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PubMed1993

Diuretics in postinfarction heart failure.

Severe left ventricular failure, as evidenced by radiographic pulmonary edema or raised left ventricular filling pressure, accompanying acute myocardial infarction, carries a high mortality risk. In this situation, the intravenous loop-diuretic furosemide induces a rapid reduction in the raised left ventricular filling pressure due to an immediate and substantial increase in systemic venous compliance accompanied by increasing diuresis. This diuretic-induced venodilatation is probably due to the release of prostaglandins. The transient systemic arterial constriction and small increase in systemic blood pressure that follows intravenous furosemide probably results from the release of renin and subsequent activation of angiotensin. These diuretic induced hemodynamic changes are accompanied by restoration of the vasodilator reflex, which enables the heart to accommodate an acute volume load. Orally administered loop diuretics achieve slower, but similar, directional hemodynamic changes. There is no information on hemodynamic or neuroendocrine dose-response effects of loop diuretics, and there is no information pertaining to the use of other diuretic groups in this situation. The hemodynamic changes induced by furosemide summate with the changes induced by other anti-heart-failure drugs. In this subset of patients with acute myocardial infarction and severe heart failure, the influence of the diuretics on morbidity incidence and mortality risk remains to be measured.

Cardiac Output, Low↗
PubMed1982

Molecular actions of diuretics.

The criteria upon which diuretics are classified is based upon their site of action within the nephron. Carboanhydrase inhibitors act in the proximal tubule, high-ceiling diuretics in the ascending loop of Henle, the thiazides in the early distal tubule and the potassium-sparing diuretics in the late distal tubule and in the collecting duct. On the molecular level diuretics do not inhibit Na+-K+-ATPase but interfere with the permeability of the tubule membranes or transport systems for certain ions and thus also influence the potential differences in the different parts of the nephron. Since carboanhydrase is located in the proximal tubule cells, not only in the cytosol but also in the brushborders and in the peritubular membranes, acetazolamide and other carboanhydrase inhibitors act on three different sites in these cells. The loop diuretics inhibit the secondary active chloride reabsorption. The receptors in this part of the nephron are stereospecific. Only the levorotatory isomere of ozolinone has active diuretic properties whereas the dextrorotatory isomere does not. Perfusion experiments of the loop of Henle with different lectins give evidence that glycoproteins containing alpha-1-fucose are involved in the reabsorption of Na+ and Cl-. Experiments on the isolated stripped rabbit colon under the condition of chloride secretion reveal striking similarities between the receptors for chloride reabsorption in the luminal cell membranes of the ascending loop of Henle and in the serosal cell membranes of the colon. The potassium-sparing diuretics amiloride and triamterene act by blocking sodium channels in the distal parts of the nephron. Thus the lumen negative potential difference decreases and (passive) potassium secretion is diminished.

Acetazolamide↗
PubMed2003

[Diuretics-first line treatment for hypertension?].

STUDY RESULTS: The role of diuretics in the treatment of arterial hypertension remains a matter of controversy. On the basis of the results of recent studies and economic considerations a broader use of diuretics in the initial antihypertensive therapy has been proposed. The present review analyses two aspects of diuretics which are of interest in this debate. Thus, several studies demonstrate that diuretic therapy is associated with a greater incidence of new-onset diabetes as compared to calcium channel blockers, ACE-inhibitors and AT(1)-antagonists. The clinical relevance of this effect becomes clear when calculating the "numbers needed to treat" (NNT) on the basis of a long-term therapy over several decades. Based on the assumption of linear increases in the incidence of diabetes over time NNT then become remarkably small and in some studies number < 10. Another problem associated with diuretics is the low compliance and persistence with this type of drugs established in "real life" studies in which patients were not disciplined by the study design. These characteristics of diuretic therapy of hypertensive patients challenge the proposed medical and also economic benefit of diuretics as compared to more "modern" antihypertensive agents.

Adrenergic beta-Antagonists↗
PubMed1998

Low-dose theophylline increases urine output in diuretic-dependent critically ill children.

OBJECTIVE: Determine the effect of low-dose theophylline on urine output and the urinary adenosine: cAMP (cyclic adenosine monophosphate) excretion ratio (a measure of phosphodiesterase inhibition) in diuretic-dependent critically ill children. DESIGN: Observational clinical case series and animal laboratory experiment. SETTING: A university pediatric intensive care unit and a pharmacology research laboratory. PATIENTS: 10 consecutive oliguric patients treated with theophylline for diuresis. INTERVENTIONS: Urine output, fluid intake, diuretic dosages, and number of pressors (including dopamine) were monitored over the 24-h period prior to and the 24-h period immediately after theophylline was started. Hourly collections of urine were obtained at baseline and 1 and 3 h after theophylline was started and urinary excretion rates of adenosine and cAMP were measured and calculated. MEASUREMENTS AND RESULTS: Mean theophylline level in the children was 5.0 microg/ml. Urine output increased from 1.58 +/- 0.46 to 3.75 +/- 0.77 ml/kg per h (p = 0.008, paired t-test) after theophylline administration. There was no significant change in fluid intake, vasoactive agents, or dosages of other diuretics during the study periods. Intrarenal infusion of the IC50 concentration of isobutylmethylxanthine for phosphodiesterase activity resulted in a reduction of the adenosine: cAMP urinary excretion ratio in rats (p < 0.05). Low-dose theophylline had no effect on the adenosine: cAMP urinary excretion ratio in children. Concurrent therapy with dopamine was associated with an enhanced diuretic effect of theophylline (with dopamine, 1.30 +/- 0.30 to 5.07 +/- 0.77 ml/kg per h vs without dopamine, 1.77 +/- 0.76 to 2.86 +/- 1.08 ml/kg per h; p = 0.03, two-way ANOVA). There was no interaction between dopamine and low-dose theophylline on the urinary adenosine: cAMP excretion ratio (p = 0.56, two-way ANOVA). CONCLUSIONS: Theophylline increased urine output in diuretic-dependent critically ill children and the diuretic effect may have been potentiated by concurrent use of dopamine. Adenosine receptor antagonism may be a more likely mechanism for the diuretic effect of theophylline than phosphodiesterase inhibition.

Adenosine↗
PubMed2002

Rat NKCC2/NKCC1 cotransporter selectivity for loop diuretic drugs.

It is generally assumed that bumetanide possesses some selectivity for the renal Na-K-Cl cotransporter NKCC2, although the results are scarce in the literature and comparisons were done with extra-renal NKCC1 at its basal, almost silent state. Here we investigated NKCC2/NKCC1 selectivity of loop diuretic drugs (bumetanide, piretanide and furosemide) as a function of the NKCC1 activated state (NKCC1 was activated by hypertonic media). NKCC2 activity was measured in isolated rat medullary thick ascending limb (mTAL) and NKCC1 in rat thymocytes and erythrocytes. When NKCC2 was compared with NKCC1at its activated state, all three diuretic drugs inhibited NKCC2 and NKCC1 with the same potency (bumetanide pIC50=6.48, 6.48 and 6.47; piretanide pIC50=5.97, 5.99 and 6.29; and furosemide pIC50=5.15, 5.04 and 5.21 for mTAL NKCC2, erythrocyte NKCC1 and thymocyte NKCC1, respectively). Basal NKCC1 exhibited a lower diuretic sensitivity, although with marked differences depending on the diuretic drug and the cell type in consideration and with the notable exception of furosemide in erythrocytes. Molecular modelling showed that bumetanide and piretanide possess four potentially active groups, of which three are shared with furosemide at similar intergroup distances. Of these three common groups, one should not bind to basal NKCC1 in thymocytes. The fourth (phenoxy) group (absent in furosemide) confers higher lipophilicity and should not bind to basal NKCC1 in erythrocytes. In conclusion, loop diuretics had no NKCC2/NKCC1 selectivity, when NKCC1 is measured at its activated state. Basal NKCC1 has a reduced diuretic sensitivity, of very different magnitude depending on the diuretic drug and cell type in consideration.

Animals↗
PubMed1987

Diuretics, serum potassium and ventricular arrhythmias in the Multiple Risk Factor Intervention Trial.

To examine the relation between diuretic use and ventricular premature complexes (VPCs) in the Multiple Risk Factor Intervention Trial, data derived from the baseline and annual rest electrocardiograms were analyzed for men in the special-intervention (SI) and usual-care (UC) groups. At baseline, age, diuretic use and presence of other rest electrocardiographic abnormalities were significantly associated with the prevalence of VPCs. Among diuretic users at baseline, those with lower serum potassium levels were most likely to have VPCs. Over the follow-up period among nonhypertensive persons the relative risk (SI/UC) for the occurrence of VPCs during follow-up was 0.83, and for hypertensives this relative risk increased linearly from 1.08 to 1.42, with higher levels of diastolic blood pressure at entry (p less than 0.01 for linear trend of relative risk estimates). This was due to an increasing risk among the SI group, and the risk was independent of the presence or absence of rest electrocardiographic abnormalities at baseline. The relative risk estimate, diuretic vs no diuretic, for development of VPCs was approximately 1.2 (p = 0.04) for SI men and 1.1 (p = 0.35) for UC men. The reduction in serum potassium level was greater for those with VPCs, and regression analysis showed that low serum potassium levels were significantly associated with the incidence of VPCs in both study groups. These data confirm and quantify the relation between diuretic drugs and VPCs and suggest that at least 1 mechanism of diuretic-induced VPCs is potassium depletion.

Adult↗
PubMed1987

Exercise-induced arrhythmias in diuretic-treated patients with uncomplicated systemic hypertension.

Although hypertensive patients have been shown to have a higher prevalence of arrhythmias during ambulatory monitoring when treated with diuretic drugs than when untreated, the effects of maximal aerobic stress on arrhythmia frequency in such patients is unknown. The incidence of arrhythmias during graded maximal treadmill exercise in a group of 68 subjects with mild, clinically uncomplicated systemic hypertension treated chronically with diuretics alone for a median of 4.5 years was compared with that in an age-matched normotensive control group. The prevalence of exercise-induced arrhythmias was higher in the group treated with diuretics than in the control group, 57% vs 38% (p less than 0.05). This difference was entirely due to the higher incidence of isolated atrial or ventricular premature complexes in the diuretic-treated patients, 44% vs 26% (p less than 0.05). There was no difference in the incidence of frequent (more than 10% of beats) or complex supraventricular or ventricular premature complexes between the diuretic-treated and control groups. Within the diuretic group, no difference in the incidence of simple or complex arrhythmia was found between men and women, between those with and those without rest or exercise-induced electrocardiographic abnormalities or between those with a serum potassium level of less than 3.7 mEq/liter vs those with a level of 3.7 mEq/liter or greater. Thus, patients with uncomplicated hypertension treated with chronic diuretic monotherapy do not appear to be at increased risk for major arrhythmias during aerobic exercise.

Adult↗
PubMed1992

A novel quinolinone diuretic, M12285, and its activation mechanism through sulfate conjugation.

The diuretic activity of a quinolinone oxime diuretic, M12285, was examined after renal arterial, i.v. and portal injection in rats. M12285 injected into the renal artery at a dose of 1 mg/kg caused no diuretic effect, whereas i.v. and portal injections induced marked diuresis dose dependently. The minimum effective dose with portal injection was lower (1 mg/kg) than that with i.v. injection (3 mg/kg) and the start of the effect was faster with portal injection. These results indicated that some metabolic modification in the liver is necessary for the diuretic activity to appear. Accordingly, we performed in situ rat liver perfusion with M12285 and obtained several metabolites. Renal arterial injection of each fractionated metabolite of M12285 revealed that all the diuretic activity derived from one of these metabolites. From IR and 1H-nuclear magnetic resonance (1HNMR) measurements, the chemical structure of this active metabolite was assumed to be a sulfate-conjugated form of M12285 at the oxime moiety. Based on this tentative chemical structure, we synthesized the oxime sulfate of M12285 (potassium salt, M17000) and confirmed the identity of IR and 1HNMR spectra. Administration of M17000 into the renal artery induced apparent diuresis in a dose-dependent manner in both rats and dogs. These results indicate that the oxime sulfate of M12285 is responsible for the diuretic activity of M12285. Therefore, we synthesized several derivatives of M17000 and confirmed their possible therapeutic value as a novel family of diuretics, namely quinolinone oxime sulfonic acids.

Animals↗
PubMed2006

Practical applications of intravenous diuretic therapy in decompensated heart failure.

Intravenous (IV) loop diuretics play an important role in the treatment of decompensated heart failure (DHF). They inhibit the Na(+)-K(+)-2Cl(-) reabsorptive pump in the thick ascending limb of the loop of Henle, and the resultant natriuresis and diuresis decreases volume load, improves hemodynamics, and reduces DHF symptoms. However, loop diuretics have a short half-life and their efficacy may be limited by postdiuretic sodium rebound during the period between doses in which the tubular diuretic concentration is subtherapeutic. Moreover, they can produce electrolyte abnormalities, neurohormonal activation, intravascular volume depletion, and renal dysfunction. Several studies have reported an association between diuretic therapy and increased morbidity and mortality. In addition, many patients, especially those with more advanced forms of heart failure (HF), are resistant to standard doses of loop diuretics. These high-risk, resistant patients may benefit from pharmacologic and/or nonpharmacologic interventions to improve hemodynamic performance, treatment of renovascular disease, discontinuation of aspirin and other sodium-retaining drugs, manipulation of the route of delivery or combination of diuretic classes, or hemofiltration. Despite >50 years of use, many questions regarding the use of intravenous diuretic agents in patients with DHF are still unanswered, and there remains a compelling need for well-designed randomized, controlled clinical trials to establish appropriate treatment regimens that maximize therapeutic benefit while minimizing morbidity and mortality.

Diuretics↗
PubMed2002

Evaluating routine diuretics after coronary surgery: a prospective randomized controlled trial.

BACKGROUND: Routine diuretic administration after cardiopulmonary bypass is common despite the lack of evidence for its benefit. We performed a prospective study to evaluate if diuretics assist in weight loss or alter clinical outcome. METHODS: Seventy-nine patients undergoing primary elective coronary bypass surgery were randomized to either diuretic (fusemide and amiloride) or placebo (lactose) postoperatively until preoperative weight was achieved or for 5 days in total. Proportions were compared with chi2 or Fisher's exact test. RESULTS: Forty patients were randomized to diuretics and 39 to placebo. By day 5, 97% of patients (37 of 38) still in the diuretic arm, and 74% of patients (29 of 39) in the placebo arm, achieved preoperative weight (p = 0.02). There were no differences in clinical outcomes. CONCLUSIONS: Routine diuretics promote an earlier diuresis but no clinical benefits are apparent in low risk patients with normal renal function. Clinicians should reconsider routine diuretic prescription in this setting.

Aged↗
PubMed1989

Pharmacology of diuretics in the newborn.

Diuretics are used in various conditions with fluid overload. Their efficacy in the management of congestive heart failure is well documented. In contrast, the indication of diuretics in chronic lung disease and central nervous system disorders of the newborn have not been clearly established. Substantial pharmacologic knowledge of diuretics in the young infant remains to be described. Most investigations on diuretics in the sick newborn infant have examined furosemide. In contrast, the pharmaco-dynamics, pharmacokinetics, clinical indications, and toxicity of other diuretics used in the newborn require considerable further evaluation. Future studies using a combination of diuretics, acting at different segments of the nephron, also may provide newer therapeutic modalities to overcome or prevent the development of frequently observed tolerance to diuretics, as well as to treat refractory edema.

Acute Kidney Injury↗
PubMed1999

Albumin improves the response to diuretics in patients with cirrhosis and ascites: results of a randomized, controlled trial.

BACKGROUND/AIMS: Diuretic treatment of ascites could result in intravascular volume depletion, electrolyte imbalance and renal impairment. We investigated whether intravascular volume expansion with albumin exert beneficial effects in cirrhosis with ascites. METHODS: In protocol 1, 126 cirrhotic inpatients in whom ascites was not relieved following bed rest and a low-sodium diet, were randomly assigned to receive diuretics (group A) or diuretics plus albumin, 12.5 g/day (group B). In protocol 2, group A patients continued to receive diuretics and group B diuretics plus albumin (25 g/week) as outpatients and were followed up for 3 years. End points were: disappearance of ascites, duration of hospital stay (protocol 1), recurrence of ascites, hospital readmission and survival (protocol 2). RESULTS: The cumulative rate of response to diuretic treatment of ascites was higher (p < 0.05) and hospital stay was shorter (20 +/- 1 versus 24 +/- 2 days, p < 0.05) in group B than in group A patients. After discharge, group B patients had a lower cumulative probability of developing ascites (19%, 56%, 69% versus 30%, 79% and 82% at 12, 24 and 36 months, p < 0.02) and a lower probability of readmission to the hospital (15%, 56%, 69% versus 27%, 74% and 79%, respectively, p < 0.02). Survival was similar in the two groups. CONCLUSIONS: Albumin is effective in improving the rate of response and preventing recurrence of ascites in cirrhotic patients with ascites receiving diuretics. However, the cost/benefit ratio was favorable to albumin in protocol 1 but not in protocol 2.

Adult↗
PubMed1994

Diuretic drugs and the treatment of edema: from clinic to bench and back again.

Despite wide variations in dietary NaCl intake, homeostatic mechanisms ensure that renal NaCl excretion matches intake at steady state. This does not imply, however, that extracellular fluid volume is maintained within narrow limits. In contrast with blood pressure, which appears to be tightly controlled, extracellular fluid volume varies significantly, even in normal individuals, when dietary NaCl intake changes. Cardiac, liver, or renal disease can perturb the relationship between NaCl intake and extracellular fluid volume and lead to symptomatic edema. All major classes of diuretic drugs in use today were developed between 1950 and 1970. These drugs were developed empirically, without knowledge of specific ion transport pathways, but experimental work during the past 15 years has shown that each major class of diuretic inhibits a specific ion transport protein in the kidney. These transport proteins have been characterized physiologically and the mechanisms by which each diuretic drug inhibits ion transport have been defined. Antibodies directed against these transport proteins have localized ion transport pathways to specific cell types along the nephron. Most recently, isoforms of each class of diuretic-sensitive Na transport pathway have been cloned. Ongoing experimental work is aimed at exploring relationships between families of transporters, determining the structural prerequisites for ion transport, and studying molecular mechanisms of transport regulation. Treatment of edema with diuretics is often straightforward, but can lead to adaptive changes in nephron structure and function. These adaptations can limit the effectiveness of diuretic drugs; maneuvers aimed at blocking these processes can be effective approaches to patients who are resistant to diuretic drugs.

Animals↗
PubMed2003

Dehydration in black and white older adults using diuretics.

PURPOSE: To assess the association between dehydration and ethnicity in older adults; and to determine if diuretic use can help explain the disparity between blacks and whites in diagnosis of dehydration. METHODS: We conducted a case-control study in black and white older adults in a pharmaceutical assistance program who were hospitalized during 1997. Cases were all those diagnosed with dehydration (N=9186). Randomly selected controls were 4:1 frequency matched to cases by sex and age group (N(Total)=45585). RESULTS: Patients taking loop, potassium-sparing, thiazide or combination diuretics were more likely to have a diagnosis of dehydration. Dehydration diagnosis was associated with being black (odds ratio (OR)=1.49, 95% confidence interval (CI), 1.36-1.63, p<.001), independent of diuretic use or dosage. That association remained when examining loop (OR=1.36, 95% CI, 1.10-1.63, p<.004) and thiazide diuretic users (OR=1.59, 95% CI, 1.09-2.34, p=.017), but not potassium-sparing or combination diuretic users. CONCLUSION: Diuretic use is significantly associated with dehydration diagnosis, but the greater likelihood of older blacks being diagnosed with dehydration is independent of diuretic use. The increased risk of morbidity and mortality associated with dehydration suggests that further examination of the root cause of this disparity in risk is warranted.

Black or African American↗
PubMed2000

Diuretic downsides--but in low doses they still seem among the best authenticated antihypertensives.

Diuretics in low doses have the greatest support among current available antihypertensives in that they have been shown to reduce total mortality, coronary mortality, stroke, and congestive heart failure in an important meta-analysis by Psaty. Recently, Messerli has linked longterm diuretic use to renal cell carcinoma in women. In some patients, diuretic use leads to increasing blood cholesterol and blood sugar levels. Impotence is a recognized side effect, with rates rising about twofold with low-dose chlorthalidone and fourfold with a higher dose. Certain population groups such as younger (<60 years) white males often do not respond to low-dose diuretic therapy with an adequate blood pressure fall. In females of a similar age group, Messerli calculates that prolonged diuretic therapy will prevent only one stroke and no coronary events nor any deaths for every renal cell carcinoma that is provoked. Despite these evident problems, the outcome data on hard endpoints in trials with initial low-dose diuretic therapy remain valid and convincing. Thus, it is argued, low- but not high-dose diuretics retain their primacy in the ranking of antihypertensive therapy.

Antihypertensive Agents↗
PubMed2000

[Potential dangers of diuretics...].

A chronic diuretic abuse is common among healthy young women. An acute cessation of diuretic intake causes renal sodium retention with formation of edema due to diuretic-induced secondary hyperaldosteronism. Therefore, diuretics should be tappered over weeks or even months in these patients. Other clinical situations where therapy with diuretics is potentially deleterious are pregnancy and systemic sclerosis. In pregnant women, diuretic-induced acute or chronic depletion of the plasma volume can lead to placental hypoperfusion and preeclampsia. Patients with systemic sclerosis have very high levels of blood renin. Diuretic-induced volume depletion provides another stimulus of the renin-angiotensin system and may cause a rapidly progressive renal failure requiring dialysis within days or weeks. The sclerodermal renal crisis is associated with a high early mortality. There is evidence that sclerodermal renal crisis can be avoided when patients are treated with an Angiotensin Converting Enzyme (ACE) inhibitor.

Acute Kidney Injury↗
PubMed2000

Role of EDHF in the vasodilatory effect of loop diuretics in guinea-pig mesenteric resistance arteries.

1. Relaxing effect of loop diuretics, piretanide and furosemide in comparison with acetylcholine (ACh) was investigated in guinea-pig isolated mesenteric resistance arteries. 2. Concentration-response curves to ACh (0.001 - 10 microM) and diuretics (0.0001 - 1 microM) were constructed in noradrenaline (10 - 30 microM)-precontracted arteries incubated either in normal physiological salt solution (PSS) or in 30 mM KCl PSS (K-PSS). 3. In PSS, maximal relaxations (R(max)) and pD(2) to ACh were 87+/-2% and 7.1+/-0.1 (n=10). L-N(G)-nitro-arginine methyl ester (L-NAME, 100 microM) reduced R(max) by 20% (P<0.01, n=7) and pD(2) by 10% (P<0.01). In contrast, indomethacin (10 microM) increased R(max) by 19% (P<0.01, n=8) and pD(2) by 10% (P<0.05). Combination of L-NAME+indomethacin reversed the effect observed with either of these inhibitors used alone. In K-PSS, R(max) was attenuated by 40% (P<0.001, n=6) compared to PSS. L-NAME reduced R(max) by 65% (P<0.01, n=5) and increased pD(2) by 15 fold. L-NAME+indomethacin suppressed the resistant relaxation. 4. In PSS+L-NAME+indomethacin, inhibitors of small (SK(Ca); apamin, 0.1 microM) and large (BK(Ca); iberiotoxin and charybdotoxin, 0.1 microM) conductance Ca(2+)-sensitive K(-)-channels used alone had little effect on the ACh-response. Combination of apamin+iberiotoxin reduced R(max) by 40% (P<0.05, n=7) while apamin+charybdotoxin fully abolished the resistant relaxation. 5. In PSS, piretanide and furosemide induced relaxation with R(max): 89+/-3% vs 84+/-5% and pD(2): 8.5+/-0.1 vs 7.7+/-0.2 (P<0.01) for piretanide (n=11) and furosemide (n=10), respectively. Endothelial abrasion suppressed relaxation to diuretics. L-NAME and indomethacin used alone or in combination did not significantly modify the response to diuretics. 6. In K-PSS, piretanide-induced relaxation was abolished whereas that to furosemide was reduced by 70% (P<0.001, n=9) compared to PSS and was suppressed by L-NAME+indomethacin. In PSS+L-NAME+indomethacin, apamin slightly reduced relaxation to diuretics whereas charybdotoxin or iberiotoxin abolished the response. 7. These results indicate that ACh-evoked relaxation is mediated by both NO/PGl(2)-dependent and -independent mechanisms. The EDHF-dependent component relies on activation of Ca(2+)-activated K(+) channels, is sensitive to a combination of apamin+charybdotoxin and to a smaller degree to a combination of apamin+iberiotoxin. Loop diuretic-induced relaxation is endothelium-dependent, appears to be mediated by NO, PGl(2) and EDHF for furosemide and EDHF only for piretanide. For the two diuretics, opening of BK(Ca) channels may be involved in the relaxation.

Acetylcholine↗
PubMed2002

Diuretics in the therapy of hypertension.

Antihypertensive monopharmacotherapy with diuretics renders blood pressure (BP) values under control in a large percentage of patients suffering from essential hypertension, and it reduces cardiovascular morbidity and mortality. Diuretics are effective in adult and elderly hypertensive subjects, independently of their race. Treatments with classic (high) doses of antihypertensive diuretics, such as 25 mg hydrochlorothiazide once daily, raise the activity of the RAA system, decrease plasma potassium and magnesium concentrations, and cause untoward changes in carbohydrate metabolism and in the plasma lipid profile. These changes appear to limit the positive response of cardiovascular prognosis to antihypertensive therapy with classic doses of diuretics. Lower doses of diuretics reduce high BP to the sought extent in many patients, and they do not elicit or cause only mild unfavourable neuroendocrine and metabolic changes. When a low dose of an antihypertensive diuretic substance is used as monopharmacotherapy, it may take 12-14 weeks after the initiation of treatment for BP to attain final stable values. The following low-dose oral formulations of diuretics constitute effective once-daily monopharmacotherapies for mild-to-moderate uncomplicated essential hypertension: bendrofluazide 1.25 mg, chlorthalidone 12.5 and 15 mg, cicletanine 50 mg, cyclopenthiazide 0.125 mg, HCTZ 12.5 mg, and torasemide 2.5 and 5 mg. These formulations are safer than classically used high-dose formulations such as hydrochlorothiazide 25 and 50 mg.

Diuretics↗