantial differences in side-effects were reported between the groups, and laboratory changes were those consistent with known metabolic effects of thiazide and thiazide-like diuretics. This study showed a much lower reversion rate after treatment withdrawal than previously reported by other investigators. It also showed significant increases in BP of placebo patients who did not revert. Long-term diuretic therapy retains its effectiveness in responsive mild hypertensive patients, potentially offering protection against the increased risks of mortality and morbidity associated with even slight elevations of BP. Withdrawal of diuretics cannot be recommended for patients with mild hypertension without use of other equally effective interventions to maintain optimum BP control.

Adult↗
PubMed2002

Differential actions of vasopeptidase inhibition versus angiotensin-converting enzyme inhibition on diuretic therapy in experimental congestive heart failure.

BACKGROUND: Omapatrilat (OMA), a vasopeptidase inhibitor, simultaneously inhibits angiotensin-converting enzyme (ACE) and neutral endopeptidase, which degrades vasodilatory factors (eg, ADM) and natriuretic peptides. Based on the beneficial cardiorenal and humoral properties of the natriuretic peptides, we hypothesized that an acute vasopeptidase inhibitor with or without diuretic would result in more favorable cardiorenal and hormonal actions than ACE inhibition plus diuretic (ACEI+D) in congestive heart failure. METHODS AND RESULTS: We compared the actions of OMA alone and with diuretic (OMA+D) to ACEI+D in a model of pacing-induced congestive heart failure. OMA+D decreased pulmonary arterial and pulmonary capillary wedge pressures to a greater level than OMA alone or ACEI+D. Glomerular filtration rate was lower with ACEI+D than with either OMA group. Plasma renin activity and aldosterone immediately increased with ACEI+D, whereas OMA+D resulted in higher plasma renin activity and a delayed increase in aldosterone. OMA alone did not increase plasma renin activity and aldosterone, but resulted in a sustained increase in plasma adrenomedullin, with higher urinary atrial natriuretic peptide, adrenomedullin, and cGMP excretions than with ACEI+D. CONCLUSIONS: Acute administration of OMA with or without diuretic results in more favorable cardiorenal and humoral responses in experimental congestive heart failure than does ACEI+D. There is no acute activation of renin and aldosterone with OMA alone such as occurs with ACEI+D and OMA+D. Thus, OMA with or without a diuretic possesses beneficial cardiorenal and humoral actions comparable to those observed with ACEI+D that can be explained by potentiation of natriuretic peptides.

Adrenomedullin↗
PubMed1983

Indapamide: a unique diuretic?

Indapamide (Lozol) is a new diuretic and antihypertensive agent. The drug appears to have a unique mechanism of action, combining diuretic effects with a direct vascular action, presumably secondary to calcium channel blockade. Available studies indicate that indapamide is comparable to hydrochlorothiazide, chlorothiazide, furosemide, and other diuretic agents in the management of hypertension and edema. The drug produces toxicity similar to that of the thiazide and loop diuretics; however, it does not appear to increase cholesterol levels. Although it is claimed that indapamide produces no effect on glucose levels, hyperglycemia has been reported. Indapamide is safe and effective for treatment of hypertension in mild to severe renal impairment, but advantages over furosemide are questionable. Indapamide is a unique diuretic, but does not appear to offer advantages over other available agents.

Antihypertensive Agents↗
PubMed1994

Hypertension: are beta-blockers and diuretics appropriate first-line therapies?

OBJECTIVE: To review the existing data on the use of diuretics or beta-blockers as first-line therapy for the treatment of mild to moderate hypertension, and to examine the issues surrounding the impact of these classes as well as the angiotensin-converting enzyme (ACE) inhibitors, calcium-channel blockers (CCBs), alpha-blockers, and alpha-beta-blockers on cardiovascular risk factors and cardiovascular morbidity and mortality. DATA SOURCES: A MEDLINE search of applicable articles on antihypertensive therapies and their impact on morbidity and mortality. In addition, a MEDLINE search of relevant articles regarding cardiovascular risk factors and the influence of the various antihypertensive therapies on these parameters. DATA SYNTHESIS: The literature was evaluated with regard to outcome. Trials examining the impact of antihypertensive pharmacotherapy, primarily with diuretics and beta-blockers, have shown them to decrease the incidence of stroke by 33-50 percent. However, their effect on coronary heart disease has been disappointing, showing only a 14 +/- 5 (mean +/- SD) percent decrease. Examination of numerous clinical trials assessing the impact of the various antihypertensive therapies on cardiovascular risk factors, including blood pressure, plasma lipids, diabetic control/insulin sensitivity, and left ventricular hypertrophy was done. The classes included beta-blockers, diuretics, alpha-blockers, ACE inhibitors, and CCBs; the results show a diversity of effect. Diuretics and beta-blockers tend to worsen cardiovascular risk status, whereas the alpha-blockers, ACE inhibitors, and CCBs all show a beneficial effect. CONCLUSIONS: Diuretics and beta-blockers can effectively reduce cerebrovascular morbidity and mortality, but have a limited effect on reducing cardiovascular disease, especially myocardial infarction. This may be explained, at least in part, by the negative, or lack of positive, effect on individual patients' overall cardiovascular risk status.

Adrenergic alpha-Antagonists↗