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PubMed1990

Furosemide blocks basolateral membrane Cl- permeability in gallbladder epithelium.

In Necturus gallbladders bathed in a NaCl Ringer solution buffered with 10 mM HCO3(-)-1% CO2, furosemide (added to the serosal solution) caused a concentration-dependent hyperpolarization of both cell membranes that was slow and reversible. At 10(-3) M furosemide, the basolateral membrane voltage (Vcs) increased significantly from -71 +/- 3 to -85 +/- 3 mV, the depolarization of Vcs elicited by a 10-fold rise in serosal [K+] increased from 34 +/- 4 to 50 +/- 1 mV, the depolarization elicited by lowering serosal [Cl-] from 98 to 8.1 mM was reduced from 15 +/- 1 to 1 +/- 1 mV, and the depolarization in response to lowering serosal [HCO3-] from 10 to 1 mM was reduced from 13 +/- 1 to 5 +/- 0.4 mV. Furosemide could in principle decrease the basolateral membrane Cl- conductance (Gcl), increase the basolateral membrane K+ conductance, or have a combined effect. To distinguish among these possibilities, we estimated the resistance of the basolateral membrane (Rb) by means of two-point intraepithelial cable analysis experiments. Furosemide increased Rb by 22%, which indicates that furosemide reduces basolateral membrane Gcl. The effect cannot be attributed to inhibition of apical membrane anion exchange by serosal addition of furosemide, because base secretion from cells to lumen is unchanged. We conclude that furosemide blocks reversibly basolateral membrane electrodiffusive Cl- permeability. A concomitant stimulation of basolateral membrane electrodiffusive K+ permeability is also possible.

Animals↗

PubMed1995

Effects of renal denervation on cardiovascular response to furosemide in conscious lambs.

The cardiovascular response to furosemide in the newborn and the role of renal sympathetic nerves in influencing this response have not been investigated. We hypothesized that in conscious lambs, furosemide would decrease blood pressure, the response being accentuated in the absence of renal sympathetic nerves. Pulsatile pressures and heart rates were measured before and after furosemide (2 mg/kg) administration to chronically instrumented lambs with either bilateral renal denervation (denervated, n = 8) or renal nerves intact (intact, n = 6). In intact lambs, mean arterial pressure remained constant after furosemide; in denervated lambs there was an increase in arterial pressure 20 min after furosemide (P < 0.001), and control levels were reached by 100 min. Basal heart rate was higher in denervated than in intact lambs (P = 0.009). In both groups of lambs, heart rate increased 40 min after furosemide and remained elevated. These data provide new information that, in conscious newborn animals, renal sympathetic nerves influence the blood pressure response to furosemide, as well as basal control of heart rate.

Animals↗

PubMed1997

Furosemide-induced airway relaxation in guinea pigs: relation to Na-K-2Cl cotransporter function.

This study tested the hypothesis that airway relaxation to furosemide is mediated via the Na-K-2Cl cotransporter. If this mechanism exists in airway smooth muscle like in vascular smooth muscle, changes in airway relaxation should be associated with changes in Na-K-2Cl cotransporter function, and both should be substrate dependent. Tracheal rings from newborn guinea pigs were bathed in standard (STD) or varying low Cl- concentration ([Cl-]) N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES). Isometric relaxation to 300 microM furosemide or 10(-8) to 10(-5) M salbutamol was measured. Airway segments were incubated with rubidium-86 (86Rb) in STD or varying low [Cl-] HEPES, with and without 300 microM furosemide or 25 microM salbutamol. Furosemide was unable to reduce 86Rb uptake at 10 mM [Cl-], although relaxation was still observed in 10 mM [Cl-]. Salbutamol did not affect 86Rb uptake. This study demonstrated that there is a furosemide-sensitive Na-K-2Cl cotransporter in newborn guinea pig trachea. However, the effect of furosemide on cotransporter function did not always directly correspond to differences in relaxation, suggesting that the Na-K-2Cl cotransporter may play a major, but not exclusive, role in furosemide-induced airway relaxation.

Animals↗

PubMed1999

Roles of aldosterone and angiotensin in maturation of sodium appetite in furosemide-treated rats.

When rats are treated with furosemide, there is a rapid natriuresis. However, increased sodium appetite does not occur until some time later. One hypothesis to explain this delay is that increased circulating levels of the hormones of sodium depletion prime or sensitize the brain circuits involved in sodium appetite, perhaps by induction of target gene(s). In the present study, we describe the time course of the temporal maturation of sodium appetite after furosemide treatment and the associated changes in plasma levels of ANG II and aldosterone and in plasma volume. Sodium appetite is modest 3 h after furosemide treatment, is increased after 12 h, and is still larger after 24 h. This pattern is evident with repeated testing. Plasma levels of aldosterone and plasma renin activity are substantially increased 3 h after furosemide treatment, and so the NaCl appetite cannot result simply from progressively increasing levels of these hormones. Furthermore, activation of the subfornical organ and the ventral lamina terminalis, assessed with c-Fos immunocytochemistry, did not differ across these three times. Metyrapone, an inhibitor of adrenal steroid synthesis, was used to examine sodium appetite in the absence of elevations in aldosterone after furosemide treatment. Although metyrapone effectively blocked the increase in aldosterone, it was without effect on the appetite 3 or 24 h after furosemide treatment. Furthermore, elevations of plasma aldosterone by the use of minipumps for several days before furosemide treatment did not prime or potentiate but instead tended to inhibit the induced sodium appetite, despite achieving levels of aldosterone and plasma renin activity typically associated with a robust sodium appetite. Infusions of DOCA gave a similar result. Lastly, minipump infusions of ANG II also did not potentiate sodium appetite. Thus neither addition nor subtraction of these hormones alone influenced sodium appetite under these conditions.

Aldosterone↗

PubMed1980

Effect of furosemide on thoracic duct lymph flow in the dog.

Furosemide 20 mg/kg was given intravenously to 12 anesthetized dogs with clamped renal pedicles. Thoracic duct lymph flow (TDLF) increased promptly by 38% (P less than 0.05), an increment that lasted 80 min. Because in 6 of 12 dogs there was a transient increase in splanchnic blood flow, in separate groups splanchnic blood flow was either markedly constricted or markedly increased by intravenous isoproterenol. Thoracic duct lymph flow increased by 95 and 90%, respectively, following furosemid despite no further change in splanchnic blood flow. Furosemide had no effect on blood pressure, lymph protein, or plasma sodium. In four chronic caval dogs, TDLF was increased by 400%, yet furosemide produced a further increment in lymph flow of 30% (P less than 0.05). Infusion of a 25% albumin solution to contract the interstitial fluid did not abolish the furosemide effect, but a 10% mannitol solution did. Furosemide increased TDLF even after the infusion of papaverine reduced blood pressure to 60 mmHg. We conclude that furosemide increases TDLF by acting directly on splanchnic capillaries to allow increased filtration of fluid in the absence of increased splanchnic blood flow or capillary hydrostatic pressure.

Abdomen↗

PubMed1983

Furosemide action on collecting ducts: effect of prostaglandin synthesis inhibition.

The effect of furosemide on inner medullary collecting duct chloride reabsorption has not been determined, and the blunting of furosemide action by drugs that inhibit prostaglandin synthesis, while known to occur, has not been examined in detail. The effect of indomethacin and meclofenamate on furosemide diuresis was studied in the rat using clearance and collecting duct microcatheterization methods. Furosemide-treated control animals showed complete inhibition of chloride, sodium, and water reabsorption in the inner medullary collecting duct. Rats given indomethacin or meclofenamate before and during furosemide administration showed marked reduction of the chloriuresis, natriuresis, and diuresis. Reduced delivery of sodium and chloride to the beginning of the inner medullary collecting duct, associated with a decrease in glomerular filtration rate and increased reabsorption in more proximal nephron segments, was largely responsible for the reduced natriuresis and chloriuresis during inhibition of prostaglandin synthesis. In addition, indomethacin increased collecting duct NaCl reabsorption toward normal, but meclofenamate showed no such effect. The results indicate that furosemide inhibits medullary collecting duct reabsorption of chloride, sodium, and water in the rat. The blunting of diuretic action seen with inhibition of prostaglandin synthesis is largely, although not entirely, due to effects of indomethacin and meclofenamate on furosemide action at nephron sites proximal to the collecting duct.

Animals↗

PubMed1991

Thirst and salt appetite in horses treated with furosemide.

When a preliminary experiment in sodium-replete ponies revealed an increase, but not a significant increase, in salt consumption after furosemide treatment, the experiment was repeated using sodium-deficient horses in which aldosterone levels might be expected to be elevated to test the hypothesis that a background of aldosterone is necessary for salt appetite. Ten Standardbred mares were injected intravenously with furosemide or an equivalent volume of 0.9% sodium chloride as a control to test the effect of furosemide on their salt appetite and blood constituents. Sodium intake and sodium loss in urine, as well as water intake and urine output, were measured and compared to determine accuracy of compensation for natriuresis and diuresis. Plasma protein and packed cell volume showed significant increases in response to furosemide treatment (F = 29.31, P less than 0.001 and F = 11.20, P less than 0.001, respectively). There were no significant changes in plasma sodium concentration or osmolality in response to the treatment (P greater than 0.05). The furosemide-treated horses consumed 126 +/- 14.8 g salt, significantly more than when they were given the control injection (94.5 +/- 9.8 g; t = 2.22, P = 0.05). In response to furosemide, horses lost 962 +/- 79.7 and consumed 2,170 +/- 5 meq sodium; however, compared with control, they lost 955 meq more sodium and ingested only 570 meq more sodium, so they were undercompensating for natriuresis. The furosemide-treated horses drank 9.6 +/- 0.8 kg of water, significantly more than when they received the control injection (6.4 +/- 0.8 kg; t = 6.9, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1999

Effect of furosemide on pulmonary blood flow distribution in resting and exercising horses.

We determined the spatial distribution of pulmonary blood flow (PBF) with 15-micron fluorescent-labeled microspheres during rest and exercise in five Thoroughbred horses before and 4 h after furosemide administration (0.5 mg/kg iv). The primary finding of this study was that PBF redistribution occurred from rest to exercise, both with and without furosemide. However, there was less blood flow to the dorsal portion of the lung during exercise postfurosemide compared with prefurosemide. Furosemide did alter the resting perfusion distribution by increasing the flow to the ventral regions of the lung; however, that increase in flow was abated with exercise. Other findings included 1) unchanged gas exchange and cardiac output during rest and exercise after vs. before furosemide, 2) a decrease in pulmonary arterial pressure after furosemide, 3) an increase in the slope of the relationship of PBF vs. vertical height up the lung during exercise, both with and without furosemide, and 4) a decrease in blood flow to the dorsal region of the lung at rest after furosemide. Pulmonary perfusion variability within the lung may be a function of the anatomy of the pulmonary vessels that results in a predominantly fixed spatial pattern of flow distribution.

Animals↗

PubMed2000

Differential effects of furosemide on porcine bronchial arterial and airway smooth muscle.

Furosemide attenuates airway obstruction in asthmatic subjects when administered as an aerosol pretreatment. This protective effect of furosemide could be related to relaxation of bronchial smooth muscle or to increased bronchial blood flow. To determine whether furosemide dilates bronchial smooth muscle, isometric contractile responses in distal bronchi from young pigs were studied. In bronchial smooth muscle rings that were precontracted with 10(-5) M acetylcholine, significant relaxation occurred with 10(-8) to 3 x 10(-6) M isoproterenol but not with 10(-8) to 10(-3) M furosemide. In contrast, bronchial arteries that were precontracted with either 10(-4) M norepinephrine or 10(-8) M vasopressin significantly relaxed in response to 10(-4) to 3 x 10(-3) M and 10(-3) to 3 x 10(-3) M furosemide, respectively. We conclude that furosemide, under the described experimental conditions, relaxes airway vascular smooth muscle but not bronchial smooth muscle. These results are consistent with previous suggestions that inhaled furosemide increases blood flow to airway tissues (Gilbert IA, Lenner KA, Nelson JA, Wolin AD, and Fouke JM. J Appl Physiol 76: 409-415, 1994).

Animals↗

PubMed1999

Cross-desensitization to furosemide and salbutamol in isolated neonatal guinea pig airways.

Airway hyperresponsiveness in neonatal chronic lung disease is treated with both furosemide, a diurectic that inhibits the Na-K-2Cl cotrasporter, and salbutamol, a beta2-adrenoceptor agonist. Tachyphylaxis to both drugs in vitro has been described. This study was conducted to determine if the relaxation response in newborn guinea pig airways to furosemide and salbutamol can be cross-desensitized in vitro. Tracheal ring segments from 4- to 7-day-old guinea pigs were suspended in HEPES buffer for measurement of isometric tension. Segments were pre-treated with either furosemide (300 microM, 1 h) or salbutamol (10 microM, 30 min). After constriction with 3 microM acetylcholine, relaxation response to salbutamol or furosemide, respectively, was measured. Pretreatment with furosemide diminished relaxation response to salbutamol [87 +/- 3% (n = 11) vs. 117 +/- 8% (n = 10), p < 0.05], as compared to saline-treated controls. In addition, pretreatment with salbutamol diminished relaxation response to furosemide [53 +/- 2% (n = 11) vs. saline-treated (83 +/- 7%, n = 7, p < 0.05) and DMSO-treated controls (69 +/- 5%, n = 5, p < 0.05)]. Measurements of 86Rb uptake, cyclic AMP levels and responses in the presence of charybdotoxin make it unlikely that Na-K-2Cl cotransporter activity, stimulation of cAMP, or opening of maxi-K+ channels are mechanisms involved in the cross-desensitization to furosemide and salbutamol in vitro.

Acetylcholine↗

PubMed1987

Influence of furosemide on rubidium-86 uptake and alpha-adrenergic responsiveness of arterial smooth muscle.

Furosemide-induced inhibition of 86Rb uptake was measured in rat and rabbit aorta and compared with its ability to inhibit contractions induced by alpha-adrenergic agonists. In both rat and rabbit tissues, furosemide defined a portion of 86Rb uptake (IC50 = 2.5 microM) which was distinct from the ouabain-sensitive fraction. Furosemide-sensitive 86Rb uptake was [Cl-]ext dependent and required Na+ and K+ for optimal activity, suggesting that it reflected a Na+-K+ cotransport process. Furosemide-sensitive 86Rb uptake was found to be greater in HEPES buffer than in bicarbonate buffer. Phenylephrine-induced contractions of rat and rabbit aorta were inhibited by furosemide; however, rat responses were far more sensitive. Agonist-induced uptake of 45Ca was reduced by furosemide in rat aorta, but not in rabbit aorta. Agonist-induced 45Ca efflux stimulation was reduced in both species. These findings indicate the presence in arteries of a furosemide-sensitive, Cl-dependent Na+-K+ cotransport process. Along with other monovalent transport processes, it may modulate Ca2+ availability and thereby influence arterial contractility.

Animals↗

PubMed1984

Amelioration of hyperchloremic acidosis with furosemide therapy in patients with chronic renal insufficiency and type 4 renal tubular acidosis.

In hypoaldosteronemic patients with chronic renal insufficiency, administration of a mineralocorticoid steroid such as fludrocortisone can ameliorate hyperkalemia and metabolic acidosis, but this therapy is not always safe owing to the deleterious consequences of extracellular fluid volume expansion resulting from mineralocorticoid-induced sodium chloride retention. In the present study of 8 patients with renal hyperchloremic acidosis, mild hyperkalemia and chronic glomerular insufficiency, we evaluated the therapeutic effect of chronic administration of a natriuretic/chloruretic agent, furosemide, a renoactive drug that is known to increase renal acid excretion in experimental animals without increasing body content of sodium chloride. 4 patients had hyporeninemic hypoaldosteronism. During 8 days of treatment in 6 patients who received furosemide alone, metabolic acidosis was significantly ameliorated. Urinary net acid excretion increased, except in the 2 patients who had the most severe hypoaldosteronism. For the group as a whole, the cumulative change in net acid excretion correlated positively with the rate of aldosterone excretion (r = 0.94, p less than 0.01). Thus, the aciduric response to furosemide is attenuated by aldosterone deficiency. When furosemide was administered in combination with fludrocortisone (4 subjects), an amelioration of metabolic acidosis occurred that was greater than that observed in the group treated with furosemide alone. Combined therapy ameliorated acidosis in the patient with the most severe degree of hypoaldosteronism, the same patient in whom administration of furosemide without fludrocortisone was ineffective even after 6 months of treatment. The findings in this study indicate that chronic furosemide therapy, alone or in combination with fludrocortisone, is a safe and effective means of ameliorating metabolic acidosis in patients with chronic renal insufficiency, including those with hypoaldosteronism.

Acidosis↗

PubMed1989

Furosemide accelerates gentamicin accumulation in cultured renal cells (LLC-PK1 cells).

Furosemide is known to potentiate gentamicin nephrotoxicity. The mechanism of potentiation is unclear. In our previous studies, we demonstrated that furosemide enhanced gentamicin accumulation in rabbit renal tissues when injected as a bolus [Kidney int. 33:363, 1988] or repeatedly subcutaneously [Diuretics II, Elsevier, New York 1987, pp.693]. In this study, we evaluated the effects of furosemide on gentamicin accumulation in cultured renal cells (LLC-PK1) and hepatoma cells (H4IIE). Thus, we excluded effects secondary to furosemide-elicited hemodynamic changes. Seven days after seeding, the culture medium was exchanged for medium containing 1 mM gentamicin alone [G] or 1 mM gentamicin +1 mM furosemide [GF]. In LLC-PK1 cells, gentamicin concentration in [GF] was significantly higher than that in [G], while gentamicin was not detected in H4IIE cells with or without furosemide. We conclude that furosemide can accelerate gentamicin accumulation in renal tissues and potentiate gentamicin nephrotoxicity.

Animals↗

PubMed1985

Protection by magnesium of renal calcinosis in furosemide-treated weanling rats with moderate magnesium deficiency.

Prolonged treatment of premature infants with the potent diuretic furosemide has resulted in hypercalciuria, sometimes with renal calcinosis and other complications. Furosemide was administered to weanling rats to explore its effect on magnesium and calcium metabolism. The animals were fed purified diets providing 40 mg magnesium/100 g diet or 10 mg magnesium/100 g. Half of each dietary group (40-F or 10-F) received 18 doses of furosemide, 20 mg/kg body weight, intraperitoneally between days 7 and 35, and half received normal saline intraperitoneally (40-O or 10-O). Furosemide had little effect on the magnesium-sufficient animals (40-F), but comparison of 10-O and 10-F data showed that it aggravated the magnesium-deficiency syndrome. Comparison of data from 40-F and 10-F animals showed the protective effect of magnesium in preserving calcium homeostasis in furosemide-treated animals: the elevation of calcium values in 10-F rats was greater in plasma (p less than 0.0005), heart (p less than 0.0025), and kidney (p less than 0.0005). Stated another way, furosemide was associated with severely disordered calcium metabolism only in animals fed suboptimal magnesium. Studies exploring the role of magnesium in furosemide-treated infants can be recommended.

Animals↗

PubMed1990

Furosemide increases total calcium in kidney and cytoplasmic free calcium in blood mononuclear cells of guinea pigs.

Nephrocalcinosis has been observed in premature infants treated with furosemide. To see whether furosemide-induced renal calcium accumulation is reflected in easily accessible extrarenal cells, we measured cytosolic free calcium ([Ca2+]i) in blood mononuclear cells and kidney tissue calcium of guinea pigs chronically treated with furosemide. At week 0, the mean [Ca2+]i in blood mononuclear cells using the fluorescent indicator quin2 was 105 +/- 4 nM. After 2 weeks of treatment with furosemide, the high dosage (10 or 20 mg/kg/day) caused a significant increase in [Ca2+]i. There was no change in cell volume after 1 or 2 weeks of treatment with furosemide at this dosage. The kidney total calcium concentration and histological calcium accumulation increased with increasing furosemide dosages. These observations suggest that calcium accumulation in blood mononuclear cells may reflect the calcium accumulation in the kidney after furosemide treatment.

Analysis of Variance↗

PubMedDate not supplied

Alteration in capillary permeability of horseradish peroxidase in the stria vascularis and movement of leaked horseradish peroxidase after administration of furosemide.

The permeability of horseradish peroxidase (HRP) from the capillaries of the stria vascularis and the movement of leaked HRP in this site were investigated over time after the administration of furosemide, a loop diuretic, for the purpose of clarifying the function of the stria vascularis. Guinea pigs were used as experimental animals. The stria vascularis became markedly edematous at 10 min after the administration of furosemide, while the vascular permeability of HRP was decreased. This edema was thought to result not from the high permeation of strial capillaries, but from the blockage of water transport into the ductus cochlearis by inhibition of the Na+/2Cl-/K+ cotransport system on the cell membrane of the marginal cells and the exudation from the intermediate cells due to change of cell membrane permeability. A large amount of the leaked HRP from the strial capillaries was taken into vacuoles of marginal cells 1 h after furosemide administration. In the present study, no leakage of HRP was observed in the ductus cochlearis. Destroyed or degenerated cells were observed in vacuoles of marginal cells 2 and 3 h after furosemide administration, suggesting that marginal cells have a phagocytic function. Two hours after furosemide administration, the vascular permeability of HRP and the function of intermediate cells was still at a decreased level, although the stria vascularis was almost restored to normal morphology. Three hours after furosemide treatment, the vascular permeability of HRP and the intake of HRP into intermediate cell vesicles were generally normalized, suggesting near restoration of stria vascularis function. In the non-furosemide-treated control group, no vacuolation was observed in marginal cells, nor was HRP intake observed in these cells.

Animals↗

PubMed1991

Effects of furosemide on the renal functions of the unanesthetized newborn rat.

In neonates pharmacokinetics of furosemide is very slow, as compared to adult individuals, because it is eliminated through glomerular filtration and tubular secretion, mechanisms that are not fully developed in the newborn mammal. In addition, Henle's loop, the main site of action of this diuretic, is shorter in the neonate than in the adult animal. The aim of this study was to measure the response to furosemide in the unanesthetized newborn rat and to compare it with that of the adult. Furosemide (0.5, 1, 1.5, 2, 5 or 10 mg/kg body weight, i.p.) or vehicle were administered to newborn and adult rats and the effects on sodium, potassium and water balance were assessed. Despite the physiological characteristics of the neonatal kidney, furosemide induced a more marked sodium excretion and decrease in free water clearance in the newborn than in the adult rat. In contrast, urinary potassium losses elicited by furosemide were higher in the adult than in the newborn rat at similar doses. At both ages, the effects of the diuretic were dose-dependent. Plasma sodium decreased, whereas plasma potassium and hematocrit increased in the newborn rats, after the highest doses of furosemide. In the adult rat changes were less marked. Our results suggest that the neonatal kidney is more sensitive to equivalent doses of furosemide than the adult kidney.

Aging↗

PubMed1995

A comparison of the effects of inhaled furosemide and ethacrynic acid on sodium-metabisulfite-induced bronchoconstriction in subjects with asthma.

Inhaled furosemide prevents bronchoconstriction induced by a number of challenges in asthma. One approach to determine the mechanism underlying this protection has been to examine the effects of diuretics with different or overlapping pharmacologic effects. We have compared the effects of furosemide on sodium metabisulfite-induced bronchoconstriction with those of equivalent diuretic doses of ethacrynic acid, a loop diuretic that, unlike furosemide, does not interact directly with the membrane Na/K/Cl cotransporter protein or inhibit carbonic anhydrase. Eight subjects with mild asthma were studied on five occasions, receiving nebulized furosemide (20 and 40 mg), ethacrynic acid (25 and 50 mg), or placebo (normal saline) in random order and double-blind 10 min before a cumulative dose challenge with inhaled sodium metabisulfite. After placebo the geometric mean sodium metabisulfite PD20 was 7.9 mumol. Furosemide 20 mg and 40 mg increased the PD20 by a mean 1.1 (95% confidence interval, -0.2-2.4; p > 0.05) and 1.6 (0.4-2.9; p < 0.02) doubling doses to 17.1 and 24.7 mumol, respectively. After inhaled ethacrynic acid 25 mg and 50 mg, the geometric mean PD20 was increased by 0.9 (-0.4-2.2; p > 0.05) and 1.5 (0.2-2.8; p < 0.05) doubling doses to 14.5 and 22.4 mumol, respectively. Thus, equivalent diuretic doses of furosemide and ethacrynic acid have a similar inhibitory effect on sodium metabisulfite-induced bronchoconstriction in asthma. This suggests that interaction with the Na/K/Cl cotransporter protein, or carbonic anhydrase inhibition, is not relevant to the effects of furosemide in asthma.

Administration, Inhalation↗