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PubMed2001

Low sodium and furosemide-induced stimulation of the renin system in man is mediated by cyclooxygenase 2.

The aim of this study was to examine the effects of highly selective inhibition of cyclooxygenase 2 (COX-2) with rofecoxib on the renin system during long-term stimulation and after short-term stimulation. Six healthy male volunteers received, in a randomized crossover design, a low-sodium diet for days 1 through 9 with or without 25 mg rofecoxib twice daily on days 5 through 9 and, in addition, 20 mg of furosemide intravenously on day 8. Plasma renin activity increased 2 to 3 times over baseline with a low-sodium diet and 5 times over baseline 30 minutes after intravenous furosemide; it was still elevated nearly 5 times on day 9. These effects were completely blocked by rofecoxib. Plasma aldosterone and urinary aldosterone concentrations basically reflected the findings with plasma renin activity. Urinary sodium excretion decreased during a low-sodium diet and increased after intravenous furosemide without being significantly affected by rofecoxib. We have concluded that low-sodium and furosemide-stimulated renin and aldosterone secretion is completely blocked in healthy volunteers during COX-2 inhibition with rofecoxib, suggesting that intact COX-2 is of major importance for stimulation of the renin system under these conditions in man.

Adult↗
PubMed2002

Development of an optimal furosemide infusion strategy in infants with modeling and simulation.

BACKGROUND: The optimal dosing strategy for continuous intravenous furosemide infusion is unknown in pediatric patients. Eighteen patients less than 1 year old were studied after cardiac surgery during routine clinical care. The current strategy starts with a continuous infusion of 0.1 mg/kg x h, which may be adapted. METHODS: A pharmacokinetic-pharmacodynamic model was developed that linked furosemide dose to furosemide serum concentrations, renal function (creatinine clearance), and urine output. Various regimens were simulated that adapt according to urine production. The modified dosing schedule was prospectively tested in a subsequent population of 18 pediatric patients after cardiac surgery. RESULTS: Data from the follow-up study suggest that urine production is more controlled for the proposed regimen. CONCLUSIONS: Both the modeling and simulation results and the follow-up study indicated that a bolus dose of 1 mg/kg followed 6 hours later with a 1- or 2-mg/kg loading dose and a 0.2-mg/kg x. h intravenous infusion provides a rational starting point for furosemide therapy after cardiac surgery in pediatric patients less than 1 year old. Adjustment of this regimen every 12 hours in steps of 0.1 mg/kg x h on the basis of clinical assessment should lead to adequate control over urinary output.

Drug Administration Schedule↗
PubMed1983

Phorbol ester inhibits furosemide-sensitive potassium transport in BALB/c 3T3 preadipose cells.

The tumor promoter phorbol 12-myristate 13-acetate (PMA) rapidly decreased the rate of 86Rb+ uptake into BALB/c 3T3 preadipose cells. The component of total 86Rb+ influx affected by PMA is insensitive to ouabain but sensitive to the diuretic furosemide. Experiments designed to investigate the characteristics of the K+ transport system sensitive to PMA revealed that: (i) 86Rb+ uptake is highly dependent on external Na+, (ii) 86Rb+ uptake is highly dependent on external Cl-, (iii) 22Na+ uptake is dependent on external K+, and (iv) a major component of 86Rb+ efflux that is sensitive to PMA and furosemide is not dependent on extracellular K+. These features strongly implicate a Na+K+/Cl- cotransport system as the target of PMA and furosemide in these experiments. PMA caused a net intracellular accumulation of K+ within 15 min in these cells, presumably via its inhibitory effect on furosemide-sensitive K+ transport. Within 30 min after PMA treatment, the mean cell volume was significantly reduced in treated compared to control cells, with a maximum decrease of 21% attained at 4 hr after PMA. The significance of these findings for biologic changes induced by PMA is discussed.

Adipose Tissue↗
PubMed1976

Furosemide inhibition of chloride transport in human red blood cells.

The chloride self-exchange flux across the human red cell membrane is rapidly and reversibly inhibited by 10(-4) M furosemide, a potent chloruretic agent. Furosemide reduces the chloride flux at all chloride concentrations and increases the cellular chloride concentration at which the flux is half-maximum. Kinetic analysis of the flux measurements made at several furosemide and chloride concentrations yields a pattern of mixed inhibition with a dissociation constant for the inhibitor-transport mechanism complex of 5 X 10(-5) M. From this pattern of inhibition and other observations, including that the percent inhibition is independent of pH (range 5.6-8.9), we conclude that the anionic form of furosemide interacts primarily with the chloride transport mechanism at a site separate from both the transport site and the halide-reactive modifier site.

Binding Sites↗
PubMed1980

Furosemide-induced thiamine deficiency.

Male Wistar rats were separated into 4 groups: group 1, thiamine sufficient diet (control); group 2, thiamine sufficient diet with intraperitoneal administration of furosemide (20 mg . kg-1 of body weight); group 3, thiamine deficient diet; group 4, thiamine deficient diet within tra-peritoneal administration of furosemide. After 4 weeks, the rats were killed and the thiamine levels and activity of transketolase were assayed. Thiamine concentration and transketolase activity were significantly decreased and thiamine pyrophosphate effect was significantly increased in the blood, and various tissues in group 2 and 4 compared with group 1 and 3, respectively. The intraperitoneal administration of various concentrations of furosemide (20 mg, 10 mg, and 2 mg . kg-1 of body weight) resulted in a significant increase in urinary thiamine excretion. Thus, it is assumed that long-term administration of furosemide could induce a thiamine deficiency.

Animals↗
PubMed2003

Up-regulation of organic anion transporter 1 protein is induced by chronic furosemide or hydrochlorothiazide infusion in rat kidney.

BACKGROUND: Thiazide and loop diuretics are secreted from the proximal tubule via the organic anion transport system to reach their principal sites of action. Recently, a multispecific organic anion transporter 1 (OAT1) was identified in rat kidney and was localized to the basolateral membrane of the S2 segment in the proximal tubule. We postulated that interactions between thiazide or loop diuretics and OAT1 may play a role in the adaptation to long-term diuretic use, and investigated whether OAT1 is regulated in vivo by chronic administration of diuretics at the protein level. METHODS: Semi-quantitative immunoblotting and immunohistochemistry were carried out in kidneys from male Sprague-Dawley rats using a polyclonal peptide-derived antibody to OAT1. Furosemide (12 mg/day/rat, n = 6), hydrochlorothiazide (3.75 mg/day/rat, n = 6) or vehicle (1.7% ethanolamine, n = 6) were infused subcutaneously for 7 days using osmotic minipumps. Experimental and vehicle-control rats were pair-fed, and two bottles of drinking water were provided, one containing tap water and the other containing a solution of 0.8% NaCl with 0.1% KCl. RESULTS: Overt diuretic responses were observed to both furosemide and hydrochlorothiazide infusions. There were no differences in body weight or creatinine clearance between the experimental and control rats. Although OAT1 protein abundance in cortical homogenates was increased by furosemide infusion (271 +/- 35 vs 100 +/- 15%, P < 0.05), Na-K-ATPase alpha1 subunit protein abundance was not affected (113 +/- 14 vs 100 +/- 8%, P = 0.42). Immunohistochemical localization in tissue sections confirmed a strong increase in OAT1 expression in the basolateral membrane of the S2 segment of proximal tubule. OAT1 protein abundance in cortical homogenates was also increased by hydrochlorothiazide infusion (181 +/- 25 vs 100 +/- 7%, P < 0.01), whereas Na-K-ATPase alpha1 subunit protein abundance was not affected (105 +/- 4 vs 100 +/- 4%, P = 0.34). CONCLUSION: Chronic furosemide or hydrochlorothiazide infusion caused increases in OAT1 protein abundance in rat kidney. These results suggest that OAT1 may be up-regulated in vivo by substrate stimulation at the protein level.

Animals↗
PubMed2006

Increased systolic blood pressure with rofecoxib in congenital furosemide-like salt loss.

BACKGROUND: To analyse whether congenital furosemide- or thiazide-like renal salt loss protects against the potential prohypertensive effects of two cyclooxygenase (COX) inhibitors: rofecoxib, a COX-2 selective inhibitor, and indomethacin, an unselective COX-inhibitor. METHODS: In a retrospective analysis, the effects of rofecoxib and indomethacin on blood pressure (bp: transformed into age-independent standard deviation scores (SDS) values), creatinine clearance (CRC), fractional excretion of sodium (FeNa), and renal excretion of systemic prostaglandins were studied in 28 patients with a genetically proven congenital hypokalaemic salt-losing tubulopathy (SLT) (11 female and 17 male, age: 2-25 years), 19 with a furosemide-like SLT, and nine with a thiazide-like SLT. RESULTS: In furosemide-like SLT patients, systolic SDS bp values were significantly higher with rofecoxib (1.03 +/- 0.16 SDS, n = 107) compared with indomethacin (0.56 +/- 0.09 SDS, n = 282; P = 0.007, 95% CI: 0.12-0.8). Without the drugs, systolic SDS bp values were elevated by 0.63 +/- 0.11 SDS, n = 164. Both drugs reduced renin and aldosterone-plasma levels to a similar extent. SDS values were significantly correlated with the excretion of the vasoconstrictor thromboxane (T x B2) (R2: 0.038, P = 0.021, n: 159), but not with CRC or FeNa. Blood pressure was not increased in thiazide-like SLT patients treated with rofecoxib. CONCLUSION: Congenital furosemide-like renal salt loss does not protect against the prohypertensive effects of rofecoxib. The positive correlation between bp SDS values with T x B2 but not with FeNa or CRC point towards an altered vascular homeostasis as one mechanism increasing blood pressure.

Adolescent↗
PubMed1996

Combination of high-dose furosemide and hydrochlorothiazide in the treatment of refractory congestive heart failure.

OBJECTIVE: We studied the synergism between high-dose furosemide and hydrochlorothiazide in patients with severe congestive heart failure and impaired renal function showing diuretic resistance to a daily dose of furosemide of at least 250 mg. DESIGN AND SETTING: An open study. A general hospital in The Netherlands. METHODS: In 20 patients with severe congestive heart failure (stage III-IV according to the New York Heart Association) with an oedematous mass of more than 5 kg and a proven diuretic resistance to high-dose furosemide, hydrochlorothiazide (25-100 mg daily) was added to the medication for 3-12 days, leaving the other medication unchanged. After correction of the hydration state, hydrochlorothiazide was withdrawn. Variables included body weight, serum electrolytes, renal function and natriuresis. RESULTS: Addition of hydrochlorothiazide resulted in a mean (+/-standard deviation) body weight reduction of 6.7 +/- 3.3 kg per patient. Mean daily urine volume increased from 1899 +/- 958 ml to 3065 +/- 925 ml (P < 0.001). Fractional sodium excretion increased significantly from 3.5 +/- 3.2% to 11.5 +/- 9.0% (P < 0.001). The most important side effect of this combination therapy appeared to be hypokalaemia. Mean endogenous creatinine clearance decreased (not significantly) from 32.7 +/- 22.5 ml. min-1.1.73 m-2 to 27.6 +/- 22.5 ml. min-1.1.73 m-2. CONCLUSIONS: Addition of hydrochlorothiazide to high-dose furosemide is a powerful diuretic tool, even in patients with a significantly reduced renal function. Because of its potentially dangerous side effects (hypokalaemia), it should be used in a carefully controlled setting.

Adult↗
PubMed1998

Brain damage due to episodic alcohol exposure in vivo and in vitro: furosemide neuroprotection implicates edema-based mechanism.

Adult rats intubated with a single dose of ethanol (alcohol; approximately 5 g/kg) for 5 to 10 successive days incur neurodegeneration in the entorhinal cortex, dentate gyrus, and olfactory bulbs accompanied by cerebrocortical edema and electrolyte (Na+, K+) accumulation. The brain damage is not lessened by cotreatment with the NMDA receptor antagonist MK-801; also, as reported elsewhere, MK-801 as well as non-NMDA receptor and Ca2+ channel antagonists are not neuroprotective in a similar, but more compressed, intoxication protocol. However, cotreatment with the electrolyte transport inhibitor/diuretic furosemide reduces alcohol-dependent cerebrocortical damage by 75-85% while preventing brain hydration and electrolyte elevations; olfactory bulb neurodegeneration is not attenuated. In parallel in vitro studies, rat organotypic entorhinal/hippocampal slice cultures exposed to alcohol (50-200 mM) 15 h/day for 6 days, mirroring episodic intoxication in vivo, demonstrate concentration-related release of the cytotoxic indicator, lactate dehydrogenase. Analogous to the in vivo findings, furosemide blocks this alcohol-induced in vitro cytotoxicity. Our results showing neuroprotection by furosemide indicate that brain edema and swelling are essential events in the brain damage induced by episodic alcohol exposure. Furosemide and related agents might be useful as neuroprotective agents in alcohol abuse. We suggest that the neurodegeneration is elicited in part by edema-dependent oxidative stress, but the regional selectivity of the damage may be best explained by physical (mechanical) compression of the limbic cortex against the adjacent tympanic bulla and subsequent neuronal cytoskeletal collapse. A scheme for these apparently nonexcitotoxic metabolic and mechanical pathways initiated by repeated alcohol exposure is proposed.

Alcoholic Intoxication↗
PubMed1990

Diminished response to furosemide in I-123 Hippuran renal studies of renovascular hypertension caused by unilateral renal artery stenosis.

Dynamic I-123 Hippuran renal studies to measure furosemide response (FR) were performed in three groups of patients: 1) 57 patients with renovascular hypertension due to a poststenotic, ischemic kidney; 2) 23 patients with essential hypertension; and 3) 50 nonhypertensive patients with healthy kidneys (control group). FR was observed as renal parenchymal tracer washout within 10 minutes after the injection of 40 mg of furosemide. The retention index (RI) took into consideration the renal parenchymal tracer content before and 10 minutes after furosemide injection. In the control group, the FR was greater than 50% and the RI was less than 20. Patients with essential hypertension revealed no differences in the amounts of FR and RI compared with the control group. In renovascular hypertension, the FR was diminished and the RI was raised significantly. The values of FR and RI showed a good correlation to the degree of the renal artery stenosis before and after percutaneous transluminal angioplasty. It is concluded that the stimulation of diuresis with furosemide and its quantification represent an important additional step in the evaluation of dynamic I-123 Hippuran studies to detect renal ischemia.

Furosemide↗
PubMed1981

The renal and hemodynamic effects of furosemide in acute myocardial infarction.

Renal and hemodynamic effects of furosemide were studied in 30 patients with acute myocardial infarction. When marked congestion of lungs was absent, the effects of furosemide were somewhat different from those of recent reports. The changes of pulmonary arterial pressure and wedge pressure were biphasic; there was first pressure rise in many occasions followed by reduced pressure; the latter is commonly believed to be the beneficial effect of furosemide. In these patients without marked congestion but in an acute state of myocardial infarction, within 5 min of furosemide administration, there was marked increase in urine volume, sodium and potassium excretion along with increases in creatinine clearance which is commonly found in the other conditions, but is in contrast to the recent reports on patients with acute myocardial complicated with pulmonary congestion.

Aged↗
PubMed1996

Acute hemodynamic and neurohoromonal effects of furosemide in critically ill pediatrics patients.

OBJECTIVES: To study the acute hemodynamic effects of furosemide in critically ill pediatrics patients, the temporal relationship between hemodynamic changes and changes in neuroendocrine axis, and the temporal relationship between hemodynamic changes and urine output. DESIGN: Prospective study. SETTING: Pediatric intensive care unit in a tertiary care university center. PATIENTS: Fourteen critically ill pediatric patients who clinically required diuretic therapy. INTERVENTIONS: Before and after furosemide administration, hemodynamic and neurohormonal measurements were taken. MEASUREMENTS AND MAIN RESULTS: Hemodynamic and neurohormonal responses to acute diuretic therapy were measured in 14 pediatric patients treated with furosemide (1 mg/kg/dose). Cardiac index deteriorated by 10 mins after drug administration (-9.4+/-3.9%, p<.05) and was associated with an increase in systemic vascular resistance (17.1+/-4.8%, p<.05). There was a subsequent increase in cardiac index (20+/-4.9%, p<.05) at 30 mins, with a decrease in systemic vascular resistance (-11.5+/-5.2%, p<.05). These hemodynamic changes were associated with marked increases in renin and norepinephrine concentrations and an increase in urinary prostaglandin release. The hemodynamic and neurohormonal effects had their onset before maximum diuresis. CONCLUSION: Intravenous furosemide administration in acutely ill pediatric patients results in an acute but transient deterioration in cardiac function that appears to parallel the neuroendocrine changes rather than the acute diuresis.

Adolescent↗
PubMedDate not supplied

Involvement of kallikrein in the antihypertensive response to furosemide in essential hypertension.

Twelve white men with essential hypertension were treated for 1 month in randomized order with either placebo or low-dose furosemide (40 mg/day) and compared to 22 race-, age-, and diet-matched normal controls. Furosemide therapy significantly reduced mean arterial pressure (108.6 +/- 2.4 vs. 101.0 +/- 2.7 mm Hg, p < 0.02) in association with a significant increase in 24 hr urinary kallikrein activity (7.9 +/- 1.8 vs. 13.4 +/- 2.8 esterase units/24 hr, p < 0.02). Normal controls on no therapy excreted 19.4 +/- 2.6 esterase units/24 hr of urinary kallikrein activity, significantly greater than hypertensives on placebo (p < 0.01) but not hypertensives on furosemide (p > 0.1). A significant (p < 0.05) inverse correlation between mean arterial pressure and urinary kallikrein activity suggests a possible role for the kallikrein-kinin system in the antihypertensive mechanism of furosemide.

Aldosterone↗
PubMedDate not supplied

Time course of blood pressure changes after intravenous administration of propranolol or furosemide in hypertensive patients.

The time course of changes in supine and standing blood pressures, heart rate, plasma renin activity, and plasma noradrenaline concentration after intravenous administration of propranolol (0.20 mg . kg-1, with a maximum of 15 mg) or furosemide (40 mg) was studied for a period of 8 h in hypertensive patients. Twenty minutes after intravenous injection of propranolol or furosemide, supine blood pressure was unchanged. Thereafter, blood pressure started to decrease gradually. Maximum reduction was obtained after 4-5 h. Twenty minutes after administration of propranolol, heart rate and plasma renin activity were reduced, and remained so during the following 8 h. Supine plasma noradrenaline concentration did not change significantly after propranolol, but standing levels, showed a tendency to increase as blood pressure fell. Twenty minutes after administration of furosemide, plasma renin activity was increased and remained elevated during the following 8 h. Heart rate and plasma noradrenaline concentration were unchanged after 20 min, but both increased gradually as blood pressure started to fall. The results show that intravenous administration of both propranolol and furosemide leads to a delayed reduction of blood pressure. The increase in total peripheral resistance, which prevents blood pressure from falling acutely after intravenous injection of propranolol, is not reflected in an acute rise in plasma noradrenaline. The delayed hypotensive response does not seem to be due to a return of sympathetic activity to pretreatment levels, since plasma noradrenaline concentration shows a tendency to rise as blood pressure falls.

Adult↗
PubMed1987

Probenecid interferes with the natriuretic action of furosemide.

The interaction between probenecid and furosemide was studied in eight hospital patients (ages 20-65 years) who had been treated with oral furosemide, 40 mg daily, and moderate salt restriction for 10 days or longer. After stabilization of drug therapy and diet for at least 3 days, probenecid, 0.5 g twice a day, was given for 3 days and then discontinued. The 24-h urinary sodium excretion (UNaV) significantly decreased from 56.3 +/- 7.2 to 35.9 +/- 7.1 mmol/day when probenecid was added to the treatment regimen (p less than 0.01), and then significantly increased to 61.7 +/- 10.3 mmol/day after probenecid was discontinued (p less than 0.01). Parallel with the changes in UNaV, there were also significant corresponding changes (p less than 0.01) in urinary excretion of uric acid (392.4 +/- 46.5, 600.9 +/- 102.1, and 345.0 +/- 33.2 mg/day, respectively), renal clearance of uric acid (3.7 +/- 0.3, 14.3 +/- 2.4, and 4.1 +/- 0.3 ml/h/kg, respectively), and serum uric acid concentration (7.7 +/- 0.5, 3.3 +/- 0.2, and 6.3 +/- 0.3 mg/dl, respectively). Before and after discontinuing probenecid therapy, there were no significant differences in these parameters (p greater than 0.05). In conclusion, the natriuretic action of furosemide was attenuated by concurrent probenecid therapy, probably owing to a reduction of furosemide delivery to the luminal side of renal tubules.

Adult↗
PubMed1996

Comparison of chronic neutral endopeptidase inhibition and furosemide in an ovine model of heart failure.

The hemodynamic, hormonal, and metabolic effects of chronic neutral endopeptidase (NEP) 24.11 inhibition and furosemide were compared in the pacing model of ovine heart failure (HF). Intravenous SCH 39370 induced a dose-related inhibition of NEP activity during 4-days treatment, in association with a transient increase in plasma atrial natriuretic peptide (ANP) and, at the higher dose, an increased mean level of plasma cyclic guanosine monophosphate. There was a significant and persistent decrease in left atrial pressure, a brief increase in cardiac output (CO), and a tendency for arterial pressure to be reduced. Significant dose-related diuresis and natriuresis were also observed. Furosemide induced a similar hemodynamic response, associated with greater diuresis and natriuresis. Both agents significantly reduced plasma aldosterone levels. Coinfusion of captopril on day 4 of treatment resulted in similar responses in both the SCH 39370- and furosemide pretreated groups. Chronic NEP inhibition significantly alters circulatory and renal function and appears to be as effective as furosemide in reducing cardiac preload in this model of congestive HF.

Animals↗
PubMed1978

Deafness associated with oral furosemide.

A patient with Hodgkin's disease and renal insufficiency became deaf while being treated with high dose oral furosemide. Cessation of furosemide was associated with improvement in his hearing. However, at the time of his death, 11 days after stopping the furosemide, significant hearing impairment was still present. It is suggested that oral furosemide be considered potentially ototoxic, particularly in patients with compromised renal function.

Aged↗
PubMed1982

A sensitive assay method of furosemide in plasma and urine by high-performance liquid chromotography.

A sensitive assay method of furosemide in plasma and urine by high-performance liquid chromatography (HPLC) is described. The minimum measurable concentrations of furosemide in plasma and urine were 0.2 and 5.0 microgram/ml, respectively; whereas the coefficients of variation of furosemide levels were found to be 7.8% for plasma and 2.0% for urine. These are within the acceptably low limits. Hence, the present method of furosemide is sensitive, reproducible, and accurate for therapeutic drug monitoring. The significance of this HPLC assay method is discussed.

Chromatography, High Pressure Liquid↗