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PubMed1985

Loop diuretics may fail to inhibit (Na+, K+, Cl-) 'cotransport' in human red cells.

The inhibition of passive K+ influx into human red blood cells (RBC) by loop diuretics was found to be dependent on the external Na+ concentration. In the absence of external Na+, there was minimal inhibition but the influx remained dependent on Cl- ions. Thus, raising the external Na+ concentration increased the affinity of the putative (Na+, K+, Cl-) cotransport system in human RBC for loop diuretics.

Biological Transport, Active↗
PubMed1981

Diuretic treatment and serum lipoproteins: effects of tienilic acid and indapamide.

Treatment with the commonly used diuretic, chlorthalidone, has previously been found to increase the serum low-density-lipoprotein cholesterol (LDL-C) fraction. Therefore, the effects of two new agents, tienilic acid (a combined diuretic-uricosuric) and indapamide on serum lipid and lipoprotein levels were assessed. Six weeks of treatment with tienilic acid, 250 mg/day, markedly decreased serum uric acid and significantly increased LDL-C and triglycerides in 16 men. In contrast, indapamide 2.5 mg/day, had no apparent influence on serum lipids or lipoproteins in 18 men.

Diuretics↗
PubMed1983

Cellular mechanism of the action of loop diuretics on the thick ascending limb of Henle's loop.

During the passed few years the cellular mechanisms responsible for the NaCl reabsorption in the thick ascending limb of the Henle loop of mammalian nephron and of the early distal tubule of amphibian kidney have been extensively studied. From these studies a new type of secondarily active transport mechanism, i.e. the Na+--2Cl- --K+ symport has emerged. Meanwhile it has been recognized that this system is also present in many other epithelia. All these epithelia share in common that they are sensitive to the so called loop diuretics. The present article summarizes our current knowledge of how the loop diuretics, by reversible interaction with the above cotransport system, inhibit the NaCl reabsorption in the thick ascending limb of Henle's loop. It is shown that these drugs transfer the thick ascending limb cell to a state in which not only transepithelial NaCl reabsorption ceases but in which also very little energy is consumed since then K+ and Cl- "relax" to passive distribution across both cell membranes and Na+ entry into the cell is blocked.

Absorption↗
PubMed1982

Responses of catecholamines and blood pressure to beta-blockade in diuretic-treated patients with essential hypertension.

Twenty patients (mean age 49 +/- 4 (SEM) yr) with mild to moderate essential hypertension were studied during placebo conditions, following 6 weeks of chlorthalidone monotherapy and 6 to 28 weeks of combined beta-blocker-chlorthalidone treatment, or vice versa. Compared to chlorthalidone therapy alone, addition of a beta-blocker to this diuretic caused a further blood pressure reduction in 11 patients (Responders); in 9 patients addition of a beta-blocking agent failed to further reduce blood pressure (Non-responders). Supine and upright plasma renin, aldosterone, norepinephrine and epinephrine levels and catecholamine excretion rates were always comparable between Responders and Non-responders. In both groups plasma and urinary norepinephrine or epinephrine values were not significantly altered following addition of a beta-blocker; heart rate and plasma renin activity were decreased in both groups to a similar extent. It is concluded that the antihypertensive mechanism of beta-blockers given to diuretic treated patients with essential hypertension is independant of renin and not associated with changes in plasma or urinary catecholamines.

Adrenergic beta-Antagonists↗
PubMed1986

Effects of standard diuretics and RPH 2823 on transepithelial Na+ transport in isolated frog skin.

Short-circuit current (SCC) techniques were used to monitor the effects of various diuretic agents on Na+ transport in isolated frog skin, a model for the late distal tubule and the collecting duct of the mammalian kidney. Acetazolamide, hydrochlorothiazide, torasemide, and ethacrynic acid did not affect sodium transport (as indicated by the SCC) or transepithelial electrical resistance when added either to the apical (outer) or to the inner (basolateral, corial) bathing solution of the tissue. However, Na+ transport was sensitive to amiloride, the triamterene derivate dimethylamino-hydroxypropoxytriamterene (RPH 2823), and to furosemide. Whereas apical amiloride, and RPH 2823 induced a dose-dependent decrease in SCC and increase in transepithelial electrical resistance, apical furosemide resulted in a dose-dependent increase in SCC and a decrease in electrical resistance. None of the three diuretic agents caused a significant change in SCC when applied to the inner bathing Ringer's solution. The small furosemide-induced decrease in resistance compared with the huge increase in SCC suggests that furosemide affects Cl- permeability as well as Na+ permeability. Evidence for this notion was achieved by the following findings: The decrease in resistance after furosemide was more pronounced in tissues bathed in Cl(-)-free solutions compared with Cl(-)-containing solutions. n contrast, SCC stimulation by apical furosemide is Cl(-)-ion independent, but strongly Na+-ion dependent. SCC stimulation by furosemide is amiloride-sensitive. With respect to the onset, locus, and reversibility of action, it seems reasonable to assume that amiloride, RPH 2823, and furosemide all influence transepithelial Na+ transport by interacting with the Na+ channel or a regulator site of it within the apical membrane. The stoichiometry of the amiloride (RPH 2823)-receptor site interaction revealed Hill-coefficient(s) of less than 1, indicating a negative cooperativity among the receptor sites. The interaction between Na+ ions and amiloride or RPH 2823 displayed mixed competitive-noncompetitive inhibition. Taken together, these results support the hypothesis that amiloride and Na+ as well as RPH 2823 and Na+ may act at different loci on the apical entry mechanism in Rana esculenta skin.

Amiloride↗
PubMed1990

Drag-reducing polymers: a novel class of diuretic and natriuretic compounds.

Previous studies have demonstrated that Separan AP-30, a drag-reducing polymer, significantly decreased the formation of atherosclerotic plaques in rabbits fed a high-cholesterol diet. Furthermore, Separan AP-273, a polymer similar to but longer than Separan AP-30, markedly increased cardiac output in open-chest rats. Preliminary studies in our laboratory have described diuresis and natriuresis following the intravenous infusion of Separan AP-273. These studies did not determine whether this natriuresis was common to drag-reducing polymers or unique to Separan. In the present study the renal effects of two chemically dissimilar drag-reducing polymers of molecular lengths approaching approximately 100 microns were compared. Sprague-Dawley rats (250-300 g) were anesthetized (Nembutal) and a tracheostomy was performed. A baseline level of sodium and water excretion was established by the infusion of saline (0.097 ml/min, IV). Separan (0.004%), an anionic polyacrylamide; Polyox (0.4%), a poly(ethylene oxide); or mannitol (20%), an osmotic diuretic, was infused into the jugular vein at 0.0034 ml/min. Separan and Polyox both increased the excretion of sodium and water (p less than 0.05). At the doses tested, potassium excretion was unaltered in both groups. Separan, but not Polyox, produced a modest increase in blood pressure. Creatinine clearance was unaltered. At this infusion rate, only hypertonic concentrations of mannitol (20%) induced a similar effect. These results indicate that drag-reducing polymers may represent a novel class of potassium-sparing diuretic and natriuretic compounds. The ability of this class of polymers to decrease the formation of atherosclerotic plaques, increase blood flow, and produce a potassium-sparing natriuresis may be of practical clinical significance.

Acrylic Resins↗
PubMed1990

Effects of nifedipine versus hydralazine on sympathetic activity and cardiac function in patients with hypertension persisting on diuretic plus beta-blocker therapy.

In patients with hypertension persisting on combined diuretic and beta-blocker therapy, the effects of an additional 9-week therapy with a calcium antagonist (nifedipine) versus a classical arterial vasodilator (hydralazine) were compared for changes in blood pressure (BP), plasma catecholamines (n = 15), and left ventricular (LV) systolic and diastolic function (n = 6). Both drugs lowered BP, but nifedipine was significantly more effective in lowering systolic BP. Hydralazine increased both supine and standing plasma norepinephrine, nifedipine increased them only in the standing position and to a lesser extent. Patients on beta1-selective (n = 5) versus nonselective (n = 10) blockade showed similar responses. Left ventricular systolic function was not affected by hydralazine, whereas nifedipine increased the rate of ejection. In contrast, LV diastolic function was not affected by nifedipine, whereas hydralazine improved the peak filling rate. We conclude that arterial vasodilation by a calcium antagonist causes less sympathetic activation than caused by a classical arterial vasodilator. However, during short-term therapy in patients already on a diuretic and a beta blocker, nifedipine appears not to improve decreased LV diastolic function.

Adrenergic beta-Antagonists↗
PubMed1990

Acute and chronic effects of a diuretic monotherapy with piretanide in congestive heart failure--a placebo-controlled trial.

To evaluate the acute and chronic effects of diuretic monotherapy with 3 mg piretanide bid, 46 patients (pts) with congestive heart failure (NYHA II-III) secondary to coronary artery disease were studied. Within 3 weeks of therapy, the patients lost 1.6 kg body weight. Forty-four patients reported a subjective feeling of improvement. Echocardiographically, a highly significant (p less than 0.001) reduction of diastolic and systolic diameters was found, as well as an increase of fraction shortening. Chest x-ray indicated a reduction of heart volume from 1012 +/- 263 ml to 936 +/- 233 ml (p less than 0.001). The serum potassium level remained unchanged. A subgroup of 26 pts underwent invasive hemodynamic examinations. IV injection of 6 mg piretanide resulted in an acute reduction of pulmonary wedge pressure (pc) from 20.2 +/- 5.3 mmHg to 11.9 +/- 5.0 mmHg (p less than 0.001); simultaneously a slight decrease of cardiac index from 3.2 +/- 0.6 l/min/m2 to 3.0 +/- 0.4 l/min/m2 was observed. Invasive control after 3 weeks of oral therapy showed no decline of the piretanide effect. The exercise tolerance increased clearly from 135 +/- 161 Wmin to 249 +/- 268 Wmin (p less than 0.05). A control group of further 14 pts was treated with placebo only and did not show any significant changes of pc (20.0 +/- 6.4 mmHg vs. 22.8 +/- 19.2 mmHg), exercise tolerance, or other clinical parameters. Thus, the diuretic monotherapy of congestive heart failure with piretanide is highly effective and shows a significant improvement in all clinical and hemodynamic parameters in the absence of any remarkable side effects.

Adult↗
PubMed1995

A comparison of the effects of low- and conventional-dose thiazide diuretic on insulin action in hypertensive patients with NIDDM.

In conventional doses, thiazide diuretics impair glucose tolerance and decrease insulin sensitivity, making them an unpopular choice for treating diabetic patients with hypertension. However, use of low-dose thiazide diuretics may avoid the adverse metabolic effects seen with conventional doses. In a double-blind, randomised crossover study we assessed peripheral and hepatic insulin action in 13 hypertensive non-insulin-dependent diabetic patients after a 6-week placebo run-in and following two 12-week treatment periods with either low (1.25 mg) or conventional (5.0mg) dose bendrofluazide. There were no differences between doses in their effects on systolic and diastolic blood pressure. Bendrofluazide 1.25 mg had significantly less effect on serum potassium, uric acid, fasting glucose and HbA1C concentrations than the 5.00 mg dose. Exogenous glucose infusion rates required to maintain euglycaemia were significantly different between doses (p < 0.05) with conventional-dose bendrofluazide worsening peripheral insulin resistance compared to baseline (23.8 +/- 2.9 vs 27.3 +/- 3.5 mumol.kg-1.min-1, p < 0.05) and low-dose bendrofluazide producing no change compared to baseline (26.8 +/- 3.6 vs 27.3 +/- 3.5 mumol.kg-1.min-1, p = NS). Postabsorptive endogenous glucose production was higher on treatment with bendrofluazide 5.0 mg compared to 1.25 mg (11.7 +/- 0.5 vs 10.2 +/- 0.3 mumol.kg-1.min-1, p < 0.05) and suppressed to a lesser extent following insulin (4.0 +/- 0.7 vs 2.0 +/- 0.4 mumol.kg-1.min-1, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Diuretic contrast-enhanced magnetic resonance urography versus intravenous urography for depiction of nondilated urinary tracts.

Diuretic contrast-enhanced magnetic resonance urography (MRU) is analogous to conventional intravenous urography (IVU) and, hence, designated as excretory MRU. It is performed with a T1-weighted fast gradient-echo sequence to obtain breath-hold, dynamic MRU after intravenous injection of low-dose furosemide (5-10 mg) and gadolinium (Gd) chelate. The combination of Gd and furosemide is the key for achieving a uniform distribution of the contrast material inside the entire urinary tract. It provides high-resolution images of nondilated urinary tracts and information about the renal function. This pictorial essay reviews the technical aspects and practical consideration of diuretic Gd-enhanced MRU and underlines its diagnostic capability in comparison with IVU in the depiction of nondilated collecting systems. We discuss its potential applications, as in young patients with anatomic anomalies, patients with renal transplants, patients allergic to iodinated contrast medium, and avoiding multimodality work-up in the evaluation of kidney donors and patients with renal and extrarenal tumor diseases.

Adult↗
PubMed2004

Aminophylline as an adjunct diuretic for neonates--a case series.

Aminophylline is an adenosine receptor antagonist. Adult and paediatric studies have demonstrated a diuretic effect of aminophylline due to increased renal blood flow and the inhibition of solute reabsorption in various segments of the nephron. We report a case series of five infants with volume overload despite frusemide treatment. Aminophylline was successfully used as an adjunct diuretic with increased urine output and effective weight loss occurring in all five neonates following its introduction.

Aminophylline↗
PubMed2000

Torasemide is an effective diuretic in the newborn rabbit.

The effect of intravenous (i.v.) torasemide on diuresis and renal function was evaluated in three groups of normoxemic, 5- to 10-day-old, newborn New Zealand White rabbits. The animals of group 1 received 0.2 mg/kg of torasemide i.v., whereas in group 2 an i.v. dose of 1.0 mg/kg was given. The third group of animals received a bolus i.v. dose of 1.0 mg/kg torasemide with continuous i.v. replacement of estimated urinary fluid and electrolyte losses. Torasemide proved to be an effective, potassium-sparing diuretic, without significant effect on glomerular filtration rate (GFR). Renal blood flow (RBF) fell and the renal vascular resistance (RVR) rose in all three groups of animals, although the rise in RVR in group 3 was not significant. These changes in renal hemodynamics were most pronounced in the animals of group 2 and are probably secondary to torasemide-induced hypovolemia (2.8% loss of body weight) and accompanying humoral reactions, such as an increase in angiotensin II (not measured). When the latter is prevented by simultaneous re-infusion of an electrolyte solution (group 3), replacing urinary losses, GFR increases and the changes in RBF and RVR are blunted. We conclude that torasemide is an effective, potassium-sparing diuretic in newborn rabbits. No evidence was found for a vasodilatory action of the drug.

Animals↗
PubMed2006

Is population-wide diuretic use directly associated with the incidence of end-stage renal disease in the United States?

In the quest for "evidence-based" medicine, an accepted hierarchy of evidence has been proposed. This hierarchy places in vitro studies and animal data at the base, and puts systematic reviews, meta-analyses, and randomized controlled trials at the pinnacle. However, when clinical medicine faces questions that have not yet been studied by the "gold standard" methods, how is one to proceed? Often, the best evidence at hand falls short of randomized controlled trials and meta-analyses. Using this framework, a review of the evidence supporting the hypothesis that population-wide diuretic use is directly associated with end-stage renal disease in the United States is presented. Publications pertaining to diuretic use in recent clinical trials are also discussed.

Animals↗
PubMed1982

Postural hypotension during tilt with chronic captopril and diuretic therapy of severe congestive heart failure.

The hemodynamic mechanism by which patients with chronic congestive heart failure (CHF) maintain their blood pressure (BP) in the upright posture is distinct from that of normal and hypertensive individuals. There are little data regarding the effects of chronic vasodilator therapy on the mechanisms controlling this response, especially in the presence of diuretic therapy. Therefore, 10 consecutive patients with severe chronic CHF underwent hemodynamic tilt study following acute and chronic captopril therapy. One patient developed orthostatic hypotension following first-dose captopril, but 6 of 10 had a mean BP decrease of 70 +/- 6 to 56 +/- 3 mm Hg on tilt following chronic captopril. This associated with significant reduction of plasma aldosterone, and was abolished on re-tilt following acute saline infusion. Therefore, during chronic captopril therapy of CHF, a reduction of diuretic dosage may be necessary to prevent orthostatic hypotension.

Adult↗
PubMed1983

Metabolic disturbances increasing the risk of coronary heart disease during diuretic-based antihypertensive therapy: lipid alterations and glucose intolerance.

The treatment of hypertension reduces the incidence of stroke and congestive heart failure. Surprisingly, however, no reduction in morbidity from coronary heart disease (CHD) has been found in any of the placebo-controlled trials of hypertension treatment. This observation is unexpected because hypertension is a major risk factor for CHD. The one clinical trial demonstrating reduction of CHD with treatment of hypertension was not placebo controlled, thus provoking uncertainty about the cause of improvement. This article is a summary of the evidence that modest increases of 5% to 7% in serum total cholesterol during diuretic-based antihypertensive therapy offset, in part, the benefit expected from the lowering of blood pressure. Correlative data suggest a link between the lipid disturbance and the long-known glucose intolerance caused by diuretic drugs. The findings raise the possibility that treatment regimens free of these metabolic disturbances may provide the means for greater gains against CHD in patients with hypertension.

Age Factors↗
PubMed1988

Central nervous system considerations in the use of beta-blockers, angiotensin-converting enzyme inhibitors, and thiazide diuretics in managing essential hypertension.

The most common mild side effects occurring with use of beta-blockers, thiazide diuretics, and angiotensin-converting enzyme inhibitors for blood pressure control are central nervous system symptoms, specifically lethargy, sedation, and fatigue. These symptoms affect 5% to 10% of patients taking these drugs. The mechanism by which beta-blockers may induce central nervous system effects is uncertain. Relative lipophilicity as a factor affecting penetrance of the blood-brain barrier has not proved to be a reliable predictor of whether the drug will cause such disturbances. Comparisons of atenolol (hydrophilic) and metoprolol (lipophilic) have shown no differences between these drugs with respect to side effects of the central nervous system. The incidence of central nervous system effects with angiotensin-converting enzyme inhibitors is similar to that for most beta-blockers. The precise role of the angiotensin-converting enzyme in the central nervous system is not well defined. Most thiazide diuretics are not associated with major complications of the central nervous system, although electrolyte imbalance may occasionally lead to complaints of neurologic symptoms. Because the incidence of central nervous system effects with these three classes of drugs is so low, concern for the side effects of the central nervous system is not a prime consideration in the choice of an initial antihypertensive agent.

Adrenergic beta-Antagonists↗
PubMed1991

Intractable heart failure despite angiotensin-converting enzyme inhibitors, digoxin, and diuretics: long-term effectiveness of add-on therapy with pimobendan.

In 25 patients whose chronic congestive heart failure (CHF) had recently worsened to New York Heart Association class IV, pimobendan (5 to 20 mg/day) was added to maximum conventional therapy consisting of digoxin, diuretics, angiotensin-converting enzyme inhibitors, coumadin derivatives to prevent thromboembolic complications, and amiodarone to suppress serious ventricular rhythm disturbances. CHF was fatal in less than 1 month in five patients (two had shown some initial improvement). The other 20 had sustained improvement by at least one functional class, interrupted by episodes of CHF that usually responded to intravenous therapy. Median survival was 12 months (range 10 days to greater than 3 years); five patients died suddenly, 12 died of intractable CHF, and two died of other causes. Six patients were alive 3 years after the onset of treatment with pimobendan. Add-on therapy with pimobendan produced a sustained improvement in many patients with severe CHF that was no longer responding to a combination of digoxin, diuretics, and angiotensin-converting enzyme inhibitors.

Aged↗