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PubMed2000

Effect of thiazide on established furosemide-induced nephrocalcinosis in the young rat.

A previous study on furosemide-induced nephrocalcinosis (NC) showed only partial resolution of the calcifications after discontinuation of the diuretic. We investigated whether treatment with chlorothiazide (CTZ) will expedite the resolution of established furosemide-induced NC. Seventy-eight weanling male Sprague-Dawley rats were divided into eight groups. Three groups were studied for 1 week: A, control; B, furosemide 40 mg/kg per 24 h; C, CTZ 100 mg/kg per 24 h. Five groups were studied for 5 weeks: D, control; E, F, G, furosemide 40 mg/kg per 24 h for 1 week followed by 4 weeks of observation (E), CTZ 50 mg/kg per 24 h (F), and CTZ 100 mg/kg per 24 h (G) and; and CTZ 100 mg/kg per 24 h (H) for 5 weeks. At the end of each study period urine and blood were collected, one kidney was studied histologically and the contralateral ashed for quantitative calcium (Ca) analysis. Animals in group B developed NC with a kidney Ca content of 1,844 +/- 203 micrograms/g dry tissue compared with group A 248 +/- 86 (P < 0.05) and group C 256 +/- 56 (P < 0.05). There were no differences among the three groups with regard to creatinine clearance, urine phosphate (P) or Ca excretion, although the latter tended to be lower in group C. Animals in group E showed a reduction in the magnitude of NC, with kidney Ca of 550 +/- 398 micrograms/g dry tissue, which was lower than in group B (P < 0.05) but still higher than in groups D (140 +/- 27) (P < 0.05) or H (162 +/- 63) (P < 0.05). Kidney Ca content in groups F (497 +/- 142) and G (489 +/- 271 micrograms/g dry tissue) was similar to that in group E. There were no differences among the five groups with regard to creatinine clearance or urine P excretion. Urine Ca excretion was significantly lower in groups F and G than groups D and E. We conclude that once established, NC caused by furosemide is not affected by CTZ therapy in spite of the anticalciuric property of the latter.

Animals↗
PubMed2005

The Na+-excreting efficacy of indapamide in combination with furosemide in massive edema.

BACKGROUND: Massive systemic edema is often observed in patients with severe nephrotic syndrome, including diabetic nephropathy. Although furosemide, a loop diuretic, is often administered to these patients, some patients do not respond to this treatment, still showing massive edema. METHODS: The efficacy of indapamide which has a thiazide-like effect on distal convoluted tubules in combination with furosemide, was evaluated in eight patients with massive edema, in regard to both Na+ excretion and diuresis. Indapamide 2 mg was administered once a day, in the morning, to patients in whom it was considered that furosemide treatment of 40-120 mg a day for 1 week was ineffective. RESULTS: Urinary Na+ excretion was markedly increased, from 83.7 +/- 82.2 mEq/day to 140.7 +/- 33.8 mEq/day after 1 week of the combination therapy compared with furosemide alone (P < 0.01); urine volume was also increased, from 1070 +/- 230 ml to 1359 +/- 296 ml after 1 week of the combination therapy (P < 0.05). In this context, body weight was significantly decreased, from 57.2 +/- 12.3 kg to 53.4 +/- 12.8 kg, after the combination therapy (P = 0.01). Indapamide in combination with furosemide was well tolerated, and no significant changes in serum levels of creatinine and potassium were observed. CONCLUSIONS: This combination therapy appears to be effective in patients with massive edema, as it increased diuresis, and achieved potent Na+ excretion.

Adult↗
PubMed1985

Effect of furosemide on ion transport in the turtle bladder: evidence for direct inhibition of active acid-base transport.

The diuretic furosemide inhibits acid-base transport in the short-circuited turtle bladder. It inhibits luminal acidification when present in either mucosal or serosal bathing fluids, but decreases alkalinization only from the serosal side of the tissue. The inhibition of both acid-base transport processes is independent of ambient Cl-; and the disulfonic stilbene, SITS, an inhibitor of Cl--HCO3- exchange, fails to prevent the furosemide-elicited inhibition of alkalinization. These results preclude an absolute requirement of a furosemide-sensitive Cl--HCO3- exchange by these transport processes. The drug also interferes with the CO2-induced stimulation of acidification and alkalinization. The inhibition of the residual acidification in acetazolamide-treated, acidotic bladders, however, suggests an action at sites other than cytosolic carbonic anhydrase. Although active Na+ and Cl- reabsorption and tissue oxygen uptake are also decreased by furosemide, the rate of oxygen consumption uncoupled by 2,4-dinitrophenol is not diminished, indicating a primary inhibition of the various ion transport processes, not of metabolism. It is proposed that inhibition of transepithelial acid-base transport by furosemide in the turtle bladder includes inhibition of the acid-base pumps.

2,4-Dinitrophenol↗
PubMed1977

Increase of free arachidonic acid by furosemide in man as the cause of prostaglandin and renin release.

Arachidonic acid (C20 :4) plasma renin activity (PRA), PGF2alpha, and sodium excretion were determined before and after furosemide in men. C20 : 4 and PRA increase (p less than 0.005) within 10 min after furosemide, PRA then decreased again whereas C20 : 4 levels remained elevated. Maximal exretion of PGF2alpha and sodium occurred 30-60 min after furosemide. Indomethacin prevented the rise of C20 : 4, PRA and PGF2alpha after furosemide, leaving sodium excretion unaltered. The release of C20 : 4 is assumed to be the primary mechanism of furosemide to increase PG biosynthesis and renin release.

Adult↗
PubMed1986

Inhibitory action of furosemide on the active chloride transport of papillary heart muscle in rabbit.

The action of furosemide on the intracellular chloride activity, ai(Cl), of rabbit papillary muscle was investigated with Cl ion selective microelectrodes. With furosemide concentrations greater than 1 microM, ai(Cl) decreased. Furthermore, the decrease in ai(Cl) was larger as the furosemide concentration increased. Lowering the extracellular sodium concentration, [Na]o, by replacing Na with choline, significantly reduced the effect of furosemide on ai(Cl). The results provide evidence that the membrane of rabbit heart cells possess a furosemide sensitive chloride transport mechanism related to [Na]o.

Animals↗
PubMed1988

Furosemide-induced glucose intolerance in mice is associated with reduced insulin secretion.

The effect of furosemide on carbohydrate metabolism was studied in ob/ob mice. Intraperitoneal injection of a single dose of furosemide (200 mg/kg body weight) into fasted mice resulted in acute hyperglycaemia and two days after such a single dose, the mice showed fasting hyperglycaemia and glucose intolerance. Pancreatic islets from mice that had been injected with furosemide (200 mg/kg body weight) two days prior to the in vitro experiments showed increased basal (3 mmol/1 D-glucose) and decreased glucose-stimulated (20 mmol/1) insulin release. Islets from furosemide- or saline-injected animals showed no difference in islet insulin content. The results show that furosemide has both acute and long-term effects on carbohydrate metabolism in ob/ob mice. It is suggested that this, at least in part, is due to an effect on the pancreatic beta-cells.

Animals↗
PubMed1988

Effects of chronic furosemide treatment on rat exocrine glands.

It has been suggested that a defective chloride transport is the primary cellular basis for the disease cystic fibrosis (CF). Therefore, the effects of chronic furosemide treatment on the structure and function of rat exocrine glands were investigated. X-ray microanalysis of the submandibular gland showed an increase in the cellular Ca and Mg concentrations, and a decrease in the cellular Cl concentration. Transmission electron microscopy showed intracellular accumulation of mucus and the presence of mucus in acinar and ductal lumina. The volume of saliva secreted by the submandibular gland after pilocarpine stimulation was markedly reduced in furosemide-treated animals; the salivary concentrations of Na and Ca were higher, and that of K was lower, than in control animals. The protein concentration in submandibular saliva was not significantly affected. The response of the submandibular gland to isoproterenol stimulation was reduced in furosemide-treated animals. In the parotid gland, chronic furosemide treatment caused an accumulation of immature zymogen granules in the acinar cells and a decrease in the cellular Cl concentration. In the pancreas, the acinar lumen was dilated and completely filled with secretory material, and the acinar cells contained less Na and somewhat less Cl than in control animals. The chronically furosemide-treated rat shows a number of parallels with other animal models for CF, in particular the chronically reserpinized rat. There is also agreement with the human disease itself.

Animals↗
PubMed1990

Effects of potassium or potassium/magnesium supplementation on potassium content of body tissues and fluids in furosemide-treated rats on magnesium-deficient or magnesium-sufficient diet.

Persistent Mg2+ deficiency may interfere with restoration of normal tissue K+ levels. This study examined: a) the effects of chronic furosemide treatment on K+ of sartorius, aorta and ventricle of rats fed Mg2(+)-deficient (100 ppm) or Mg2(+)-sufficient (400 ppm) diet and deionized water; b) whether normal tissue K+ is restored by oral K+ or K+/Mg2+ supplementation with continued furosemide therapy. Levels of Mg2+ were also measured. Furosemide (20 mg/kg i.p.) decreased K+ in sartorius, aorta and ventricle by 5.5, 4.3 and 19.9 microEq/gm (p less than .05), respectively, in rats fed 100 ppm Mg2+ diet. Furosemide did not alter K+ levels in rats fed 400 ppm Mg2+ diet. K+ supplementation (1 mEq/kg for 7 days) restored K+ to normal in sartorius but the addition of Mg2+ supplementation was necessary to restore K+ levels to normal in ventricle and aorta. These data indicate that furosemide can decrease tissue K+ in rats on a Mg2(+)-deficient diet. This decrease can be reversed during diuretic administration by K+ supplementation in sartorius, or K+ plus Mg2+ supplementation in ventricle and aorta.

Animals↗
PubMed1990

Chronopharmacological study of furosemide; (V). Influence of pretreatment with 6-hydroxydopamine.

Our previous indirect evidences suggested that the adrenergic nervous system is involved in the mechanisms responsible for the time-dependent changes in the effects of furosemide in Wistar rats. In the present study, the role of this system was examined more directly by means of 6-hydroxydopamine-induced sympathectomy. Thirty mg/kg of 6-hydroxydopamine hydrobromide (6-OH-DA) (n = 9) or its vehicle alone (n = 9) was injected intra-arterially (i.a.) twice in Wistar rats. Furosemide (5 mg/kg) was administered i.a. at 1000 hrs (03HALO*) or at 2200 hrs (15HALO). Urine was collected for 60 min after the drug and urinary excretion of sodium and furosemide were determined respectively. Urine volume and urinary excretion of sodium and furosemide were significantly greater at 1000 hrs (03HALO) than at 2200 hrs (15HALO) in the vehicle-injected rats as observed in the previous study. However these administration-time-dependent changes in the effects of furosemide disappeared in the rats with 6-OH-DA. Thus, the present study provides more direct evidence and supports our original hypothesis concerning the mechanisms of this chronopharmacological phenomenon of the agent. Since 6-OH-DA does not penetrate the central nervous system from the blood stream, the present data also indicate that the peripheral adrenergic system is involved in this event.

Animals↗
PubMed1984

Effect of furosemide on cerebrospinal fluid composition.

Electrolyte composition of the cerebral spinal fluid (CSF) is important in central respiratory drive. The relationship between [Cl-] and [HCO3-] is of particular interest in maintenance of electrolyte balance. Therefore, the effect of furosemide, an inhibitor of sodium-coupled chloride transport, on CSF electrolyte homeostasis was studied under conditions of normocapnia and hypercapnia in anesthetized dogs. The drug was given intravenously (IV) or in the lateral cerebral ventricles (CV). With normocapnia, there was no change in CSF or arterial PCO2, pH, [K+], [Cl-], or [HCO3-], while CSF [NA+] decreased 1.7 mM in dogs receiving IV furosemide. With 5% CO2 breathing and IV furosemide, CSF PCO2, pH, [K+], [Cl-], and [HCO3-] changed as has been reported for 5% CO2 breathing alone. 5% CO2 and CV furosemide, however, led to a greater reduction in CSF [Cl-] and no change in CSF [HCO3-]. Thus CV furosemide alters the CSF [Cl-] and [HCO3-] in hypercapnia, suggesting that sodium-coupled chloride transport plays a role in regulation of CSF acid-base homeostasis.

Acid-Base Equilibrium↗
PubMed1993

The effects of oral ibopamine in patients with mild heart failure--a double blind placebo controlled comparison to furosemide. The Ibopamine Study Group.

The effect of ibopamine and furosemide in 130 patients with NYHA Class I and II heart failure were studied in a parallel, double-blind, randomized placebo-controlled multi-centre trial. Ibopamine 200 mg b.i.d. was compared to furosemide 40 mg q.d. and placebo. A 1- to 2-week single-blind run-in period was followed by an 8-week double-blind treatment period. Reproducible treadmill exercise test times with the modified Naughton-Balke protocol were required for randomization. Exercise times increased significantly in comparison to the placebo group after 8 weeks of therapy for both the furosemide group (1.2 min, P < 0.035) and the ibopamine group (1.3 min, P < 0.025). Neither furosemide nor ibopamine affected quality of life assessments. Adverse clinical experiences were generally mild and similar in frequency amongst the three treatment groups. The results of this study show the usefulness of both ibopamine and furosemide as monotherapy in patients with mild congestive heart failure.

Administration, Oral↗
PubMed1989

Reduction of portal pressure by acute administration of furosemide in patients with alcoholic cirrhosis.

In patients with cirrhosis, it has been demonstrated that blood volume and degree of portal hypertension are correlated. Hence, a reduction of blood volume by furosemide could decrease portal pressure and could thereby be useful in the treatment of portal hypertension. Splanchnic and systemic haemodynamics were evaluated before and 1 h after intravenous administration of furosemide (0.75 mg/kg) in 10 patients with cirrhosis. Furosemide significantly increased haemoglobin from 12.4 to 13.0 g/dl and patients passed more than 1 l of urine within the 3 h following furosemide administration. These findings confirm that blood volume decreased after diuretic administration. Cardiac output significantly decreased from 6.6 +/- 2.3 to 5.5 +/- 2.2 l/min, while arterial pressure and heart rate did not change significantly. Furosemide significantly decreased wedged hepatic venous pressure from 31.1 +/- 6.2 to 27.7 +/- 5.2 mmHg, but not free hepatic venous pressure. Accordingly, the hepatic venous pressure gradient significantly decreased from 22.1 +/- 5.4 to 19.5 +/- 4.0 mmHg. Azygos blood flow and hepatic blood flow also significantly decreased from 0.40 +/- 0.17 to 0.31 +/- 0.13 l/min and from 1.49 +/- 0.50 to 0.82 +/- 0.30 l/min, respectively. These results show that diuretic therapy markedly influences splanchnic haemodynamics.

Adult↗
PubMed1982

Effect of furosemide on the in vitro prostaglandin biosynthesis in human platelets.

Effect of furosemide at various concentrations (0.05-4 mM) was examined on the in vitro biosynthesis of prostaglandins in human platelets. At lower furosemide concentrations (0.05 and 0.1 mM) no effect was observed. At 1 and 2 mM concentrations, PGE2 significantly (P less than 0.01) increased. At 3 and 4 mM concentrations PGE2 increased though not significantly probably because of the small number of samples (n=5). A decrease in PGD2 formation was noted at 1-4 mM furosemide concentrations, though significantly only at 3 mM conc. At 1 and 2 mM concentrations, TxB2 and HHT increased whereas at 3 and 4 mM concentrations these metabolites were decreased. These effects were, however, not significant. No effect was observed on endoperoxide generation at 1 and 2 mM conc. Furosemide at 1 and 2 mM concentrations inhibited ADP- and arachidonic acid induced platelet aggregation. An increased platelet formation of PGE2 in the presence of furosemide may point to the fact that this drug shows its effect mainly on the formation of PGE2 which has been found to exert a profound effect on renal blood flow and thus ameliorates some forms of hypertension.

Arachidonic Acid↗
PubMed1982

The loop diuretic furosemide as non-competitive inhibitor of C1-/HCO3-ATPases of vertebrate kidneys and insect rectum.

1. The effect of the diuretic drug furosemide was studied in detail on ouabain-insensitive, SCN- and OCN- -sensitive C1-/HCO-3-ATPase in homogenates from larval dragonfly rectum (Aeshna cyanea), frog (Rana temporaria) and mouse (Mus musculus) kidney. 2. The in vitro inhibition by the drug studied on the HCO-3-activated enzyme is non-competitive with an inhibitor constant of Ki=4.3 mM furosemide in the case of insect rectum and Ki=0.9 mM furosemide in the case of frog and mouse kidney. 3. Furosemide even at 10 mM concentration which completely inhibits the anion-dependent ATPase has only a little inhibitory effect on the Na+/K+-ATPase of the 3 tissues. 4. The data suggest that furosemide may affect an active chloride transport system involving a C1-/HCO-3-ATPase.

Adenosine Triphosphatases↗
PubMed1994

Determination of furosemide with its acyl glucuronide in human plasma and urine by means of direct gradient high-performance liquid chromatographic analysis with fluorescence detection. Preliminary pharmacokinetics and effect of probenecid.

Furosemide is metabolized in humans by acyl glucuronidation to the 1-O-glucuronide (Fgluc). Furosemide (F) and the conjugate can be measured directly by gradient high-performance liquid chromatographic analysis without enzymic deglucuronidation. The glucuronide conjugate was isolated by preparative HPLC from human urine samples. Furosemide and its acyl glucuronide were present in plasma. No isoglucuronides were present in acidic urine of a volunteer. Calibration curves were constructed by enzymic deconjugation of samples containing different concentrations of isolated F-acyl glucuronide. The limit of quantitation of F in plasma is 0.007 microgram/ml, Fgluc 0.010 microgram/ml. The limits of quantitation in urine are respectively: F 0.10 microgram/ml, Fgluc 0.15 microgram/ml. A pharmacokinetic profile of furosemide is shown, and some preliminary pharmacokinetic parameters of furosemide obtained from one human volunteer are given. Probenecid does not inhibit the formation of the acyl glucuronide of F, but inhibits the renal clearance of both compounds.

Chromatography, High Pressure Liquid↗
PubMed1992

The effect of furosemide on evoked otoacoustic emissions in guinea pigs.

After recording transiently evoked otoacoustic emissions (TEOAEs) to a click stimulus in guinea pigs by using the IL088 which was developed by Bray and Kemp (1987) for easy recording and analysis of TEOAE, the changes after intravenous administration of furosemide (30 mg/kg or 50 mg/kg) were examined. The wave of the TEOAE could be detected from 20 of 24 ears (83%). After the i.v. injection of furosemide (30 mg/kg), TEOAE powers (total echo power and highest peak power in FFT pictures) decreased quickly and showed minimum values after 5-10 min. Then they increased rapidly and recovered normally within 60 min after injection. However, no ears showed TEOAEs during the 5- to 10-min period following the injection of the 50-mg/kg dose of furosemide. They then recovered slowly as compared with the group treated with the lower dose of furosemide (30 mg/kg). These changes are similar to those of the endocochlear potential (EP) after furosemide injection. These data support the notion that the EP can contribute to the mechanism of TEOAE generation.

Acoustic Stimulation↗
PubMed1992

The inhibitory effect of furosemide on the contractile response of equine trachealis to cholinergic nerve stimulation.

The effects of furosemide on the responses of equine trachealis muscle with and without epithelium to electrical field stimulation (EFS) and exogenous acetylcholine (ACh) were investigated in organ baths. Tissues were pretreated with guanethidine and the parameters used for EFS were those previously demonstrated to activate postganglionic cholinergic neurons. In tissues with intact epithelium, furosemide (100 microM) shifted the frequency-response curve to the right. In the preparations without epithelium, furosemide did not affect the response to EFS. Neither in epithelium-on nor in epithelium-off tissues was the ACh dose-response curve affected by the administration of furosemide. We conclude that furosemide (100 microM) decreases the equine tracheal smooth muscle responses to EFS through inhibition of cholinergic neurotransmission, and that this effect is dependent on epithelium.

Acetylcholine↗
PubMed2004

Development and in vitro evaluation of furosemide transdermal formulations using experimental design techniques.

The in vitro skin permeation of furosemide, a commonly used loop diuretic, through human epidermis, as a preliminary step towards the development of a transdermal therapeutic system, was examined. A screening study was carried out, in order to estimate the effects of the type, the concentration of enhancer and the concentration of gelling agent on the cumulative amount of furosemide permeated through human epidermis, using a 3(3) factorial design. The type and the concentration of enhancer were further evaluated as they were found to affect significantly furosemide permeation. In order to further increase the amount of the drug permeated, the combination of two enhancers, Azone and oleyl alcohol, at three concentration levels was employed, using an optimization technique. The results indicated that higher amounts of furosemide permeated were observed when Azone was used at 5.0-6.5% (v/v) and oleyl alcohol at 7.5-9% (v/v), in the gels used. These formulations seem to be suitable for possible transdermal delivery of furosemide for pediatric use.

Adjuvants, Pharmaceutic↗