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PubMed2006

Carvedilol accelerate elevation of serum potassium in chronic heart failure patients administered spironolactone plus furosemide and either enalapril maleate or candesartan cilexetil.

OBJECTIVE: To retrospectively investigate the effect of carvedilol and spironolactone plus furosemide, administered concomitantly with an angiotensin II converting enzyme inhibitor (ACE-I) or an angiotensin II receptor blocker (ARB) to patients with chronic heart failure (CHF). METHODS: Patients with CHF, who visited Departments of Cardiovascular Internal Medicine at the National Hospital Organization Osaka Medical Center, were enrolled for this study. Serum potassium, blood urea nitrogen (BUN), serum creatinine (Scr) and serum sodium were measured in every patient at the time of start of treatment and after 3 and 12 months of treatment. Data from patients in groups A (20 mg/day carvedilol + 25 mg/day spironolactone + 40 mg/day furosemide + an ACE-I) and B (20 mg/day carvedilol + 25 mg/day spironolactone + 40 mg/day furosemide + ARB) were compared. RESULTS: When 20 mg/day carvedilol plus 25 mg/day spironolactone plus 5 mg/day enalapril maleate (enalapril, group A) or 8 mg/day candesartan cilexetil (candesartan, group B) plus 40 mg/day furosemide were used concomitantly, the mean serum potassium increased significantly in both groups of patients. Seven of 59 (11.9%) patients had hyperkalemia (>5.5 mEq/L) during 12 months of treatment whereas 8.5% of patients (five of 59) had hypokalemia (< or =3.5 mEq/L). CONCLUSION: When carvedilol is used concomitantly with spironolactone, furosemide and enalapril or candesartan, it is necessary to monitor serum potassium concentration, even if spironolactone is administered at a low dose of 25 mg/day.

Adult↗
PubMed1991

Combination of long-acting furosemide and instant-acting amiloride: pharmacokinetics and pharmacodynamics in human subjects.

The pharmacokinetics and pharmacodynamics of the combination of amiloride (2 x 2.5 mg) and long-acting furosemide (2 x 10 mg) were compared with amiloride (5 mg) and furosemide (20 mg) in 12 healthy male volunteers aged 26.2 +/- 1.6 years and weighing 68.8 +/- 6.2 kg, after random order administration. Furosemide and amiloride plasma or urine concentrations were determined by HPLC with fluorimetric detection. The rate of absorption (tmax = 3 h) and the bioavailability of the two diuretics were not significantly modified by their combination. Furosemide plasma half-life was 2.77 +/- 1.04 h after the combination treatment and 2.76 +/- 0.98 h alone, amiloride plasma half-life was respectively 15.7 +/- 4.6 h and 14.6 +/- 3.7 h. The urinary elimination of furosemide was significantly higher in the 2-4 h interval in the combination treatment, accompanying its delayed maximum effect of diuresis. A synergistic effect was observed after the combination administration of the two diuretics; between the 2nd and the 8th hour, the sodium elimination was significantly increased (P less than 0.01) and the potassium excretion was significantly decreased (P = 0.05). After a single dose, no modification of plasma or erythrocyte magnesium levels was observed. This study shows that the combination of the two drugs entails a synergy of their activities which does not involve pharmacokinetic changes.

Adult↗
PubMed1988

The effect of furosemide on vascular smooth muscle is influenced by plasma protein.

The effect of furosemide on vascular smooth muscle was studied on segments of rabbit blood vessels. Furosemide (20 micrograms/ml) induced small (3-4%) decreases in resting tension whereas nitroglycerin (0.5 micrograms/ml) induced decreases from 8 to 13%. The addition of albumin (45 g/l) abolished the furosemide response whereas the nitroglycerin response was unaffected. Similarly the pronounced effect of nitroglycerin on electrically evoked contractions was unaffected by the presence of albumin whereas the furosemide effect was weakened by albumin. The biologically determined free fraction of furosemide increased with increasing drug concentrations from 13% at 16 micrograms/ml to 35% at 256 micrograms/ml.

Animals↗
PubMed1997

The effect of aerosolized furosemide in infants with chronic lung disease.

To investigate whether aerosolized furosemide would improve pulmonary function in premature infants with chronic lung disease, we enrolled eight preterm ventilator-dependent infants in a cross-over, double-blind, placebo-controlled trial. Either aerosolized furosemide (2 mg/kg) or placebo (0.9% saline) was administered, and serial pulmonary function tests were performed before and at 1 and 2 h after each inhalation. After furosemide inhalation, static respiratory compliance increased significantly by 24.3% and 23.2% as percentage change from the baseline value at 1 and 2 h (p = 0.014 and 0.022, respectively). Also, tidal volume increased significantly by 33.8% and 28.7% at 1 and 2 h, respectively (p = 0.004 and 0.009). In contrast, no changes were observed in them after placebo inhalation. Total respiratory resistance was unchanged after both furosemide and placebo inhalation. There were no differences in urine volume in two groups. These data suggested that aerosolized furosemide improved pulmonary function in infants with chronic lung disease without excessive diuresis.

Administration, Inhalation↗
PubMed1988

Furosemide causes acute and long-term hyperglycaemia and reduces glucose tolerance in mice.

The effect of furosemide on carbohydrate metabolism was studied in mice. Single-dose administration (200 mg kg-1 body weight) resulted in transient hyperglycaemia and a rise in the glucose/insulin ratio within 60 min. The glucose tolerance was impaired with elevated serum glucose and reduced insulin response 2 h after the furosemide injection, but had recovered within 24 h. In mice made hypoglycaemic by prior injection of insulin, the basal serum glucose and the glucose tolerance were impaired 22 h after the injection of furosemide. It is suggested that furosemide has both acute and long-term effects on carbohydrate metabolism in mice and that, at least in part, this is due to reduced insulin secretion. Glucose may protect against the diabetogenic action of furosemide.

Animals↗
PubMedDate not supplied

Exercise induced alterations in the serum muscle enzymes, erythrocyte potassium and plasma constituents following feed withdrawal or furosemide and sodium bicarbonate administration in the horse.

Six thoroughbreds were used in each of three trials to examine the effect of potassium depletion on exercise-associated muscle damage. Horses were exercised after a control period (Treatment 1), a 72-hour fast (Treatment 2), and furosemide and sodium bicarbonate (Treatment 3). During the preexercise period, feed withdrawal for 72 hours caused decreases in body weight, plasma sodium, chloride, and serum calcium. There were no changes in plasma potassium, erythrocyte potassium, or serum creatine phosphokinase (CK) activity. Furosemide and sodium bicarbonate administration resulted in a decrease in plasma potassium, chloride, serum calcium, and magnesium in the pre-exercise period. Erythrocyte potassium and serum CK activity were unchanged. Body weight initially decreased following furosemide and sodium bicarbonate and then increased upon access to water. In all three treatment groups plasma sodium, potassium, L-lactate, serum calcium, and magnesium were increased immediately following exercise. There was a significant increase (P less than 0.05) in serum CK activity in the furosemide and sodium bicarbonate-treated horses compared to control and withholding feed treatment groups by 30 minutes following exercise. Erythrocyte potassium was decreased immediately following exercise in the furosemide and sodium bicarbonate group but not in the other treatment groups. Potassium depletion may play a role in exercise-induced muscle damage but could not be implicated as the sole cause of the serum CK activity increase in this study.

Animals↗
PubMedDate not supplied

Short-term compatibility of furosemide with crystalloid solutions.

Parenteral veterinary furosemide is a 50-mg/mL solution with a pH of 8.0-9.3. The purpose of this study was to determine whether a commonly used veterinary formulation of 50 mg/mL of furosemide solution could be diluted in vitro without precipitation. Furosemide 50 mg/mL was diluted to concentrations of 10 and 5 mg/mL with 5% dextrose in water (D5W), 0.9% saline, lactated Ringer solution (LRS), and sterile water. Acidic sterile water and basic sterile water solutions were made by the addition of hydrochloric acid and sodium hydroxide, respectively, for use as controls to assess the effect of pH extremes for each concentration. After furosemide dilution, the final pH of each sample was measured, and samples were grossly and microscopically examined for clarity and crystal formation immediately and 1, 3, 5, and 8 hours after dilution. Gross precipitation and microscopic crystals were immediately observed in the acidic controls. Solutions of 5 mg/mL in LRS and 0.9% saline became slightly cloudy immediately, but no crystals were observed microscopically for 8 hours. Solutions of 10 mg/mL in D5W, 0.9% saline, LRS, and sterile water and solutions of 5 mg/mL in D5W and sterile water and the basic control were grossly clear, and no microscopic crystals were observed for 8 hours. On the basis of the results obtained in this in vitro investigation, this veterinary formulation of furosemide 50 mg/mL can be diluted without precipitation to a concentration of 10 mg/mL with D5W, 0.9% saline, LRS, or sterile water and to 5 mg/mL with D5W or sterile water and held for 8 hours.

Animals↗
PubMedDate not supplied

Furosemide continuous rate infusion in the horse: evaluation of enhanced efficacy and reduced side effects.

Continuous rate infusion (CRI) of furosemide in humans is considered superior to intermittent administration (IA). This study examined whether furosemide CRI, compared with IA, would increase diuretic efficacy with decreased fluid and electrolyte fluctuations and activation of the renin-angiotensin-aldosterone system (RAAS) in the horse. Five mares were used in a crossover-design study. During a 24-hour period, each horse received a total of 3 mg/kg furosemide by either CRI (0.12 mg/kg/h preceded by a loading dose of 0.12 mg/kg IV) or IA (1 mg/kg IV q8h). There was not a statistically significant difference in urine volume over 24 hours between methods; however, urine volume was significantly greater after CRI compared with IA during the first 8 hours ([median 25th percentile, 75th percentile]: 9.6 L [8.9, 14.4] for CRI versus 5.9 L [5.3, 6.0] for IA). CRI produced a more uniform urine flow, decreased fluctuations in plasma volume, and suppressed renal concentrating ability throughout the infusion period. Potassium, Ca, and Cl excretion was greater during CRI than IA (1,133 mmol [1.110, 1,229] versus 764 mmol [709, 904], 102.7 mmol [96.0, 117.2] versus 73.3 mmol [65.0, 73.5], and 1,776 mmol [1,657, 2.378] versus 1,596 mmol [1,457, 1,767], respectively). Elimination half-lives of furosemide were 1.35 and 0.47 hours for CRI and IA, respectively. The area under the excretion rate curve was 1,285.7 and 184.2 mL x mg/mL for CRI and IA, respectively. Furosemide CRI (0.12 mg/kg/h) for 8 hours, preceded by a loading dose (0.12 mg/kg), is recommended when profound diuresis is needed acutely in horses.

Animals↗
PubMed1982

Ions and energy metabolism in duck salt-gland: possible role of furosemide-sensitive co-transport of sodium and chloride.

1. The effects of methacholine on net ionic movements and energy metabolism of the avian salt-gland have been studied, using slices of glands taken from salt-adapted Pekin ducks. The slices were equilibrated with media and drugs for 120 min at 1 degrees C before the experimental incubation at 38 degrees C.2. During incubation at 38 degrees C the slices accumulated K(+) and lost Na(+) and Cl(-). In the presence of methacholine, they retained more Na(+) and Cl(-) and accumulated less K(+), the maximal effects being given by 0.5-1.0 mM-methacholine. Similar results were obtained whether the medium contained 10 mM-Tris (used in most experiments) or 25 mM-HCO(3) (-) as the major buffer.3. The higher final levels of cell Na(+) and Cl(-) induced by methacholine were not seen when furosemide (1 mM) was also present. Methacholine did not induce a higher level of cell Na(+) when medium Cl(-) was replaced by I(-), NO(3) (-) or SO(4) (2-), and did not induce a higher Cl(-) content when medium Na(+) was replaced by choline or Li(+). The fall of K(+) accumulation caused by methacholine was also prevented by furosemide or by replacing Cl(-) in the medium with other anions. The anion-transport inhibitors, SCN(-) (up to 10 mM) and 4,4'-diisothiocyano-2,2'-disulphonic acid stilbene (DIDS) (up to 2 mM) did not prevent the effects of methacholine.4. Methacholine stimulated respiration and lowered the slice ATP contents, and these effects were both prevented by ouabain or furosemide. Ouabain, but not furosemide, also reduced the basal (i.e. in the absence of methacholine) rate of respiration and raised the ATP level. SCN(-) and DIDS had no effect on basal or stimulated respiration or on ATP contents.5. The respiratory stimulation and fall of ATP induced by methacholine were totally prevented if medium Na(+) was replaced by choline. Replacement of Na(+) by Li(+) caused some stimulation of basal respiration; it also permitted some loss of ATP in the presence of methacholine, but the loss was smaller than that seen in the normal Na(+) medium.6. The respiratory stimulation and fall of ATP induced by methacholine were prevented if medium Cl(-) was replaced by SO(4) (2-). The effects of methacholine were partially blocked when NO(3) (-) replaced Cl(-).7. The results are consistent with the stimulation by methacholine of a furosemide-sensitive, coupled entry of Na(+) and Cl(-) into the cells, associated with a loss of K(+). This would result in a stimulation of Na(+) extrusion by the ouabain-sensitive transport system for Na(+) and K(+) with increased consumption of ATP.

Adenosine Triphosphate↗
PubMed1982

The effects of intracochlear and systemic furosemide on the properties of single cochlear nerve fibres in the cat.

1. Tuning properties and spontaneous discharge rate of single cochlear fibres in the anaesthetized cat were determined during short- and long-term poisoning of the cochlea by locally and systemically applied furosemide.2. With intra-arterial administration of furosemide, short-term reversible elevation occurred of the low threshold sharply tuned ;tip' segment of the frequency threshold (;tuning') curve (f.t.c.) by up to 40 db, without substantial changes in the threshold of the low frequency ;tail' segment of the f.t.c. These changes could occur in part without changes in the spontaneous activity and entirely without changes in the maximal evoked activity. These effects were observed in all fibres examined, the characteristic frequencies of which ranged from 3.5 to 31 kHz.3. Intracochlear administration of furosemide in 0.9 mM concentrations produced similar changes, but these were not reversible.4. The changes correlated with the depression of the amplitude of the gross cochlear action potential. The cochlear microphonic potential, however, was either unchanged, or only slightly reduced.5. In long-term furosemide poisoning of the cochlea, fibres with anomalous response properties were found alongside fibres having normal tuning. The former exhibited either reduced excitability of the low threshold tip segment, or a tip segment attenuated in both excitability and threshold.6. It is concluded that the selective effects of furosemide on the tip segment of cochlear fibre f.t.c.s offer further evidence for a physiologically vulnerable ;second filter' in the cochlea. The selective influence of the furosemide on the low threshold tip segment provides support for the hypothesis that the normal f.t.c. is generated by two largely independent processes: one vulnerable, low threshold and sharply tuned, and the other less vulnerable, but high threshold and more broadly tuned.7. The findings, obtained with an agent known to produce reversible impairment of hearing in man, provide direct physiological evidence in support of the hypothesis that in sensorineural hearing loss of cochlear origin the frequency selectivity of cochlear nerve fibres is impaired.

Action Potentials↗
PubMed1992

Influence of hypertonic-hyperoncotic solution and furosemide on canine hydrostatic pulmonary oedema resorption.

1. This study aimed at enhancing the clearance of experimental hydrostatic pulmonary oedema in dogs using hypertonic-hyperoncotic solution (HHS) and furosemide. 2. Anaesthetized dogs (n = 20) were mechanically ventilated with a positive end-expiratory pressure of 10 cmH2O (1.0 kPa). 3. Hydrostatic pulmonary oedema was induced by inflating a balloon inserted into the left atrium and simultaneously infusing isotonic saline rapidly. Oedema formation was terminated by deflating the balloon and reducing the infusion rate. 4. Four groups were studied: A, control; B, furosemide; C, HHS and D, HHS+furosemide. HHS, 6 ml kg-1, was given as a bolus injection and furosemide, 1 mg kg-1, intravenously as a bolus followed by an infusion of 0.5 mg kg-1 h-1. All dogs were studied for 4 h. 5. Serum osmolarity, plasma colloid oncotic pressure and diuresis in groups C and D (HHS groups) substantially increased; haemoglobin concentration decreased and pulmonary arterial wedge pressure remained constant. 6. Despite the combination of these factors favouring fluid flux from the extravascular to the intravascular compartment, extravascular lung water measured with the double indicator dilution technique decreased no faster in the HHS groups than in the two other groups (from over 26 to approximately 19 ml kg-1 in groups A, C and D and to 14.7 in group B (only furosemide)). 7. This was confirmed by postmortem gravimetric measurements of extravascular lung water; A, 11.0 +/- 5.7; B, 9.7 +/- 3.3; C, 10.5 +/- 3.1 and D, 10.6 +/- 1.8 g kg-1. 8. We speculate that mechanisms other than effective Starling gradients and enhanced diuresis might define a maximal rate of pulmonary oedema clearance.

Animals↗
PubMed1983

Passive transport of K+ and Na+ in human red blood cells: sulfhydryl binding agents and furosemide.

Passive transport pathways for K+ and Na+ were studied in fresh human red blood cells (pretreated with ouabain) by measuring unidirectional influxes. The effects of the sulfhydryl binding agents N-ethylmaleimide (NEM) and p-chloromercuribenzene sulfonate (p-CMBS) and the loop diuretic furosemide were studied. Influxes were measured at equimolar K+ and Na+ concentrations (50 mM) with both ions present and also in K+-free or Na+-free media. Some experiments were carried out in Cl--free media (with NO-3 as the substitute). NEM stimulated K+ influx twofold; the stimulation required Cl- but not Na+. NEM inhibited Na+ influx 20%. Furosemide inhibited both K+ and Na+ influxes. All of furosemide-inhibitable Na+ influx required the presence of K+. However 30% of furosemide-inhibitable K+ influx did not require Na+. All of furosemide-inhibitable K+ influx required Cl-. The ratio of Na+-dependent K+ influx to K+-dependent Na+ influx was 3:1. p-CMBS stimulated both Na+ and K+ influxes. K+ influx in p-CMBS cells required neither Na+ nor Cl-. Likewise p-CMBS-promoted Na+ influx did not require K+. These various results are consistent with two Cl--dependent pathways for K+ transport, one requiring Na+ [perhaps (Na + K + Cl) cotransport] and one independent of Na+ [perhaps (K + Cl) cotransport]. The pathways promoted by p-CMBS are probably independent of the apparent cotransport systems.

4-Chloromercuribenzenesulfonate↗
PubMed1977

Effect of furosemide on renal handling of glucose in the rat.

Clearance and intratubular microinjection studies were performed in rats during extracellular volume expansion before and after furosemide administration to evaluate renal tubular transport of glucose. Three groups of animals were studied: group I, intact rats; group II, acutely thyroparathyroidectomized rats; and group III, thyroparathyroidectomized rats receiving parathyroid extract after a control period. In all groups furosemide caused a significant increase in the urinary flow rate and sodium excretion. There was no significant change in filtered glucose and glucose excretion. After early distal tubular injections of [14C]glucose, recovery was complete both before and after furosemide infusion. Furosemide had no effect on [14C]glucose recovery after the late proximal injection. These results indicate that furosemide has no effect on the renal handling of glucose in normoglycemic rats. There is no evidence for glucose reabsorption in the nephronal segments distal to the early distal tubular segment in this experimental state. Our data suggest, but do not prove, that no glucose is transported by the rat nephron beyond the pars recta during normoglycemia.

Animals↗
PubMed1981

Effect of furosemide on calcium and magnesium transport in the rat nephron.

Superficial tubules were perfused in vivo to determine the effect of intraluminal furosemide on electrolyte transport in the loop of Henle and distal tubule of the rat with special reference to calcium and magnesium reabsorption. in vivo perfusion of single tubules allowed us the opportunity to investigate separate electrolyte transfers with altering the corticomedullary concentration gradient within the kidney. Intraluminal furosemide (3 X 10(-6) and 3 X 10(-5) M) resulted in proportionately greater calcium and magnesium inhibition relative to sodium and chloride in Henle's loop. Furosemide had little effect on transport function within the perfused superficial distal tubule. Distal calcium and magnesium reabsorption was dependent on their respective deliveries to this segment. Parathyroid hormone increased fractional calcium and magnesium reabsorption in Henle's loop and the distal tubule in the presence of intraluminal furosemide. These results are consistent with a luminal effect of furosemide in the loop of Henle that inhibits calcium and magnesium transport to a greater degree than sodium chloride. Intraluminal ethacrynic acid (10(-4) M) or its cysteine complex had no effect on electrolyte transport in the perfused rat nephron.

Animals↗
PubMed1992

A micropuncture study of renal lithium reabsorption: effects of amiloride and furosemide.

The validity of the lithium clearance technique as a measure of end-proximal fluid delivery was assessed using micropuncture in sodium-replete, Inactin-anesthetized Sprague-Dawley rats. Three groups of animals were used: controls, amiloride treated, and furosemide treated. Diuretic-induced salt and water losses were replaced. Fractional lithium excretion (FELi) was 0.23 +/- 0.01, 0.24 +/- 0.02, and 0.40 +/- 0.03 in the control, amiloride, and furosemide groups, respectively. In each group, the tubular fluid-to-plasma lithium concentration ratio at the end of the proximal convoluted tubule (PCT) was significantly greater than unity (control, 1.16 +/- 0.03; amiloride, 1.16 +/- 0.02; furosemide, 1.17 +/- 0.02). In the control group, fractional lithium delivery (FDLi) at the late PCT was 0.50 +/- 0.02, while FDLi at the early distal tubule was 0.25 +/- 0.01; the latter did not differ significantly from FDLi at the late distal tubule or from FELi. Values in amiloride-treated rats were almost identical. Furosemide had no effect on FDLi at the late PCT, but raised that at the early distal tubule to 0.37 +/- 0.03. We conclude that 1) lithium reabsorption in the PCT lags slightly behind that of water, 2) substantial furosemide-sensitive lithium reabsorption occurs beyond the PCT, and 3) no significant lithium reabsorption occurs in nephron segments beyond the loop. These findings call into question the use of lithium clearance as a quantitative measure of end-proximal fluid delivery in sodium-replete animals.

Absorption↗
PubMed1984

Pulmonary vascular effects of furosemide on gas exchange in pulmonary edema.

To test the hypothesis that pulmonary vasoactivity of furosemide redistributes blood away from edematous lung, thus improving gas exchange, we studied two groups of 10 dogs each with unilobar oleic acid edema, treating one group with 1 mg/kg furosemide 2 h after the oleic acid. Pulmonary perfusion distribution was determined with radio microspheres. Shunts of the injured lobe, measured from O2 contents of lower lobar pulmonary venous blood, increased significantly (P less than 0.05) at 2 h after injury in both groups. Within 0.5 h after furosemide the lobar shunt decreased in the treated animals from 40.1 +/- 20.6 to 28.6 +/- 20.1% and increased from 21.4 +/- 14.0 to 53.8 +/- 26.9% in the control group (P less than 0.05). Mean fractional lobar perfusion to the injured lobe increased from 18.2 +/- 4.8 to 21.6 +/- 6.4% (P less than 0.05) in the furosemide group but decreased from 20.1 +/- 3.5 to 16.1 +/- 4.4% (P less than 0.05) in the controls. Wet lung-to-body weight ratios of the edematous lobes did not differ between the two groups. Our data suggest the possibility that, before decreasing edema, furosemide improved shunt through pulmonary vascular effects by preferential perfusion of nonflooded alveolar units.

Animals↗
PubMed1994

Acute respiratory acidosis: large-dose furosemide and cerebrospinal fluid ions.

NaCl cotransport carrier is known to be involved in transepithelial fluid absorption and secretion in various tissues. Recent studies indicate that Na-K-2Cl cotransport carrier also exists in the choroid plexus cells and that inhibition of the carrier decreases cerebrospinal fluid (CSF) production. In this study, we used large-dose intravenous furosemide, an inhibitor of Na-K-2Cl carrier, to determine the effects on cisternal CSF ionic composition in acute respiratory acidosis. In pentobarbital-anesthetized mechanically ventilated dogs, renal pedicles were ligated to prevent furosemide-induced diuresis. The experimental group (group II, n = 7) received 400 mg/kg of furosemide intravenously, and group I (control group, n = 7) received the vehicle. In group II, serial serum and CSF furosemide concentrations were approximately 10(-3) and 10(-5) mol/l, respectively. During 5 h of acute respiratory acidosis in both groups, the mean arterial PCO2 increased approximately 25 Torr, with comparable changes in CSF PCO2. In both groups, CSF [HCO3-] and [H+] rose approximately 3 meq/l and 20 neq/l, respectively. Changes in CSF [Na+], [K+], [Cl-], and [Na(+)-Cl-] were also similar and were not significantly different from each other when the two groups were compared. These data show that furosemide at the dose that inhibits NaCl cotransport carrier does not significantly alter ionic composition of cisternal CSF.

Acid-Base Equilibrium↗
PubMedDate not supplied

Furosemide compounds enhance urinary excretion of active kallikrein independently of their effects on urinary electrolyte excretion.

The chemical and diuretic effects of furosemide on the excretion and activation of urinary prokallikrein were investigated in rats by treatment with furosemide compounds with a range of diuretic activity or amiloride hydrochloride or the vehicle. Diuresis occurred with furosemide and benzyl furosemide, but not with isofurosemide, amiloride hydrochloride, or the vehicle. The urinary excretion rate of active kallikrein was significantly elevated above controls throughout the 72 h of treatment with all of the drugs tested, regardless of the level of diuresis or the rate of urinary electrolyte excretion. In contrast, the urinary excretion rate of total kallikrein (prokallikrein + active kallikrein) was unchanged in all groups. These data indicate that furosemide derivatives increase the activation, but not the excretion, of urinary prokallikrein and that these effects are unrelated to the chemical structure or diuretic activity of the compounds or to overall changes in urinary electrolyte excretion rates.

Animals↗