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PubMed1994

Mechanisms of renal vasoconstriction following furosemide in conscious rats.

Regional hemodynamics following intravenous injection of furosemide were studied in conscious rats instrumented with Doppler flowprobes. Furosemide caused a dose-dependent acute (within 3 min) transient increase in renal resistance (RR) followed by a later generalized vasoconstriction in the renal, mesenteric and hindquarter (HQR) vascular bed. With in vitro experiments a possible direct effect of furosemide on renal artery segments was excluded. The acute rise in RR was partly (approximately 40%) attenuated by pretreatment with phentolamine or prazosin, but not prevented by renal denervation, volume repletion or pretreatment with captopril, losartan, indomethacin, aminophylline, nifedipine, or a vasopressin V1A-receptor-antagonist. However, the acute renal vasoconstriction was absent in water diuretic rats. The later vasoconstriction was blunted by captopril (RR+HQR), losartan (RR) and phentolamine (HQR) pretreatment. We conclude that the later generalized vasoconstriction following furosemide involves regional specific stimulation of angiotensin II and alpha-adrenoceptors. The mechanism of the acute renal vasoconstriction could not be fully determined. Because of its absence in water diuretic rats, its rapid onset, transient nature and relative insensitivity for pharmacological tools in euvolemic rats, the acute increase in RR following furosemide may be caused by cell swelling as a result from dissipation of the renal medullary gradient.

Animals↗
PubMed1980

Effect of furosemide on insulin and glucagon responses to arginine in normal subjects.

This study aimed at evaluating the influence of furosemide upon insulin and glucagon responses to arginine in healthy subjects. For this purpose, six normal subjects received two consecutive arginine pulses (3 g), 60 min apart, before and after the administration of furosemide (40 mg, IV). The acute insulin response (mean change from 3-10 min) to the second arginine pulse was significantly inhibited by furosemide (mean increase: 14.8 +/- 3.0 microU/ml versus 11.7 +/- 2.5 microU/ml, p < 0.01). By contrast, the acute glucagon response was significantly increased (mean increase: 77 +/- 18 pg/ml versus 105 +/- 21 pg/ml, p < 0.01). No significant changes in plasma glucose levels occurred. In control experiments, in which saline rather than furosemide was administered, the acute insulin and glucagon response to the first arginine pulse did not differ from that observed with the second pulse. The effect of furosemide on insulin and glucagon secretion might be mediated through enhanced release of endogenous prostaglandin E.

Adult↗
PubMed1990

Effect of chronic oral furosemide administration on the 24-hour cycle of lithium clearance and electrolyte excretion in humans.

The effect of chronic furosemide treatment on the circadian cycle of lithium clearance (CLLi) and electrolyte excretion has been examined in 8 young, male volunteers, by performing two 24 h clearance experiments, before and after one week of treatment with furosemide 80 mg once daily. After 8 days on furosemide there was a significant decrease in creatinine clearance (-21%), plasma Na (-8.4 mM) and plasma K (-0.58 mM). At that time, however, there were no changes in 24 h-values of CLLi or Na excretion, although the magnitude of the circadian variation in CLLi and other renal parameters was increased. Both CLLi and CLNa were increased in the first 3 h following furosemide administration and thereafter they fell below the control level in the remaining hours of the experiment. From the absolute and fractional changes in CLLi it is suggested that compensatory Na conservation in response to chronic furosemide treatment occurs between doses, and that it involves decreased output from the proximal tubules combined with increased fractional Na reabsorption in the distal nephron.

Adult↗
PubMed1986

The influence of furosemide on heart rate and oxygen uptake in exercising man.

We recently observed that heart rate (HR) related methods for assessing physical fitness lead to an overestimation of endurance capacity in subjects treated with furosemide. To gain a more detailed description of this effect, the relationships between work load (WL), oxygen uptake (VO2), and HR were determined in the present study. To this end, nine healthy male subjects performed two incremental exercise tests (10 W increase per 30 s) on a bicycle ergometer. In one test 40 mg furosemide (Lasix) was applied orally 90 min before exercise started. Compared with control conditions, furosemide led to a change in mean blood volume of -4.5% (range: +7.8% to -11.5%). Neither the maximal VO2 (VO2max) nor the maximal work load (WLmax) were significantly altered after furosemide application. Though the WL-VO2 relationship was not significantly affected, the HR-VO2 relationship showed significant alterations which depended on both the loss of blood volume (BV) and work intensity: When the reduction in BV was less than approximately 5%, HR was found to be lowered at all workloads. When the BV reduction was greater than about 5% HR was significantly reduced only in the lower ranges of work load but significantly increased at the higher work intensities. Since BV reductions are known to increase HR during exercise, our findings suggest that, in addition to the blood volume induced changes in HR, furosemide exerts further direct or indirect effects on heart rate adjustment.

Adult↗
PubMed1984

The effect of furosemide on sodium and potassium concentrations in guinea-pig perilymph.

To observe the effects of furosemide on electrolyte concentrations in inner-ear fluids, experiments were performed on 286 normal guinea-pigs. Intravenous injection of furosemide (15 mg/kg) induced increases of Na concentration in scala tympani perilymph, scala vestibuli perilymph, and cerebrospinal fluid (CSF). K concentrations in both perilymphs and CSF were also increased by furosemide. The increased Na concentrations are thought to be due to the dehydration of body fluids induced by the diuretic action of furosemide. The increase of K concentrations in perilymphs could be attributable to either a characteristic action of furosemide on the electrolyte transport in the inner ear or a secondary change caused by a rise of K concentration in the endolymph.

Animals↗
PubMed1975

Treatment of benign essential hypertension: comparison of furosemide and hydrochlorothiazide.

Furosemide (Impugan) 12.5, 25 or 40 mg twice daily, has been compared as an antihypertensive with hydrochlorothiazide 12.5 mg twice daily and a placebo. A double blind, cross-over design was used with a run-in period of 4 weeks, preceding five 4-week periods of treatment with these compounds alone. There were 34 patients in the trial, 17 men and 17 women. Paired comparison showed that furosemide 25 or 40 mg twice daily and hydrochlorothiazide 12.5 mg twice daily had a similar hypotensive effect, irrespective of the initial blood pressure. Furosemide 40 mg twice daily and hydrochlorothiazide 12.5 mg twice daily caused a slight fall of blood pressure as compared with placebo (0.10 greater than p greater than 0.05, p less than 0.05). There was a distinct correlation between blood pressure and age. Serum K+ fell significantly during treatment, particularly with hydrochlorothiazide 12.5 mg twice daily, as well as with furosemide 25 or 40 mg twice daily. As compared with placebo, urinary output increased significantly after furosemide 12.5, 25 or 40 mg twice daily, but it rose only to a non-significant extent after hydrochlorothiazide. The fall of blood pressure and decrease in serum K+ were linearly related. There were only a few, mild side effects which did not necessitate discontinuation of the trial.

Adult↗
PubMed1976

Interactions between furosemide and vasopressin on hemodynamics and on water excretion by the isolated dog kidney.

The effects of furosemide were studied on isolated dog kidneys in the absence and in the presence of vasopressin. In the latter condition, furosemide did not modify renal blood flow and glomerular filtration rate while both parameters were decreased by the drug in the absence of vasopressin, as they were also reduced by vasopressin alone. This would indicate direct vasoactive effects of furosemide, depending on the previous tone of the vasculature. In the absence of vasopressin, furosemide decreased free water clearance through inhibition of sodium reabsorption in the ascending limb of Henle's loop. On the other hand, in the presence of vasopressin, furosemide increased free water clearance, presumably through reduction of water reabsorption in the collecting duct by enhanced distal tubular flux.

Animals↗
PubMed1981

The early phase of experimental acute renal failure. VI. The influence of furosemide.

Experiments were performed to determine whether furosemide, given in doses high enough to induce a strong diuresis and to inhibit the mechanism of tubuloglomerular feedback, offers any protection from acute renal failure induced by a nephrotoxin or ischaemia. Microperfusion of the loop of Henle revealed that a tubular furosemide concentration of 5 x 10(-5) mol x 1(-1) was necessary to fully inhibit the tubuloglomerular feedback response to a raised sodium chloride concentration at the macula densa. The infusion of furosemide systemically to achieve such concentrations in the tubule resulted in an improvement in renal function when given before or after the nephrotoxin but was without effect when given before or after ischaemia. Measurements of furosemide concentrations in the urine, however, confirmed that sufficient amounts were applied to inhibit the feedback mechanism. It is concluded from this and similar studies that furosemide is only beneficial in models of acute renal failure with an obstructive or nephrotoxic pathogenesis, in which it acts by flushing out the noxious material and not by inhibiting the mechanism of tubuloglomerular feedback.

Acute Kidney Injury↗
PubMed1981

Lack of adrenergic influence on renin release after furosemide in normal man.

The role of the sympathetic nervous system in furosemide-induced renin release was investigated in six normal subjects. After intravenous administration of furosemide, plasma renin concentrations increased more than two-fold within 15 min. Neither replacement of urinary fluid loss by intravenous infusion of saline nor pharmacological beta-blockade with d,1-propranolol changed the renin response to furosemide. The activity of the sympathetic nervous system, as estimated by measurement of plasma catecholamine concentrations, remained at the reference level after furosemide. It is concluded that the sympathetic nervous system is not involved in renin release after intravenous administration of furosemide.

Adult↗
PubMed1995

Mineral excretion following furosemide compared with bumetanide therapy in premature infants.

Mineral excretion following single doses of furosemide were compared with bumetanide in a random cross-over trial in 17 premature infants. The mean birthweight and gestational age were 889 +/- 85 g and 27 +/- 2 weeks. Following furosemide therapy, significantly higher chloride losses and urine volumes were noted in the first 8-h period compared with the second or third 8-h periods. Following bumetanide therapy, sodium, calcium, and chloride losses and urine volumes were significantly higher in the first 8 h compared with the second or third 8-h periods. Hourly sodium and chloride losses were significantly lower following bumetanide than furosemide during the first two 8-h periods. During the final 8-h period sodium, potassium, chloride, and calcium losses were significantly lower following bumetanide than following furosemide. Sodium loss per urine volume was lower with bumetanide than furosemide but calcium loss tended to be higher. Hence, bumetanide does not appear to be a calcium-sparing diuretic following single-dose therapy.

Bronchopulmonary Dysplasia↗
PubMed1983

Sequential changes in plasma renin activity and plasma catecholamines in mildly hypertensive patients during acute, furosemide-induced body-fluid loss.

To evaluate the role of adrenergic mechanisms in the acute response of renin to furosemide, plasma renin activity (PRA) and plasma catecholamine concentrations were measured for 3 h after i.v. administration of furosemide 1 mg/kg to 8 patients with mild essential hypertension. Furosemide induced a prompt and long-lasting increase in renin, with PRA more than doubled at all times. The increase in PRA within the first 30 min paralleled the peak increases in urinary water and sodium flow rates, and significant decreases in plasma volume and central venous pressure. There was no change in plasma catecholamine concentrations. Plasma noradrenaline was increased significantly at 60 min and adrenaline at 90 min, once furosemide had induced a marked loss of body-fluid and approximately 65% decrease in central venous pressure. Both catecholamines remained elevated until the end of the study, whereas urinary water and sodium flow rates had returned to their pre-treatment values by 150 min. Mean blood pressure was essentially unchanged throughout the study, whereas heart rate increased significantly after 90 min. The findings suggest that in mildly hypertensive patients adrenergic mechanisms are not involved in the initial renin response to furosemide, but they come into play later, probably as a result of reflex sympathetic activation triggered by marked volume depletion.

Adult↗
PubMed1978

[Interference of the tissue concentration of antibiotics with a salidiuretic. Behaviour of cephradine and cephalothin in brain tissue after additional administration of furosemide (author's transl)].

Serum and brain tissue concentrations were determined after i.v. administration of 4 g cephradine to 11 patients of whom 6 were additionally receiving 40 mg furosemide t.i.d. peroral. Five further patients were given 4 g cephalothin i.v. All patients were undergoing a brain operation at the time of antibiotic administration. Between 60 and 100 min after dosage, cephradine decreased in the serum from 104.9 mcg/ml to 56.7 mcg/ml and in the brain tissue from 13.02 mcg/g to 8.37 mcg/g in the mean. Cephradine concentrations in serum were higher and in brain tissue lower when furosemide was given as well. These differences are statistically significant (p less than 0.01). Serum concentrations of cephalothin over the same period and in the absence of furosemide were very low with 32.2 mcg/ml at 60 to 70 min, and extremely low in the brain tissue (0.55 mcg/g in the mean) so that a trial with furosemide was not performed. Neither antibiotic was detectable in the cerebrospinal fluid. The differences in serum and brain tissue concentrations of cephradine in the presence and absence of furosemide demonstrate that special care must be taken when administering more than one drug.

Brain Chemistry↗
PubMed1989

Isolation and reconstitution of furosemide-binding proteins from Ehrlich ascites tumor cells.

Furosemide-binding proteins were isolated from cholate-solubilized membranes of Ehrlich ascites tumor cells by affinity chromatography, using furosemide as ligand. Solubilized proteins retarded by the affinity material were eluted by furosemide. In reducing and denaturing gels, the major proteins eluted by furosemide were 100 and 45 kDa. In nonreducing, non-denaturing gels, homodimers of both polypeptides were found, whereas no oligomeric proteins containing both polypeptides were seen. It is concluded that the furosemide gel binds two distinct dimeric proteins. The isolated proteins were reconstituted into phospholipid vesicles and the K+ transport activity of these vesicles was assayed by measurement of 86Rb+ uptake against a large opposing K+ gradient. The reconstituted system was found to contain a K+ transporting protein, which is sensitive to Ba2+ like the K+ channel previously demonstrated to be activated in intact cells after cell swelling.

Animals↗
PubMed1988

Interaction of furosemide with lipid membranes.

The interaction of furosemide with different phospholipids was investigated. Its influence on the lipid structure was inferred from its effect on the phase transition properties of lipids and on the conductance of planar bilayer membranes. The thermotropic properties of dipalmitoyl phosphatidylcholine, phosphatidylethanolamine (natural), dipalmitoyl phosphatidylethanolamine, brain sphingomyelin, brain cerebrosides and phosphatidylserine in the presence and absence of furosemide were investigated by differential scanning calorimetry. The modifying effect of furosemide seems to be strongest on phosphatidylethanolamine (natural) and sphingomyelin bilayers. The propensity of furosemide to decrease the electrical resistance of planar lipid membranes was also studied and it is shown that the drug facilitates the transport of ions. Partition coefficients of furosemide between lipid bilayers and water were measured.

Cerebrosides↗
PubMed1988

Penetration of furosemide into phospholipid monolayers.

Furosemide is a surface-active anion and it tends to displace lipid monolayers from the surface at positive polarizations lowering their potential stability range. The efficiency of the penetration and the displacement increases with decreasing surface pressure of the monolayer. Lower capacitance at a wider potential range corresponds to higher surface pressure. Monolayers with higher capacitances are indeed more readily penetrated and displaced as demonstrated by further increase in their capacitance and increase in their proton conductance. Furosemide raises the capacitance of the monolayer in the stable region due to intercalation between the head groups thus reducing the thickness of the hydrocarbon layer. In pure PC monolayer about 10% increase in capacitance is observed in the presence of 6 X 10(-4)M furosemide. The effect of furosemide becomes more pronounced with increasing sphingomyelin content in the mixed monolayers. The monolayer of PE is more condensed and its capacitance is lower (approximately 1.45 microF/cm2) and is stable in a wider potential range than that of PC. It is less affected by furosemide and concentrations higher than 10(-3) M are required to narrow the stability range and to increase the capacitance.

Furosemide↗
PubMed1991

Furosemide-related renal calcifications in the premature infant. A longitudinal ultrasonographic study.

Low birthweight infants treated with chronic furosemide therapy are at risk for the development of intrarenal calcifications. A prospective longitudinal renal ultrasound investigation was conducted to study the correlation of diuretic therapy, clinical course and ultrasonographic findings. Of 117 premature infants studied ultrasonographically upon discharge from the hospital, 20 had intrarenal calcifications. Eight patients at age 16.3 +/- 2.6 months had sonographic resolution of renal calcifications, 6.6 +/- 1.1 months after furosemide therapy had been discontinued. Of the 12 patients with persistent calcifications, 4 died from severe pulmonary disease and autopsy in 3 of them confirmed the ultrasonographic diagnosis. All 12 children but 2 continued to receive furosemide for their chronic lung disease demonstrating significant association between chronic use of loop diuretics and persistence fo the renal calcifications (p less than 0.001). Two patients required nephrolithotomy and 4 suffered from recurrent urinary tract infections. In 4 patients, 5 kidneys were of small size and in 2 bilateral collecting system dilation was noted. We conclude that discontinuation of furosemide therapy is associated with resolution of the renal calcifications. On the other hand, continued treatment with furosemide is associated with high renal morbidity which indicates ongoing clinical and ultrasonographic follow-up.

Child, Preschool↗
PubMed1977

Acute intravenous administration of potassium chloride to furosemide pretreated dogs.

Twelve male mongrel dogs were used for this study; six were untreated (control) and six were given intravenous furosemide (1 mg/kg) daily for seven consecutive days before each study. Each animal received intravenous KCl 0.8, 1.6 or 3.2 mMol/kg/hr for one hour, but only one dose for each study and at least seven days were allowed between studies. The animals were given thiopentone for tracheal intubation and mechanically ventilated, maintaining a PaCO2 of 4.0 to 4.5 kPa (30-35 torr) and anaesthetized with nitrous oxide-oxygen and halothane. Daily administration of furosemide reduced serum potassium from 4.48 to 4.09 mMol/1 with no significant change in serum sodium. A greater number of furosemide-pretreated animals (6 vs 3) developed cardiac dysrhythmias during non-lethal intravenous KCl at 0.8, 1.6 mMol/kg/hr. The furosemide-pretreated group tended to succumb at a lower serum potassium concentration (12.2 vs 13.8 mMol/I, P less than 0.05) and developed earlier onset (44 vs 54 min, P less than 0.05) of cardiac standstill or ventricular fibrillation following intravenous KCl at 3.2 mMol/kg/hr. Cardiac output, heart rate and mean arterial pressure were significantly elevated during serum concentrations of 6.9-9.1 mMol/1, while no statistically significant changes were observed for stroke volume and peripheral resistance. There were no significant differences of urinary potassium excretion between the untreated and treated groups when like doses of KCl were infused. These data suggest that acute infusion of KCl in furosemide-pretreated dogs may not be an effective means of treating hypokalaemia and could be hazardous.

Animals↗
PubMed2000

Furosemide stimulates K transport in HCD57 erythroid cells.

We examined the influence of serum and furosemide on K movement and cell volume in HCD57 cells, a murine erythroleukemia cell line, which require erythropoietin (EPO) for survival. We found that maintenance of cell volume depends on the concentration of serum in the culture medium. In isotonic medium containing 20% serum, HCD57 cells maintain their steady-state volume. In contrast, the cells shrink progressively as medium serum content is reduced. In serum-free medium, raising external K to 75 mm prevents cell shrinkage and a further increase in K to 145 mm results in swelling, revealing a role for K permeability in the regulation of cell volume. Of particular interest has been a serendipitous finding with furosemide. Below an external K concentration of 2.1 +/- 0.3 mm in medium containing 2% serum, furosemide inhibits K uptake, probably stemming from its well known inhibitory action on KCl cotransport. However, above that K concentration, furosemide stimulates K uptake in a dose-dependent manner. Moreover, furosemide potentiates cell shrinkage induced by serum withdrawal. These findings suggest that the transport machinery mediating cellular shrinkage, once primed by serum depletion, becomes receptive to a second stimulus.

Animals↗