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PubMed1977

Comparison of the hypotensive and diuretic effects of 1,4-dimorpholino-7-phenylpyrido[3,4]pyridazine (DS-511) and hydrochlorothiazide in Doca, renal and spontaneously hypertensive rats.

The hypotensive and diuretic activities of a new diuretic, 1,4-dimorpholino-7-phenylpyrido[3,4-d] pyridazine (DS-511), were compared with those of hydrochlorothiazide (HC) in DOCA, renal and spontaneously hypertensive rats. The results obtained were: 1. During the developing stage of DOCA-hypertension the daily treatment of rats with DS-511 and HC showed significant hypotensive action. During this period the diuretic activity of both agents was clear. 2. During the equilibrium stage of DOCA-hypertension the hypotensive action of DS-511 was indistinct despite its diuretic activity. The hypotensive and diuretic action of HC was not clear. 3. In renal-hypertensive rats the daily treatment of DS-511 and HC caused significant, but weaker hypotension than that in the developing stage of DOCA-hypertension. In these animals the diuretic activity of both agents was clear. 4. In spontaneously hypertensive rats the daily treatment with DS-511 and HC exhibited a similar hypotensive and diuretic action. 5. In all three kinds of hypertensive rats the diuretic activity of DS-511 was similar to that of HC in the excretion of urine and sodium, but the former was less kaliuretic than the latter.

Animals↗
PubMed1984

Evaluation and comparison of the renal excretory function after different diuretics through criteria based on a mathematical model of the excretory function.

The subject of the present study is to compare various diuretic effects through a number of criteria included in a programme developed by us on the basis of an improved model of the method of W.P. Leary and A.J. Reyes for description of the dynamics of the renal excretory function. The effects compared were: of diuretics different in potency and duration of action; of different doses of one and the same diuretic; of different diuretics and placebo--0.9% solution of sodium chloride. The rate of excretion prior to the diuretic administration is graphically represented which enables the estimation of presence or absence of diuretic effect of the pharmacological substance applied. This also makes possible the evaluation of the specific effect of the diuretics with regard to different electrolytes which improves the approach when the diuretics are to be combined and helps their optimum dosage and distribution within time.

Animals↗
PubMed1983

Biochemical changes in black and Indian hypertensive patients on diuretic therapy.

Thirty-seven patients (19 Blacks and 18 Indians) suffering from mild hypertension were given each of five diuretics separately for 4 weeks after a 'washout' period on placebo of the same duration. The diuretics used were hydrochlorothiazide 25 mg/d (Dichlotride; Frosst MSD), hydrochlorothiazide 25 mg plus triamterene 50 mg (Dyazide; SKF) 1 tablet per day, amiloride hydrochloride 5 mg plus hydrochlorothiazide 50 mg (Moduretic; MSD) 1 tablet per day, chlorthalidone (Hygroton; Geigy) 50 mg/d and indapamide (Natrilix; Servier) 2.5 mg/d. The study showed that during the acute phase of diuretic therapy for the treatment of hypertension plasma potassium levels were decreased by thiazide and thiazide-like diuretics and increased by potassium-sparing diuretics. However, despite the decrease in plasma potassium levels produced by thiazide diuretics and indapamide these levels did not fall to 3.0 mmol/l or less. All the diuretics were effective in lowering the standing mean arterial pressure when compared with placebo values. In the absence of significant hypokalaemia, the choice of a diuretic for the Black hypertensive patient should therefore be determined by its cost.

Adult↗
PubMed1993

The role of low-dose diuretics in essential hypertension.

Diuretics have been used to treat hypertension since 1958. The doses used were relatively high. Dose-dependent side effects and the increasing availability of other drugs such as beta- and alpha-blockers, calcium-entry blockers, and angiotensin-converting enzyme (ACE) inhibitors, with equal antihypertensive efficacy but additional effects in cardiovascular diseases, led to a decrease in diuretic use. In controlled trials, little or no protection against coronary artery disease (CAD) was discussed as being due to the diuretics' side effects. The main side effects are hypokalemia, hyperglycemia, and hyperlipidemia. Hypokalemia occurs most often (up to 30%) in thiazide-treated hypertensive patients, and may cause arrhythmias in patients with CAD. This side effect is clearly dose-dependent and may be avoided by comedication with antikaliuretics. Glucose intolerance may develop in about 3% of diuretic-treated men and is reversible after discontinuation of the diuretic. This side effect is functionally correlated with hypokalemia and therefore is not seen when patients are given a comedication (for example, spironolactone prevents hypokalemia). Hypercholesterolemia was first reported in 1964 during long-term diuretic treatment. During the first 12 weeks of treatment, low-density lipoprotein (LDL) cholesterol increased 5-15% in men and postmenopausal women. After 1 year of therapy, the levels decreased to pretreatment values. However, in placebo-controlled trials, the placebo groups exhibited cholesterol levels falling below the diuretic group. Although the mechanisms and the clinical implications of these side effects are not completely understood, the perception grew that diuretics per se may have been at least partially responsible for the lack of protection against CAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Trials as Topic↗
PubMed1995

Effects of K-ATP blocking guanidine diuretics during experimental kaliuresis in rats and dogs.

Several guanidine diuretics related to the renal tubular K-ATP blocker U-37883A were compared to standard diuretics under high K+ excretion conditions. In conscious rats, oral KCl(0.28 mEq) increased K+ excretion 3-fold. This kaliuresis was further enhanced by oral diuretic doses of ethoxzolamide (1 and 2 mg/kg), hydrochlorothiazide (HCTZ; 0.3 and 0.9 mg/kg), and furosemide (18 mg/kg), but was significantly blunted by oral triamterene (1 and 10 mg/kg). By comparison, diuretic doses of U-37883A and analogs U-18177 (10 and 30 mg/kg) and U-38658A (3 and 9 mg/kg) did not affect K+ excretion. In conscious dogs, oral U-18177A (10 mg/kg) and HCTZ (1 mg/kg) were compared during 3- to 13-fold kaliuresis induced by oral isotonic saline (200 mL), oral KCl (30.8 mEq), subcutaneous deoxycorticosterone acetate (1.0 mg/kg), and oral acetazolamide (20 mg/kg). HCTZ was diuretic and further increased K+ excretion and its fractional clearance by 42 and 34%, respectively. Conversely, U-18177A was diuretic and slightly reduced these kaliuretic parameters by 11 and 20%. Thus, the guanidines U-18177 and U-37883A exert a relatively eukalemic diuresis under normal and high K+ excretion conditions, and their putative renal tubular K-ATP blocking action seems an effective means of inducing diuretics with less K+ imbalance than with standard diuretics.

Adamantane↗
PubMed1996

[Role of diuretics in the treatment of hypertension: from large controlled trials to international guidelines].

Diuretics were used in most of the major trials that demonstrated that lowering the blood pressure reduced cardiovascular morbidity and mortality. Nevertheless in the second half of the eighties, there were misgivings about the widespread use of thiazide diuretics, driven in part by the relative failure of the large trials to reduce myocardial infarction-to the extent predicted by large scale epidemiological studies. There was much attention on metabolic side effects of thiazide diuretics including dyslipidaemia, glucose intolerance, hypokalaemia, hyperuricaemia, and then microalbuminuria particularly in diabetic subjects. These issues were current when JNC (IV) (1988) and the WHO-ISH guidelines (1989) were being written. Three major clinical trials SHEP, STOP and MRC published in the early nineties established that thiazide diuretics alone, or in combination with beta blockers, did reduce cardiovascular morbidity and mortality in elderly subjects with hypertension. All guidelines published since 1993 include diuretics among the first line drugs. Possibly the most important factor in the restoration of diuretics has been the use of progressively lower doses that minimise the metabolic side effects. Diuretics are effective as monotherapy in the treatment of mild essential hypertension and of isolated systolic hypertension in elderly subjects. They are very useful in combination with beta blockers or with ACE inhibitors. They should be avoided in patients with gout and should not be used as first line drugs in patients with diabetes. They should only be used with caution in young obese subjects with dyslipidaemia and increased risk of coronary artery disease, facing many decades of treatment for hypertension. However there is no doubt that diuretics are effective, cheap and have a central role in the control of hypertension in all communities around the world.

Adult↗
PubMed1996

[Diuretics and diabetes mellitus].

The term "diuretics" describes a concerning pharmacological action and side effects heterogeneous class of drugs. The special advantage of using diuretics includes reducing edema and expanded plasma volume often associated with hypertension and cardiovascular disease. Diuretics are one of the 5 major classes of antihypertensive agents recommended for the initial drug therapy of hypertension. However, currently treatment of hypertension with diuretics is controversial, because of potentially adverse effects on the cardiovascular risk profile, including deterioration in glucose control especially in patients with impaired glucose tolerance. Additionally there is concern about excess mortality associated with diuretic therapy and diabetes mellitus. The metabolic side effects on glucose metabolism and lipid profile are related to the type of diuretic and its dosage. The adverse effects of thiazides on insulin action, glycemia and lipid profile are dose dependent and can be minimized by using low doses. In contrast, indapamide seems not to alter glucose metabolism and lipid profile. The choice of diuretic depends on concomitant disease. In patients with nephropathy potassium sparing agents should not be used, however furosemid can be used even in high doses. Beside focus on indication of diuretics in patients with diabetes and their metabolic side effects treatment of therapy resistant hypertension in these patients are discussed in this review.

Antihypertensive Agents↗
PubMed1992

Interaction of biofeedback-assisted relaxation and diuretic in treatment of essential hypertension.

Thirty patients with essential hypertension participated in a study designed to compare two treatments: diuretic medication alone (n = 10) and biofeedback assisted relaxation combined with diuretic (n = 20). One of 10 patients lowered BP with diuretic alone and 11 of 20 patients lowered BP with diuretic combined with biofeedback-assisted relaxation. The addition of the behavioral intervention to the diuretic therapy produced a decrease in blood pressure beyond that associated with the diuretic alone. The decrease in BP mediated by diuretic were related to high entry levels of BP, low anxiety, forehead muscle tension, anger expression and plasma renin activity. The BP decrease mediated by combined diuretic and biofeedback-assisted relaxation was associated with high pretreatment BP, anger controlled, low finger temperature and high/normal plasma renin activity.

Adult↗
PubMed1994

Randomized trial of long-term diuretic therapy for infants with oxygen-dependent bronchopulmonary dysplasia.

STUDY OBJECTIVE: To determine whether long-term oral diuretic therapy would improve the pulmonary function of preterm infants with bronchopulmonary dysplasia. DESIGN: Randomized, double-blind, placebo-controlled study. SETTING: Level III intensive care nursery. INTERVENTION: We randomly selected 43 stable patients with oxygen-dependent bronchopulmonary dysplasia to receive either orally administered spironolactone and chlorothiazide or placebo. These drugs were continued until the patients no longer required supplemental oxygen. Both groups received furosemide as needed. MEASUREMENTS AND RESULTS: Each infant had pulmonary function tests at study entry, 4 weeks after study entry, 1 week and 8 weeks after being weaned to room air and off study drugs, and at 1 year of corrected age. Pulmonary function tests include dynamic pulmonary compliance, airway resistance, thoracic gas volume, and maximal expiratory flow at functional residual capacity; most of the infants had functional residual capacity measured. Between the first and second pulmonary function tests (while the infants were receiving diuretic or placebo), the infants in the diuretic group had a significant improvement in dynamic pulmonary compliance (46%; p < 0.001) and airway resistance (31%; p < 0.05); there were no changes in compliance or resistance in the placebo group. Although patients in both the diuretic and the placebo groups required progressively less supplemental oxygen, by 4 weeks after study entry the patients in the diuretic group needed less supplemental oxygen than did those in the placebo group (p < 0.01). There were no significant differences in results of serial pulmonary function tests in either group after discontinuation of diuretic therapy. Despite the significant differences in pulmonary function between the two groups, there was no significant difference between them in the total number of days that supplemental oxygen was required. Significantly more infantsin the placebo group received more than 10 doses of furosemide on an as-needed basis. CONCLUSIONS: Long-term diuretic therapy in stable infants with oxygen-dependent bronchopulmonary dysplasia, after extubation, improves their pulmonary function and decreases their fractional inspired oxygen requirement, but does not decrease the number of days that they require supplemental oxygen. The improvement in pulmonary function associated with diuretic therapy is not maintained after treatment is discontinued.

Analysis of Variance↗
PubMed1993

Diuretic renography in the evaluation of neonatal hydronephrosis: is it reliable?

Arguments against the use of diuretic renography in the assessment of newborn hydronephrosis include immature function of neonatal kidneys, previously reported poor diuretic response and nonreproducible drainage patterns. To address these concerns we reviewed the initial and followup renal scans of 17 neonates with hydronephrosis without ureterectasis diagnosed by perinatal ultrasonography. All patients were evaluated with an initial diuretic renal scan up to the age of 28 days, and all had normal cystograms. A total of 19 dilated kidneys was studied of which 13 ultimately required pyeloplasty and 6 were managed nonsurgically. Patient study parameters included age and weight at the time of each renal scan, side of hydronephrosis, differential function of each kidney, pre-diuretic and post-diuretic urine output, and drainage half-time of each kidney. The diuretic renal scans followed a standardized protocol. There was no statistically significant difference between neonatal and followup differential function (p > 0.05), and the correlation coefficient was highly significant (r = 0.968). Comparison of response to diuretic stimulation (ml./kg. per minute) revealed no statistically significant difference as the patients aged with brisk urine output 3 to 5 times greater than previously reported. The distribution and mean drainage half-times for normal nonhydronephrotic kidneys were similar when comparing those performed as neonates and at followup. Hydronephrotic kidneys managed nonsurgically maintained almost identical patterns. Those repaired surgically demonstrated appropriate improvement in drainage but function remained unchanged. These results refute each of the criticisms against the use of diuretic renography to evaluate neonatal hydronephrosis and demonstrate its reliability in neonates.

Furosemide↗
PubMed1978

Relationship between the hypotensive and renin-stimulating actions of diuretic therapy in hypertensive patients.

1. The pressor role of renin stimulated by chronic diuretic therapy has been assessed in 31 patients with essential hypertension by infusing the angiotensin II antagonist, saralasin, immediately before and at the end of 2 weeks' treatment with the diuretic, chlorthalidone. 2. Under diuretic therapy the change in blood pressure caused by saralasin was found to be correlated to plasma renin activity values, in such a way that small pressor responses were again observed in patients whose renin was mildly stimulated by the diuretic, whereas a marked depressor response occurred in patients whose renin was markedly increased. 3. On the other hand, the hypotensive effect of chlorthalidone was correlated to values of plasma renin activity under diuretic therapy in an opposite direction: indeed little or no decrease and sometimes an increase in blood pressure were observed in patients with marked renin activation by diuretic therapy. 4. It is concluded that stimulation of renin release by chronic diuretic therapy can be considered a factor limiting the hypotensive activity of diuretic drugs.

Adult↗
PubMed1992

The relationship between diuretic dose, and the haemodynamic response to captopril in patients with cardiac failure.

The effect of diuretic dose on the haemodynamic response to captopril was assessed in nine patients with chronic cardiac failure. Each patient was given an intravenous dose of captopril while maintained on (a) a low dose diuretic regime, and (b) a high dose diuretic regime. Activity of the renin angiotensin aldosterone system, as assessed by plasma concentrations of these hormones, was greater when patients were receiving the higher dose diuretic regime. The magnitude of haemodynamic response produced by intravenous captopril was greater when the patients were maintained on the high dose diuretic regime, although no significant correlation was found between resting plasma renin activity and resting plasma angiotensin II concentration and the change produced by captopril in any haemodynamic response on either diuretic regime. An increased dosage of loop diuretic potentiates the haemodynamic effects of captopril in patients with cardiac failure. Reduction of diuretic dose prior to introduction of captopril may protect against severe first dose hypotension.

Adult↗
PubMed1986

Diuretic treatment alters clonidine suppression of plasma norepinephrine.

The effect of short-term diuretic treatment on the action of clonidine was evaluated in eight subjects with mild, uncomplicated hypertension. A single oral dose of clonidine (0.3 mg) was given before and after 1 week of therapy with hydrochlorothiazide, 50 mg, and amiloride, 5 mg, taken daily. Changes in mean arterial pressure, heart rate, plasma norepinephrine and epinephrine levels, and plasma renin activity were assessed. Diuretic treatment caused a significant weight loss, increased plasma renin activity, and reduced serum potassium concentration but did not significantly alter the absolute reduction in mean arterial pressure caused by clonidine. Absolute clonidine-induced reduction in plasma renin activity after diuretic treatment was three times greater than before treatment, although percent changes were similar. Before diuretic therapy, clonidine significantly reduced the level of norepinephrine (absolute and percent change). After diuretic treatment, clonidine failed to suppress norepinephrine, and the difference from prediuretic changes was significant. The level of epinephrine was not altered significantly either by diuretic treatment or clonidine. These results indicate that diuretic therapy alters the clonidine-activated mechanism for reduction of arterial pressure through a shift from overall suppression of sympathetic tone to pathways that are more restricted to renal tone. This shift may be due to changes in fluid or electrolyte balance that alter the action of alpha 2-adrenergic receptor-mediated pathways. Use of the clonidine suppression test for the diagnosis of pheochromocytoma may give false-positive results in diuretic-treated patients.

Administration, Oral↗
PubMed1993

Efficacy of albumin and diuretic therapy in children with nephrotic syndrome.

OBJECTIVE: To examine the efficacy and complications of albumin and diuretic therapy in the treatment of edema due to the nephrotic syndrome. METHODS: The clinical and biochemical effects of 35 treatment courses of albumin and diuretics administered to 21 children with nephrotic syndrome were retrospectively examined. Treatment consisted of intravenous infusion of 25% albumin and furosemide. A second diuretic was administered in addition to furosemide during 10 treatment courses. There was an average of 5 infusions per hospitalization. RESULTS: Albumin and furosemide therapy resulted in a 1.2 +/- 0.2% (SEM) body weight loss per infusion. The administration of albumin with two diuretics did not result in improved weight loss compared to albumin and furosemide alone. Patients whose nephrotic syndrome was in remission at the time of posthospitalization follow-up (n = 8) had a sustained weight loss both during and after albumin and diuretic treatment. Patients with persistent proteinuria (n = 27) transiently lost weight during therapy, but returned to a weight similar to their pretreatment weight at 2-week follow-up. Albumin infusion resulted in hypertension, requiring acute antihypertensive therapy in 16 treatment courses (46%) and increased maintenance antihypertensive therapy in 12 treatment courses (34%). In addition, hypokalemia, hypernatremia, and hyperbicarbonatemia developed in 40%, 17%, and 11% of treatment courses, respectively. Albumin and diuretic therapy resulted in the development of respiratory distress during four treatment courses, including one patient who developed respiratory failure and one patient who developed congestive heart failure. CONCLUSIONS: Albumin and diuretic therapy results in fluid removal and weight loss in children with the nephrotic syndrome; however, this effect is transient unless remission of proteinuria occurs. While this is a retrospective study, the findings suggest that albumin and diuretic therapy can be associated with frequent and potentially serious complications.

Adolescent↗
PubMed1995

International renal-cell cancer study. VIII. Role of diuretics, other anti-hypertensive medications and hypertension.

Risk of renal-cell cancer in relation to use of diuretics, other anti-hypertensive medications and hypertension was assessed in a multi-center, population-based, case-control study conducted in Australia, Denmark, Germany, Sweden and the United States, using a shared protocol and questionnaire. A total of 1,732 histologically confirmed cases and 2,309 controls, frequency-matched to cases by age and sex, were interviewed. The association between renal-cell cancer and the drugs was estimated by relative risks (RRs) and 95% confidence intervals (CIs). Risks were increased among users of diuretics and other anti-hypertensive medications. After adjustment for hypertension, risk for diuretics was reduced to unity, except among long-term (15+ years) users. Risk for use of non-diuretic anti-hypertensive drugs remained significantly elevated and increased further with duration of use. Overall risk was not enhanced when both classes of medications were used. Excess risk was not restricted to any specific type of diuretic or anti-hypertensive drug and no trend was observed with estimated lifetime consumption of any particular type of product. The RR for hypertension after adjustment for diuretics and other anti-hypertensive medications was 1.4 (95% CI = 1.2-1.7), although among non-users of any anti-hypertensive medications, there was little excess risk associated with a history of hypertension. Exclusion of drug use that first occurred within 5 years of cancer diagnosis or interview did not alter the associations. Our findings suggest small effects on renal-cell cancer risk associated with hypertension and use of diuretics and other anti-hypertensive medications. However, because of potential misclassifications of these highly correlated variables, it is difficult to distinguish the effect of treatment from its indication, hypertension.

Antihypertensive Agents↗
PubMedDate not supplied

Interrelationships among thiazide diuretics and calcium, magnesium, sodium, and potassium balance in normal and hypertensive man.

The benzothiadiazide diuretics are known to cause magnesium and potassium wasting and retention of calcium and uric acid. The effect of magnesium replacement on diuretic-induced changes in sodium, potassium, calcium, and magnesium balance, weight, and blood pressure was studied in 12 normal subjects and 13 hypertensive patients to determine whether oral magnesium would reduce thiazide-induced kaliuresis. The groups differed in their response to diuresis in that the normotensive subjects did not show a fall in blood pressure (despite an equivalent weight loss), returned to a state of sodium balance earlier, and developed a greater net negative potassium balance over 12 days of diuretic therapy. Both groups displayed calcium and uric acid retention and magnesium wasting during diuretic therapy. The addition of oral magnesium replacement during diuretic therapy had no effect on any measured values beyond that seen in subjects who took diuretics without magnesium replacement. Thus, magnesium replacement did not reduce urinary potassium loss. However, urinary calcium losses increased when magnesium was given to subjects who were not receiving diuretics. The data provide the first report that small doses of oral magnesium enhance calcium excretion in hypertensive subjects.

Adult↗
PubMed1983

Effect of "high ceiling" diuretics on active salt transport in the cortical thick ascending limb of Henle's loop of rabbit kidney. Correlation of chemical structure and inhibitory potency.

The group of "high ceiling" diuretics consists of a variety of chemically different potent diuretic and saluretic substances. Appart from a few exemptions direct evidence for an action of these substances in the thick ascending limb of the loop of Henle (TAL) is still lacking. For furosemide, we have reported recently that it inhibits most likely the Na+-2 Cl--K+ cotransport system present in the lumen membrane of the TAL. The present study tests: 1. whether other "high ceiling" diuretics have a similar site and mode of action, and 2. how modifications of the furosemide molecule alter the inhibitory potency. Isolated cortical TAL (cTAL) segments (n = 185) of rabbit kidneys were perfused in vitro. The equivalent short circuit current (Isc = transepithelial PD/transepithelial resistance), as a measure of active salt transport was correlated to the dose of 64 substances. Several diuretics, such as 2-aminomethyl-4-(1,1-dimethyl-ethyl)-6-iodophenol hydrochloride (MK 447), hydrochlorothiazide, muzolimine, etozoline, tizolimide, amiloride, and triamterene were ineffective both from the lumen and basolateral side at concentrations as high as 10(-4) - 10(-3) mol X 1(-1). The phenoxyacetic acids ethacrynic acid, indacrinone (MK 196), and to less an extend tienilic acid were inhibitory active. They differed from furosemide in one or more of the following criteria: delayed onset, incomplete reversibility, stronger action from the bath, different slope of the dose response curve. Similarly, 1-ozolinone acted stronger from the bath. In contrast, the diuretics of the furosemide type and related compounds (bumetanide and piretanide) showed rapid onset and complete reversibility of inhibition. These substances acted stronger from the lumen. The individual positions in the benzyl ring of the diuretics were differently affected by substitutions, leading to parallel shifts in the dose response curves with halfmaximal inhibition at concentrations ranging between 8 X 10(-8) to greater than 10(-4) mol X 1(-1). For these substances the calculated Hill coefficients were close to unity: 0.96 +/- 0.05. We conclude that the so called "high ceiling" or "loop" diuretics consist of at least 3 groups: 1. drugs that do not interfere with the active salt transport in the cTAL segment, 2. drugs that interfere by so far not characterised mechanisms, and 3. drugs of the furosemide type which inhibit the Na+-2 Cl--K+ cotransport system in the lumen membrane of the cTAL segment.

Animals↗
PubMed1993

Loop diuretics versus others in the treatment of congestive heart failure after myocardial infarction.

Most frequently, diuretic therapy in congestive heart failure has as its main objective ridding the lungs of water. The work of the muscles of external respiration is thus decreased, the fraction of cardiac output that is distributed to vascular beds other than that of the respiratory muscles is consequently increased, and the functional and clinical condition of the patient improves. Diuretic therapy does not change cardiac output significantly in most cases; in some circumstances diuretic therapy may increase cardiac output in a clinically relevant fashion, and in some other cases diuretic therapy may lower cardiac output to the extent of impairing the overall functional situation. The dose of diuretics should be the minimal compatible with the prosecution of the main clinical objective (class betterment), to minimize possible increases in the afterload to the left ventricle (intravenous administration), to minimize hemodynamically detrimental decreases in the preload, and to minimize the likelihood of development or the severity of undesired changes in plasma biochemistry (hyponatremia, hypokalemia, hypomagnesemia, hyperuricemia, etc.). Loop diuretics are preferred shortly after myocardial infarction, given the ample dose-effect range of these substances and their relatively benign effect on renal blood flow. During chronic therapy, loop diuretics at low doses may be tried first, and the dose may be increased if necessary, provided higher doses do not cause symptomatic falls in cardiac output through the striking renal excretory response that these drugs elicit shortly after dosing.(ABSTRACT TRUNCATED AT 250 WORDS)

Diuretics↗