Journal articles: 'Frusemide'

1

HINCHCLIFF, K. W., and K. H. McKEEVER. "Frusemide." Equine Veterinary Journal 27, S18 (June 10, 2010): 256–58. http://dx.doi.org/10.1111/j.2042-3306.1995.tb04932.x.

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Johnson, Valerie E., and P. J. Hilton. "Frusemide-Sensitive Sodium and Potassium Transport by Human Leucocytes." Clinical Science 68, no. 1 (January 1, 1985): 89–91. http://dx.doi.org/10.1042/cs0680089.

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1. Frusemide-sensitive sodium and potassium transport by normal human leucocytes has been studied in vitro by both isotopic and net flux techniques. 2. In physiological media the leucocyte exhibits a frusemide-sensitive influx of sodium and potassium of equal magnitude compatible with a 1:1 co-transport system. 3. Cells exposed to zero external sodium and potassium (osmolality maintained with choline) demonstrated a frusemide-sensitive sodium and potassium efflux. 4. Frusemide-sensitive potassium influx was dependent on the presence of external sodium but frusemide-sensitive sodium influx persisted unchanged in the absence of external potassium. 5. Frusemide-sensitive potassium influx was dependent on external chloride but frusemide-sensitive sodium influx was chloride-independent. 6. These last two observations make it likely that the frusemide-sensitive pathway is capable of operating in modes other than sodium-potassium co-transport.

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Jeffrey, R. F., T. M. MacDonald, M. Rutter, S. Freestone, J. Brown, R. R. Samson, and M. R. Lee. "The effect of intravenous frusemide on urine dopamine in normal volunteers: Studies with indomethacin and carbidopa." Clinical Science 73, no. 2 (August 1, 1987): 151–57. http://dx.doi.org/10.1042/cs0730151.

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1. The urine dopamine response to intravenous frusemide (30 mg) was investigated in 15 salt replete male volunteers. The effects of oral indomethacin (100 mg) and oral carbidopa (100 mg) given before intravenous frusemide were studied in the same group of subjects. 2. Frusemide produced a significant increase in urine dopamine output within 15 min. 3. Indomethacin attenuated the natriuretic and renin responses to frusemide, but did not alter urine dopamine output. 4. Carbidopa lowered urine dopamine to undetectable levels, but did not significantly affect the natriuretic and renin responses to frusemide. 5. We conclude that urine dopamine excretion after frusemide is not directly related to increased sodium excretion or renin response and it is not mediated by the prostaglandins. In addition, dopamine does not contribute to the renal actions of frusemide under normal conditions.

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Molimard, M., and C. Advenier. "Effect of frusemide on bradykinin- and capsaicin-induced contraction of the guinea-pig trachea." European Respiratory Journal 6, no. 3 (March 1, 1993): 434–39. http://dx.doi.org/10.1183/09031936.93.06030434.

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Frusemide, a loop diuretic, inhibits the bronchial response to various bronchoconstrictor stimuli in asthmatic subjects. The underlying mechanisms remain unclear. In order to determine whether frusemide inhibits pharmacologically induced C-fibre stimulation, we investigated the effect of frusemide on bradykinin-, capsaicin-, neurokinin A-, and substance P-induced contraction of the guinea-pig isolated trachea. Frusemide 10(-5) and 10(-4) M produced a significant inhibition of concentration-response curves to bradykinin, which was markedly reduced by indomethacin 10(-6) M. Frusemide significantly reduced capsaicin-induced contraction only in the presence of indomethacin 10(-6) M. Neurokinin A- and substance P-induced contractions were not affected by frusemide and/or indomethacin. Our data suggest that a cyclo-oxygenase pathway is involved in the inhibition by frusemide of the bradykinin-induced contraction, but not in the inhibition of the capsaicin-induced contraction.

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Melki, T. S., M. L. Foegh, and P. W. Ramwell. "Implication of thromboxane in frusemide diuresis in rats." Clinical Science 71, no. 6 (December 1, 1986): 647–50. http://dx.doi.org/10.1042/cs0710647.

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1. Administration of the thromboxane A2 (TXA2) synthase inhibitor OKY 1581 to rats significantly increased the urine output elicited by the loop diuretic frusemide. 2. The administration of the TXA2 receptor antagonist SQ 29548 significantly increased the diuretic effect of frusemide. 3. Another TXA2 receptor antagonist L-640,035 increased significantly the diuretic effect of frusemide. 4. Both the sodium excretion rate and urine osmolar excretion rate were significantly increased in rats treated with the TXA2 synthase inhibitor OKY 1581 and frusemide. 5. The data suggest that TXA2 is released during frusemide-induced diuresis in rats, and the released TXA2 has an opposing antidiuretic effect.

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Boles Ponto, Laura L., and Ronald D. Schoenwald. "Furosemide (Frusemide)." Clinical Pharmacokinetics 18, no. 5 (May 1990): 381–408. http://dx.doi.org/10.2165/00003088-199018050-00004.

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Boles Ponto, Laura L., and Ronald D. Schoenwald. "Furosemide (Frusemide)." Clinical Pharmacokinetics 18, no. 6 (June 1990): 460–71. http://dx.doi.org/10.2165/00003088-199018060-00003.

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8

Cardan, E. "Intrathecal frusemide." Anaesthesia 40, no. 10 (October 1985): 1025. http://dx.doi.org/10.1111/j.1365-2044.1985.tb10581.x.

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9

Yeo, CT, BJ O'Connor, M. Chen-Worsdell, PJ Barnes, and KF Chung. "Protective effect of loop diuretics, piretanide and frusemide, against sodium metabisulphite-induced bronchoconstriction in asthma." European Respiratory Journal 5, no. 10 (November 1, 1992): 1184–88. http://dx.doi.org/10.1183/09031936.93.05101184.

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We determined whether the loop diuretic, piretanide, had a similar inhibitory action against sodium metabisulphite (MBS)-induced bronchoconstriction in asthmatic subjects as frusemide and, if so, its duration of action. In the first study, we compared the effect of inhaled placebo, piretanide (24 mg), or frusemide (40 mg), on the provocative concentration of MBS needed to cause a 20% fall in baseline forced expiratory volume in one second (FEV1) (PC20MBS) in 12 mild asthmatic subjects before, immediately after, and at 1.5, 3, 6, and 24 h, after inhalation. Both piretanide and frusemide induced a significant diuresis lasting at least 24 h. Frusemide caused a mean 3.8 fold (95% confidence interval: 2.3-6.3 fold), piretanide a 2.5 fold (1.8-3.4 fold) and placebo a 1.7 fold (1.5-1.9 fold) increase in PC20MBS. The effects of frusemide and piretanide were significantly greater than that of placebo. At later time points, tachyphylaxis to the bronchoconstrictor effects of MBS was observed during the placebo limb. In the second study, we measured PC20MBS at 90 min after inhalation of either placebo, piretanide (24 mg), or frusemide (40 mg). No significant difference in PC20MBS was observed. We conclude that piretanide in addition to frusemide significantly inhibits MBS-induced bronchoconstriction and that this action is short-lived over less than 90 min. Frusemide was more potent in inhibiting MBS-induced bronchoconstriction despite causing a smaller diuretic effect than piretanide. The basic mechanism of action of the loop diuretics in the airways remains unclear.

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J. Jawad, Fatima. "A Study on the Stability of Different Frusemide Liquid Dosage Formulas: Oral Solution, Syrup, Elixir, Suspension and Emulsion." Iraqi Journal of Pharmaceutical Sciences ( P-ISSN: 1683 - 3597 , E-ISSN : 2521 - 3512) 17, no. 2 (March 30, 2017): 1–8. http://dx.doi.org/10.31351/vol17iss2pp1-8.

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The present study aim at preparing frusemide in liquid form suitable for oral use. This is achieved through preparing different liquid forms of frusemide. The frusemide liquid is prepared in the following forms: oral solution, syrup and elixir with intensity of 1, 0.4 and 0.8% weight /volume respectively and in combination with potassium carbonate, polysorbate 80, alcohol and phosphate buffer solution of pH8 to dissolve the frusemide in the above mentioned forms. The different forms of the prepared medicine have been stored in glass bottles that can provide protection against light and at 40, 50, 600C for four months. Besides the pH has been checked to decide the period of validity. The results show that the expiration date of frusemide have lasted for 1.8, 1.07 and 1.22 years respectively for the oral solution, the syrup and the elixir. The suspensions of frusemide are formulated in combination with the following: polyvinyl pyrolidine, xanthan gum, the combination of (xanthan gum and sodium carboxymethyl cellulose), the combination of (xanthan: methyl cellulose) and chitosan. The formulas which give suitable release of the drug are chosen for assessment according to the following considerations: The rat of sedimentation and apparent zero order degradation constant at 250C. In conclusion, it is found the best formula is that which includes poly vinylpyrolidine, tween20, glycerol, sorbitol, cocoa syrup and parabens at pH7. the fluidity of this chosen formula is psendoplastic type and its validity has lasted for about three years. The emulsion of frusemide is also prepared extemporaneously by using the commercial frusemide tablets in combination with acacia and olive oil. This should be consumed within 45 days of the date of production. Key word: frusemide, elixir, suspension, emulsion.

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Shirley, D. G., S. J. Walter, and R. J. Unwin. "Mechanism of the Impaired Natriuretic Response to Frusemide during Sodium Depletion: A Micropuncture Study in Rats." Clinical Science 91, no. 3 (September 1, 1996): 299–305. http://dx.doi.org/10.1042/cs0910299.

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1. The nephron sites involved in the blunted natriuretic response to frusemide during sodium depletion were investigated using micropuncture techniques in anaesthetized rats. 2. Glomerular filtration rate was lower, and fractional sodium reabsorption in the proximal convoluted tubule higher, in sodium-depleted than in sodium-replete rats. Consequently, sodium delivery to the loop of Henle was reduced (by approximately 35%) in the sodium-depleted animals. Intravenous frusemide (2.5 mg h−1 kg−1; urinary water and electrolyte losses replaced) had no effect on glomerular filtration rate or proximal tubular sodium reabsorption in either group. 3. The inhibitory effect of intravenous frusemide on fractional sodium reabsorption in the nephron segments constituting the loop of Henle (measured by free-flow micropuncture) was attenuated during sodium depletion. However, when loops of Henle were microperfused at identical rates with artificial late proximal tubular fluid, no difference in the responses of sodium-depleted and sodium-replete rats to intraluminal frusemide (10−5 mol/l) could be detected. 4. In sodium-replete animals, the increased load of sodium delivered from the loop of Henle during frusemide administration resulted in a lowering of fractional sodium reabsorption in the distal tubule. In contrast, in sodium-depleted rats given frusemide, fractional distal sodium reabsorption tended to increase, so that values in the two groups of frusemide-treated animals were markedly different (0.30 ±0.04 versus 0.51 ±0.03). 5. It is concluded that the blunted natriuretic response to frusemide during sodium depletion results from at least three factors: a reduced sodium delivery to the loop of Henle; a reduced inhibitory effect of frusemide on fractional sodium reabsorption in the loop of Henle, which may be a consequence of the reduced sodium load; and enhanced fractional reabsorption of sodium in the distal tubule, which partially buffers the diuretic-induced increase in sodium delivery from the loop.

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Crawford, R. J., S. Allman, W. Gibson, S. Kitchen, and H. H. Richards. "A Comparative Study of Frusemide–Amiloride and Cyclopenthiazide–Potassium Chloride in the Treatment of Congestive Cardiac Failure in General Practice." Journal of International Medical Research 16, no. 2 (March 1988): 143–49. http://dx.doi.org/10.1177/030006058801600209.

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Forty-seven patients entered this comparison of frusemide–amiloride and cyclopenthiazide–potassium chloride in the treatment of congestive cardiac failure in general practice. Frusemide–amiloride was ‘very satisfactory’ in 92% of the patients compared to only 55% who took cyclopenthiazide–potassium chloride. Significantly more patients were free of paroxysmal nocturnal dyspnoea and orthopnoea after taking frusemide–amiloride.

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13

Jørgensen, H., N. Anderssen, T. Silsand, and L. E. Peterson. "Long-Term Treatment with Slow-Release Frusemide Compared with Thiazide Treatment in Arterial Hypertension." Journal of International Medical Research 17, no. 6 (November 1989): 552–59. http://dx.doi.org/10.1177/030006058901700609.

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The effect of 30 mg/day slow-release frusemide given orally for 12 months was studied in 64 patients previously treated with thiazides for mild to moderate essential hypertension. Frusemide had a significant antihypertensive effect ( P<0.001), and compared to thiazides significantly reduced fasting serum glucose ( P<0.015), haemoglobin A1c ( P<0.025), albumin ( P<0.025) and serum calcium ( P<0.025), and significantly increased serum sodium and chloride concentrations ( P<0.0001). There was also a non-significant trend for frusemide to reduce serum total cholesterol, triglycerides and urate, and to increase serum potassium. Frusemide was well tolerated in all but three patients. It is concluded that slow-release frusemide has a comparable antihypertensive effect to that of thiazide diuretics, but has fewer metabolic side-effects, and should be used in preference to thiazides for the treatment of arterial hypertension when a diuretic is indicated.

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T, Tamilveeran, Karthikeyan B, and Balamurugan K. "A Comparison and Evaluation of Loop Diuretic Frusemide Generic vs Brand Tablets." Journal of Pharmaceutical Research International 36, no. 4 (March 30, 2024): 24–32. http://dx.doi.org/10.9734/jpri/2024/v36i47509.

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Branded medications are the original products developed by pharmaceutical companies and generic drugs are copies of branded drugs whose patent has expired. The research work focused on comparisons and evaluations of generic VS brand of frusemide tablets. The study includes some of the specifications that should tested in the finished products in tablets such as appearance, thickness, diameter, weight variation, hardness, friability, disintegration time, dissolution, hardness and thickness as per pharmacopoeial & non pharmacopoeial tests were performed. The generic and brand frusemide tablets quality control results showed within the range as per IP. The in vitrodrug release of generic frusemide tablets was found to be 96.7 %in 45 min and branded tablets which showed drug release 98.3% in 45 min. Hence, it can be concluded that evaluation of loop diuretic frusemide tablets generic and brand frusemide tablets showed same deviations in the quality control results as per IP.

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Itabashi, Akira, Laurence Chan, Joseph I. Shapiro, Cynthia Cheung, and Robert W. Schrier. "Comparison of the natriuretic response to atriopeptin III and loop diuretic in the isolated perfused rat kidney." Clinical Science 73, no. 2 (August 1, 1987): 143–50. http://dx.doi.org/10.1042/cs0730143.

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1. Isolated rat kidneys were perfused at a constant perfusion pressure of 90 mmHg to study the natriuretic effects of atriopeptin III (AP-III) and to compare these effects with those of frusemide. AP-III (1 μg) or frusemide (1 mg) were added to the perfusate (100 ml) after two 15 min control collection periods. 2. Compared with the control group, AP-III and frusemide increased urinary sodium excretion (UNaV, 5.6 ± 1.1 and 4.6 ± 0.6 vs control 1.8 ± 0.3 μmol min−1 g−1, mean ± sem, P < 0.01 and P < 0.05, respectively), fractional sodium excretion (FENa, 4.8 ± 1.1 and 6.7 ± 0.8 vs control 2.0 ± 0.2%, P < 0.05 and P < 0.001, respectively) and potassium excretion (UKV, 3.2 ± 0.3 and 3.0 ± 0.3 vs control 1.5 ± 0.3 μmol min−1 g−1, both P < 0.01). However, AP-III, but not frusemide, increased glomerular filtration rate (820 ± 55 vs 590 ± 24 μl min−1 g−1, P < 0.01) and urine flow rate (V 97.5 ± 8.0 vs 44.1 ± 5.2 μl min−1 g−1, P < 0.001). Calculated distal delivery of sodium (CNa + CH2O, 76.6 ± 6.8 vs 30.7 ± 3.8 μl min−1 g−1, P < 0.005) as well as fractional distal delivery of sodium [(CNa + CH2O)/CIn, 9.4 ± 0.9 vs 5.1 ± 0.6%, P < 0.01] were increased by AP-III, but not frusemide. Fractional distal reabsorption of sodium [CH2O/(CNa + CH2O), 51.9 ± 6.5 vs 59.9 ± 2.7%, NS] was not affected by AP-III but was significantly reduced by frusemide (7.4 ± 3.0%, P < 0.001). 3. The natriuretic effects of the combination of AP-III and frusemide were additive even though the distal delivery was no greater than with AP-III alone. These data indicate that AP-III has a unique natriuretic effect different from frusemide, and that the main site of natriuretic action by AP-III is proximal to the ascending loop of Henle. Because of different nephron sites, the effects of AP-III and frusemide are additive, a finding of potential clinical importance.

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Rodwell, LT, SD Anderson, J. du Toit, and JP Seale. "Different effects of inhaled amiloride and frusemide on airway responsiveness to dry air challenge in asthmatic subjects." European Respiratory Journal 6, no. 6 (June 1, 1993): 855–61. http://dx.doi.org/10.1183/09031936.93.06060855.

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Amiloride, a Na+ channel blocker, and frusemide, an inhibitor of the Na+/K+/2Cl- co-transporter on the basolateral surface of airway epithelial cells, have the potential to affect water transport across the airway epithelium. As isocapnic hyperventilation challenge (ISH) with dry air may provoke airway narrowing in asthmatic subjects by dehydrating the airways, inhaled amiloride and frusemide may reduce airway responsiveness by effecting airway hydration. Fifteen asthmatic subjects (6 females, 9 males), who had a fall in forced expiratory volume in one second (FEV1) of 20% after ISH, inhaled amiloride (11 mg), or its vehicle, from a Fisoneb ultrasonic nebulizer, within 10 min before ISH. On a separate day, eight of these subjects inhaled frusemide (38 mg), from the same Fisoneb, 10 min before ISH. After breathing, 30 l at resting ventilation, subjects breathed at 30% of their maximum voluntary ventilation (MVV i.e. predicted FEV1x35), then at 60% MVV, and finally at MVV for 3 or 4 min. FEV1 was measured 1, 3, 5, 7 and 9 min after each period, or until it was stable. Airway sensitivity was expressed as the ventilation (l-min-1) which provoked a 10, 15, 20 or 30% fall in FEV1, (PVE10, PVE15, PVE20 and PVE30, respectively). There was no significant difference in the PVE10,15,20,30 between the vehicle and amiloride treatment day; however, in the 8 subjects who inhaled frusemide, frusemide caused a significant increase in the PVE20 when compared to amiloride. In conclusion, inhaled amiloride failed to protect against ISH, whereas frusemide was effective at reducing airway responsiveness. Further studies are needed to explain the mechanism of action of frusemide.

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Ala-Houhala, I., H. Vapaatalo, and A. Pasternack. "Intravenously administered frusemide increases glomerular permeability." Clinical Science 73, no. 4 (October 1, 1987): 365–70. http://dx.doi.org/10.1042/cs0730365.

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1. The effects of frusemide on glomerular permeability were investigated in eight proteinuric patients by measuring the fractional protein and dextran clearances and correlating these observations with changes in renal haemodynamics. 2. Frusemide increased significantly the fractional albumin and IgG clearances. The fractional dextran clearances of molecules with a radius ≥ 5.4 run also increased significantly after frusemide injection. Pretreatment with indomethacin partly inhibited the increments in clearances of macromolecules. 3. The changes in the fractional protein clearances correlated significantly with those of inulin clearance There was also a high degree of correlation between the changes in fractional protein clearances and prostanoid excretion. 4. The data obtained suggest that frusemide increases glomerular permeability by influencing the effective pores of the glomerular capillary wall. The increased permeability possibly is due to changes in prostanoid synthesis.

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Mackay, I. G., K. Nath, A. D. Cumming, A. L. Muir, and M. L. Watson. "Haemodynamic and Endocrine Responses of the Kidney to Frusemide in Mild Essential Hypertension." Clinical Science 68, no. 2 (February 1, 1985): 159–64. http://dx.doi.org/10.1042/cs0680159.

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1. Prostaglandin-dependent, frusemide-induced changes in renal plasma flow, glomerular filtration rate and plasma renin activity were measured in 14 patients with mild essential hypertension. 2. The renal haemodynamic responses to frusemide were the same as in 10 normal subjects. 3. Frusemide-induced changes in urinary PGE and kallikrein excretion were also the same as in normal subjects. 4. Impaired renal release of vasodilator prostaglandins in essential hypertension is likely to be secondary to the hypertension rather than an underlying factor in its development.

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Obika, L. F. O., and M. Marin-Grez. "Urinary kallikrein response to repeated frusemide injections in rats: Effect of adrenalectomy and deoxycorticosterone acetate treatment." Clinical Science 71, no. 5 (November 1, 1986): 497–503. http://dx.doi.org/10.1042/cs0710497.

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1. The effect of repeated intravenous injections of frusemide (0.17 mg/kg) on the urinary kallikrein excretion of normal, adrenalectomized and deoxycorticosterone acetate (D0CA)-treated adrenalectomized rats was studied. 2. Adrenalectomy decreased baseline urinary kallikrein excretion, while DOCA treatment restored it to normal. 3. Frusemide injections repeatedly increased urinary kallikrein excretion in the three groups of rats studied. Compared with control and DOCA-treated animals, adrenalectomized rats were less responsive. 4. The excretion of urinary kallikrein was positively correlated with urine volume and with the excretion of sodium and potassium in all groups. The regression lines were shifted to the left in DOCA-treated adrenalectomized rats showing that mineralocorticoids enhance the effect of frusemide on urinary kallikrein excretion. The regression lines between urinary kallikrein excretion and the measured variables in adrenalectomized rats did not differ from those of control animals. 5. We conclude that the response of urinary kallikrein to frusemide is influenced by the level of mineralocorticoid activity. The effect of frusemide on urinary kallikrein excretion does not appear to be a ‘wash-out’ of the enzyme since its influence did not subside after repeated injections.

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Bianco, S., MG Pieroni, RM Refini, M. Robuschi, A. Vaghi, and P. Sestini. "Inhaled loop diuretics as potential new anti-asthmatic drugs." European Respiratory Journal 6, no. 1 (January 1, 1993): 130–34. http://dx.doi.org/10.1183/09031936.93.06010130.

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The observation that changes in bronchial osmolarity can induce bronchoconstriction in asthma inspired the experimental studies which, unexpectedly, revealed that frusemide is an effective bronchoprotective agent against a variety of osmotic and non osmotic stimuli. Although the mechanism of this protective effect is not fully understood, studies in vivo and in vitro suggest that frusemide may inhibit the activation of different cell types induced by bronchoconstrictor stimuli. Other loop diuretics also exert bronchoprotective activity, but frusemide appears to be the more effective bronchoprotective agent of this family, regardless of their diuretic potency and lipid solubility. Despite the relatively large amount of experimental evidence, there is currently little information on the clinical effectiveness of frusemide in asthma and a long-term controlled study is currently in progress. The observations that treatment with a combination of inhaled acetylsalicylate and frusemide results in a markedly increased bronchoprotective effect compared to either drug alone, opens a new perspective in the possible clinical use of these drugs. Preliminary studies suggest that the association of these drugs is well tolerated and may result in a remarkable steroid sparing effect in patients with steroid dependent asthma, for whom a convenient alternative to long-term steroid therapy is not currently available.

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Nowicki, S., E. J. Ochoa, G. Levin, and M. M. Elias. "Intrarenal dopamine participation in frusemide diuretic and natriuretic responses to frusemide." Journal of Autonomic Pharmacology 15, no. 3 (June 1995): 159–68. http://dx.doi.org/10.1111/j.1474-8673.1995.tb00300.x.

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Öhman, K. Peter, and Bengt E. Karlberg. "Plasma and tissue kallikrein–kinin systems during acute administration of frusemide in normotensive and hypertensive humans." Clinical Science 81, no. 3 (September 1, 1991): 305–11. http://dx.doi.org/10.1042/cs0810305.

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1. This study aims to further elucidate the role of the tissue and plasma kallikrein-kinin systems in blood pressure, electrolyte and volume homoeostasis. Components thereof and of the renin-angiotensin-aldosterone system were measured in conjunction with frusemide administration, in normotensive subjects and in patients with primary hypertension. 2. Frusemide increased plasma pre-kallikrein, angiotensin II and aldosterone concentrations and plasma renin activity, whereas the plasma level of tissue kallikrein remained unchanged. Basal values and the induced changes were similar in both groups. 3. Frusemide increased the urine volume and the excretion of Na+, K+, Mg2+, Cl−, aldosterone, prostaglandin E2 and tissue kallikrein. These changes were similar in both groups, but the total tissue kallikrein excretion was significantly lower in the hypertensive patients. Excretion of electrolytes and hormones was also measured during three 24 h urine collection periods and did not differ between the two groups. 4. Thus, acute administration of frusemide to hypertensive patients and normal subjects increased the plasma level of pre-kallikrein, possibly indicating less activation to kallikrein and subsequently less kinin generation in the blood stream. This also suggests a role for the plasma kallikrein-kinin system in the regulation of vascular tone and blood volume. Circulating tissue kallikrein does not seem to be acutely involved. 5. Urinary excretion of kallikrein is reduced in patients with primary hypertension after the administration of frusemide, apparently without affecting the renal excretory response.

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Obika, L. F. O., and M. MARIN-GREZ. "Amiloride inhibits the rise of urinary kallikrein excretion induced by frusemide administration in the rat." Clinical Science 72, no. 4 (April 1, 1987): 449–54. http://dx.doi.org/10.1042/cs0720449.

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1. The effect of amiloride administration on the urinary kallikrein response to the injection or continuous infusion of frusemide in normal Sprague–Dawley rats was investigated. 2. Injections of frusemide induced repeatedly an increase in urinary kallikrein excretion. This effect was suppressed by amiloride. Amiloride also blocked the response to mannitol injection. A continuous infusion of frusemide lasting 100 min also induced an increase in urinary kallikrein excretion which persisted throughout the experiment. This response was completely blocked by the injection of amiloride. 3. Urinary kallikrein excretion was directly and positively related to urine volume and urinary sodium excretion before and after amiloride injection. The regression lines had markedly decreased slopes after amiloride administration. The urinary kallikrein excretion was also positively related to the urine volume and urinary sodium excretion when frusemide was continuously infused. However, these relationships were abolished after amiloride injection. 4. In both the injection and the infusion experiments, there was a direct relationship of urinary kallikrein excretion to urinary potassium excretion. Although this relationship persisted after amiloride injection, the regression line was shifted to the left. 5. The suppression of the kallikrein stimulating effect of frusemide by the sodium channel blocker amiloride indicates that distal tubule sodium re-absorption is the triggering factor in urinary kallikrein excretion. The study suggests that the mechanism involved in the release of kallikrein by the distal tubular cells is linked to the renal mechanism affected by amiloride.

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Stone, RA, PJ Barnes, and KF Chung. "Effect of frusemide on cough responses to chloride-deficient solution in normal and mild asthmatic subjects." European Respiratory Journal 6, no. 6 (June 1, 1993): 862–67. http://dx.doi.org/10.1183/09031936.93.06060862.

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We studied the tussive effects of a chloride-deficient solution (1.26% sodium bicarbonate). Nine normal volunteers and 10 mild asthmatic subjects were studied. In two double-blind, placebo-controlled, cross-over studies, we assessed the profile of any inhibitory effects that inhaled frusemide had over these responses. Baseline cough challenge was followed by inhalation of either frusemide (40 mg), or 0.15 M NaCl control. Cough was then induced at 0.5, 2, 4 and 6 h after treatment. Forced expiratory volume in one second (FEV1) was measured before and after each challenge. Changes from the baseline cough response due to drug or control were compared nonparametrically at each time point. There was no difference in the sensitivity of normal and asthmatic subjects to the cough challenge (median cough response 15 and 14.5 on control day, 12 and 15 on frusemide day). Frusemide caused sustained inhibition of the cough response in normal subjects (p < 0.05 at 2 h, p < 0.01 at 4 h), but had only a small, nonsignificant effect in asthmatic subjects at 30 min. Falls in FEV1 of asthmatic subjects due to the chloride-deficient solution were not significant, and did not correlate with number of coughs. We conclude that mild asthmatic subjects are less sensitive than normal subjects to the influence of frusemide against low chloride challenge. This observation is not explained by bronchoconstrictor effects of the cough challenge in asthmatic subjects.

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Polosa, R., LC Lau, and ST Holgate. "Inhibition of adenosine 5'-monophosphate- and methacholine-induced bronchoconstriction in asthma by inhaled frusemide." European Respiratory Journal 3, no. 6 (June 1, 1990): 665–72. http://dx.doi.org/10.1183/09031936.93.03060665.

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Recent studies have shown that inhaled frusemide exerts a protective effect against various bronchoconstrictor stimuli in asthma including exercise, fog and allergen. Since mast cell activation seems to be a component of bronchoconstriction by these stimuli it is possible that inhibition of mediator release accounts for some or all of the inhibitory effects of frusemide in asthma. Since inhaled adenosine 5'-monophosphate (AMP) is another stimulus that produces bronchoconstriction by augmenting mast cell mediator release, we have investigated the ability of this drug to antagonise the airway effects of inhaled AMP and methacholine in a randomized, placebo-controlled, double-blind study of 12 asthmatic subjects. Inhaled frusemide (approximately 28 mg) administered 5 min prior to challenge increased the provocation concentration of inhaled AMP and methacholine required to reduce forced expiratory volume in one second (FEV) by 20% from baseline from 30 to 96 mg.ml-1 (p less than 0.01) and from 1.1 to 1.8 mg.ml-1 (p less than 0.01), respectively. The protection that frusemide afforded against AMP was significantly greater than that against methacholine (p less than 0.05). These data suggest that inhaled frusemide may serve as a functional antagonist against a smooth muscle spasmogen, such as methacholine, possibly by augmenting prostanoid generation. Its more potent activity against AMP and other bronchoconstrictor stimuli, that are considered to involve mast cell mediators, suggests an additional action on mast cell functions possibly at the level of the Ca++/Mg(++)-ATPase.

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26

Maheshwari, R. K., and J. Gupta. "NEW ECO-FRIENDLY TITRIMETRIC ANALYSIS OF FRUSEMIDE TABLETS USING MIXED HYDROTROPIC SOLUBILISATION." INDIAN DRUGS 55, no. 04 (April 28, 2018): 75–76. http://dx.doi.org/10.53879/id.55.04.11172.

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In the present study, a blend of 15% w/V sodium salicylate, 5% w/V niacinamide, 5% w/V sodium acetate and 5% w/V sodium citrate was prepared to carry out titrimetric estimation of frusemide tablets. The solubility of frusemide in distilled water at room temperature was found to be 0.64 mg/mL. The solubility of frusemide was significant in this mixed hydrotropic blend (21.39 mg/mL) with more than 33 fold enhancement in solubility. The crushed powder of tablets of frusemide was extracted using this blend. The analysis of the drug was done by titrimetric analysis with 0.1M sodium hydroxide solution. Various organic solvents like methanol, chloroform, dimethyl formamide and ethanol have been employed for solubilisation of poorly water soluble drugs to conduct their titrimetric analysis. This proposed method for analysis is recommended because it eliminates the use of toxic solvents and it is a novel, rapid, accurate and reproducible method that is economic as well. Statistical data proved accuracy, precision and reproducibility of the proposed analytical method. The proposed method uses the concept of mixed hydrotropy and provides an alternative method of analysis where the toxicity of solvents can be eliminated.

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27

Fiorino, F., B. Mattellini, M. Vento, L. Mazzocchin, L. Bianconi, and F. B. Pizzini. "Does the intravenous administration of frusemide reduce endolymphatic hydrops?" Journal of Laryngology & Otology 130, no. 3 (January 14, 2016): 242–47. http://dx.doi.org/10.1017/s0022215115003527.

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AbstractObjective:To verify the hypothesis that intravenous frusemide reduces endolymphatic hydrops, as evaluated by three-dimensional fluid-attenuated inversion recovery magnetic resonance imaging following intratympanic gadolinium administration.Methods:The study comprised 12 patients (7 females and 5 males, aged 19–74 years) with Ménière's disease. Disease duration ranged from 0.5 to 8 years, with a frequency of 0.5 to 6 vertigo spells per month, as calculated in the last 6 months. Three-dimensional fluid-attenuated inversion recovery magnetic resonance imaging was performed 24 hours after intratympanic injection of gadobutrol diluted eight-fold. Frusemide 20 mg was given intravenously immediately after imaging. Magnetic resonance imaging was repeated after 1 hour, using the same parameters and sequence.Results:All patients showed enhancement defects, indicating endolymphatic hydrops of variable degrees. No modifications occurred at the second magnetic resonance imaging performed 1 hour after frusemide administration.Conclusion:There was no evidence of endolymphatic hydrops modification 1 hour after intravenously administered frusemide. Therefore, loop diuretics in Ménière's disease, which are today used on an empirical basis, must be reconsidered. Implications of these outcomes are discussed and related to the role of endolymphatic hydrops in the development of Ménière's disease.

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Waller, Derek G., Satvinder S. Bhatia, Sara K. Campbell, Janet D. M. Albano, and J. Gavin B. Millar. "Active and Inactive Urinary Kallikrein in Man: Effects of Diuresis and Antidiuresis." Clinical Science 79, no. 2 (August 1, 1990): 117–21. http://dx.doi.org/10.1042/cs0790117.

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1. The urinary excretion of active and inactive kallikrein was studied in volunteers during diuresis induced by water loading or oral frusemide and during antidiuresis induced by desamino-d-arginine-vasopressin. 2. During acute oral water loading, excretion of active kallikrein was unchanged, despite high urine flow rates and low urine osmolalities being achieved. Excretion of inactive kallikrein correlated with the urine flow rate. 3. After desamino-d-arginine-vasopressin in eight water-loaded and six normally hydrated subjects, excretion of inactive kallikrein also correlated with the urine flow rate. There were no significant changes in the excretion of active kallikrein. 4. After frusemide there was a small transient increase in excretion of active kallikrein 1–2 h after dosing which coincided with the maximum diuresis and natriuresis. Excretion of inactive kallikrein again correlated with urine flow rate but the regression relationship between the two variables was different for water-load-induced and frusemide-induced diuresis. 5. These studies do not support a role for urinary kallikrein in the modulation of the antidiuretic action of vasopressin, but suggest that it may contribute to the natriuretic action of frusemide.

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29

Polosa, R., K. Rajakulasingam, G. Prosperini, S. Magri, C. Mastruzzo, and ST Holgate. "Inhaled loop diuretics and basal airway responsiveness in man: evidence of a role for cyclo-oxygenase products." European Respiratory Journal 8, no. 4 (April 1, 1995): 593–99. http://dx.doi.org/10.1183/09031936.95.08040593.

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Inhaled frusemide protects asthmatic airways against a wide variety of bronchoconstrictor stimuli by unknown mechanisms. To investigate whether inhaled loop diuretics modulate baseline bronchial responsiveness, a randomized, double-blind, placebo-controlled study was conducted to test the ability of frusemide (40 mg) and bumetanide (2 mg) to displace concentration-response curves with methacholine in 14 healthy volunteers. In addition, separate randomized, double-blind studies were carried out to evaluate the effects of oral flurbiprofen, a potent cyclo-oxygenase inhibitor, on the protective action of frusemide against methacholine-induced bronchoconstriction. Inhaled loop diuretics significantly increased the provocative concentration of methacholine causing a 15% decrease in forced expiratory volume in one second (PC15FEV1) from the geometric mean (range) value of 58.6 (9.2-233) mg.ml-1 after placebo administration, to 129 (13.8-505) and to 106 (6.6-510) mg.ml-1 after administration of frusemide and bumetanide, respectively. Similar results were obtained when data from partial flow-volume curves were used for analysis. In the eight subjects studied, pretreatment with oral placebo and inhaled frusemide reduced airway responsiveness to methacholine, with a geometric mean (range) PC15FEV1 value of 116 (25.4-405) mg.ml-1, and premedication with oral flurbiprofen abolished this protective effect, the geometric mean (range) PC15FEV1 methacholine being reduced to a value of 50.3 (16.6-189) mg.ml-1. In addition, oral flurbiprofen alone failed to alter airway responsiveness to methacholine. In view of these findings, it is suggested that bronchoprotective prostaglandins may mediate the effects of loop diuretics against methacholine-induced bronchoconstriction in man.

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30

Stone, Patrick, Anna Kurowska, and Adrian Tookman. "Nebulized frusemide for dyspnoea." Palliative Medicine 8, no. 3 (July 1994): 258. http://dx.doi.org/10.1177/026921639400800315.

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31

Pickkers, Peter, Tom Dormans, and Paul Smits. "Direct vasoactivity of frusemide." Lancet 347, no. 9011 (May 1996): 1338–39. http://dx.doi.org/10.1016/s0140-6736(96)90990-3.

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32

Joannidis, Michael, Sebastian J. Klein, and Marlies Ostermann. "10 myths about frusemide." Intensive Care Medicine 45, no. 4 (January 14, 2019): 545–48. http://dx.doi.org/10.1007/s00134-018-5502-4.

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33

Chung, K. F., and P. J. Barnes. "Inhaled frusemide and asthma." Lancet 335, no. 8704 (June 1990): 1539. http://dx.doi.org/10.1016/0140-6736(90)93094-6.

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34

Panayiotou, BN, MVR Prasad, and MN Zaman. "FRUSEMIDE‐INDUCED BULLOUS PEMPHIGOID." International Journal of Clinical Practice 51, no. 1 (January 1997): 49–50. http://dx.doi.org/10.1111/j.1742-1241.1997.tb09626.x.

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35

Mizuma§, Takashi, Antony F. McDonagh, Emil T. Lin, and Leslie Z. Benet. "Photoinduced covalent binding of frusemide and frusemide glucuronide to human serum albumin." British Journal of Clinical Pharmacology 48, no. 1 (July 1999): 79–87. http://dx.doi.org/10.1046/j.1365-2125.1999.00970.x.

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36

Atherton, J. C., R. Green, S. Hughes, V. McFall, J. A. Sharples, L. R. Solomon, and L. Wilson. "Lithium clearance in man: Effects of dietary salt intake, acute changes in extracellular fluid volume, amiloride and frusemide." Clinical Science 73, no. 6 (December 1, 1987): 645–51. http://dx.doi.org/10.1042/cs0730645.

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1. The effects of amiloride and frusemide on lithium clearance were studied during changes in dietary sodium chloride intake and during infusion of 0.9% NaCl in normal human volunteers. 2. Lithium and fractional lithium clearances were less on the low than on the high salt diet. Values for the medium salt diet were intermediate. Acute extracellular fluid volume expansion with 0.9% NaCl infusion and extracellular fluid volume contraction 3–4 h after intravenous frusemide caused lithium and fractional lithium clearances to increase and decrease respectively. 3. Amiloride caused small changes in lithium and fractional lithium clearances on a low salt diet, but was without effect when salt intake was medium or high. 4. Increases in lithium clearance occurred immediately after frusemide irrespective of dietary salt intake and in subjects infused with 0.9% NaCl. Only in salt-depleted subjects did frusemide cause a substantial increase in fractional lithium clearance. Changes induced under other circumstances were small. 5. It is concluded that the lithium clearance method for assessment of proximal tubule salt and water re-absorption can be used with some degree of confidence in certain circumstances (medium and high salt intake as well as in acute volume expansion) but may not be reliable when dietary salt intake is low.

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37

Wood, AM, AT Dinh Xuan, G. Cremona, A. Lockhart, and TW Higenbottam. "The alpha 1-adrenergic agonist methoxamine and the "loop" diuretic frusemide reduce nasal potential difference." European Respiratory Journal 4, no. 7 (July 1, 1991): 802–6. http://dx.doi.org/10.1183/09031936.93.04070802.

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Pretreatment by inhalation with the alpha 1-adrenergic agonist methoxamine and the "loop" diuretic frusemide reduces the bronchial response to certain airway challenges in asthma. To test whether these drugs may act by altering airway epithelial ion and water transport, their effect on nasal potential difference (PD) when applied topically in eight normal volunteers was measured. For comparison, the effect of the Na(+)-channel blocking drug amiloride and the beta 2-adrenergic agonist salbutamol was also tested. Both methoxamine and frusemide significantly reduced PD: at the highest concentration given (10(-3) mol.l-1), there was a mean drop in PD from baseline of 39.5% following methoxamine treatment (p less than 0.05) and a mean drop of 30.2% following frusemide (p less than 0.05). Neither drug was as effective as amiloride, which caused a mean drop in PD of 27.5% from baseline at 10(-6) mol.l-1 and a drop of 71.6% at 10(-3) mol.l-1 (p less than 0.01 for each concentration). Salbutamol had no significant effect on PD (p greater than 0.05). We conclude that methoxamine and frusemide may derive their protective effect on some bronchial challenge, at least in part, from their effect on airway epithelial ion flux.

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38

Baggio, Bruno, Giovanni Gambaro, Francesco Marchini, Massimo Vincenti, Giulio Ceolotto, Achille C. Pessina, and Andrea Semplicini. "Abnormal Erythrocyte and Renal Frusemide-Sensitive Sodium Transport in Idiopathic Calcium Nephrolithiasis." Clinical Science 86, no. 3 (March 1, 1994): 239–43. http://dx.doi.org/10.1042/cs0860239.

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1. Anomalous transmembrane anion transport has been observed in erythrocytes of patients with idiopathic calcium nephrolithiasis. 2. To verify whether cation transport is also abnormal, we investigated the frusemide-sensitive Na+ efflux from Na+-loaded erythrocytes and the natriuretic response to acute intravenous frusemide administration in calcium oxalate renal stone formers. 3. Frusemide administration induced a statistically significant smaller increase in the fractional excretion of Na+ in patients than in control subjects. Abnormal kinetic properties of erythrocyte Na+-K+-2Cl− co-transport were observed in approximately 60% of stone formers. The Km for Na+ of Na+-K+-2Cl− co-transport correlated with urinary Ca2+ excretion. 4. The abnormal kinetic properties of Na+-K+-2Cl− co-transport may be relevant for stone formation, hampering renal Ca2+ reabsorption in the distal nephron and determining critical physicochemical conditions for calcium/oxalate crystallization.

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39

Reid, Ian A., and Lance Chou. "Effect of Blockade of Nitric Oxide Synthesis on the Renin Secretory Response to Frusemide in Conscious Rabbits." Clinical Science 88, no. 6 (June 1, 1995): 657–63. http://dx.doi.org/10.1042/cs0880657.

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1. The enzyme nitric oxide synthase is present in the macula densa and may participate in the control of renin secretion by the adjacent juxtaglomerular cells. In the present study, we investigated the effect of inhibiting nitric oxide synthase on the renin secretory response to frusemide, which stimulates renin secretion by blocking Na+-K+-2Cl− co-transport in the macula densa. 2. Injection of frusemide in 12 conscious rabbits elicited a transient increase in mean arterial pressure from 84 ± 2 to 92 ± 3 mmHg at 5 min (P < 0.01) and a sustained increase in heart rate from 246 ± 6 to 281 ± 10 beats/min at 45 min (P < 0.01). Plasma renin activity increased from 8.0 ± 1.2 to 14.3 ± 1.8, 12.4 ± 1.6 and 11.6 ± 1.5 pmol 2 h−1 ml−1 at 15, 30 and 45 min respectively (P < 0.01). There were no changes in plasma sodium and potassium concentrations or osmolality. 3. Inhibition of nitric oxide synthase with NG-nitro-l-arginine methyl ester increased mean arterial pressure by 9 mmHg, decreased heart rate and plasma renin activity, and markedly suppressed the renin response to frusemide (from 4.6 ± 0.7 to 7.6 ± 1.7, 4.7 ± 1.0 and 4.6 ± 0.7 pmol 2 h−1 ml−1 at 15, 30 and 45 min respectively). By contrast, infusion of an equipressor dose of phenylephrine did not suppress the renin response to frusemide. 4. Histochemical studies with the NADPH diaphorase technique confirmed the presence of nitric oxide synthase in the macula densa, and suggested that enzyme activity is increased by treatment with frusemide. 5. These results are consistent with a role for the l-arginine—nitric oxide pathway in the modulation of renin secretion by the macula densa.

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Brown, Mark A., Loretta Reiter, Alison Rodger, and Judith A. Whitworth. "Impaired Renin Stimulation in Pre-Eclampsia." Clinical Science 86, no. 5 (May 1, 1994): 575–81. http://dx.doi.org/10.1042/cs0860575.

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1. Pre-eclampsia is characterized by reduced plasma active renin concentration and renal prostacyclin production. The aim of this study was to determine whether the plasma active renin concentration could be stimulated in women with pre-eclampsia by intravenous frusemide, which stimulates renin acutely through a prostacyclin-mediated mechanism. 2. Plasma active renin concentration, plasma aldosterone concentration, haematocrit and urinary sodium, creatinine and 6-keto-prostaglandin F1α were measured before (0) and 15, 30 and 60 min after intravenous frusemide in 10 non-pregnant women, 10 normal pregnant women and nine women with pre-eclampsia. Six normal pregnant and six non-pregnant women underwent the same measurements after injection of 2ml of saline to control for effects of time and posture. 3. Baseline plasma active renin concentration (but not plasma aldosterone concentration) was lower in pre-eclamptic women [4.0 (1.7–6.2) pmol of angiotensin I h−1 ml−1; median (interquartile range)] than in normal pregnant women [6.7 (5.3–12.2) pmol of angiotensin I h−1 ml−1] (P < 0.05). Baseline urinary 6-keto-prostaglandin F1α/creatinine ratio, urinary sodium excretion and fractional sodium excretion did not differ between normal pregnant and pre-eclamptic women. 4. After frusemide, plasma active renin concentration rose significantly in non-pregnant (P = 0.002) and normal pregnant (P = 0.008) women, but not in women with pre-eclampsia. Individual results showed stimulation in all non-pregnant and normal pregnant women but in only six out of nine pre-eclamptic women, significantly fewer than in normal pregnancy (P < 0.05). The overall magnitude of the response of plasma active renin concentration to frusemide was blunted significantly in pre-eclamptic compared with normal pregnant women (P = 0.022). 5. Absolute and fractional sodium excretion and haematocrit rose significantly in all groups and the magnitude of change did not differ among groups for any of these parameters. The urinary 6-keto-prostaglandin F1α/creatinine ratio increased significantly only in non-pregnant women (P = 0.01), with variable individual responses in normal and hypertensive pregnant women. 6. This study shows that normal pregnant women exhibit natriuresis and stimulation of plasma renin after frusemide similar to that of non-pregnant women. However, pre-eclamptic women, as a group, have impaired renin stimulation after frusemide but a similar natriuresis to that of normal pregnant women. The mechanisms of these changes are unclear but are consistent with the notion of ‘exhausted’ renal renin in some women with pre-eclampsia.

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41

HAAS, Marijke, Frits MOOLENAAR, Dirk K. F. MEIJER, Paul E. DE JONG, and Dick DE ZEEUW. "Renal targeting of a non-steroidal anti-inflammatory drug: effects on renal prostaglandin synthesis in the rat." Clinical Science 95, no. 5 (November 1, 1998): 603–9. http://dx.doi.org/10.1042/cs0950603.

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1.Renal specific targeting of the non-steroidal anti-inflammatory drug naproxen was obtained by coupling to the low-molecular-mass protein lysozyme. A previous study showed that conjugation to lysozyme resulted in a 70-fold increase of naproxen accumulation in the kidney with a subsequent renal release of the active metabolite naproxen–lysine. 2.In the present study we questioned whether naproxen–lysozyme is active in the rat kidney, inhibiting the urinary excretion of prostaglandin E2 and renal sodium and water excretion in salt-restricted baseline conditions as well as during frusemide treatment. 3.A high dose of free naproxen (10 ;mg·day-1·kg-1) did not affect prostaglandin E2 excretion in baseline conditions (naproxen, 11±1 ;ng/8 ;h; vehicle, 13±4 ;ng/8 ;h), whereas sodium and water excretion were, respectively, 3.0 and 1.6 times lower in the naproxen group (P< 0.05). Naproxen completely prevented the frusemide-induced increase (3-fold) in prostaglandin E2 excretion (naproxen 6.6±1.1 ;ng/8 ;h, vehicle 40±12 ;ng/8 ;h, P< 0.005). Frusemide-stimulated natriuresis and diuresis were, respectively, 1.6 (P< 0.05) and 1.8 times (P< 0.005) lower in the naproxen group. 4.A dose of 2 ;mg·day-1·kg-1 lysozyme-conjugated naproxen did not affect prostaglandin E2 excretion in baseline conditions (conjugate, 18±2 ;ng/8 ;h; vehicle, 24±5 ;ng/8 ;h). The conjugate also had no effect on sodium and water excretion. However, the naproxen conjugate completely prevented the frusemide-induced increase (2-fold) in prostaglandin E2 excretion (conjugate, 16±3 ;ng/8 ;h; vehicle, 48±13 ;ng/8 ;h, P< 0.05). Surprisingly, frusemide-induced natriuresis and diuresis were not affected by the conjugate. 5.In conclusion, a renal specific delivery of the non-steroidal anti-inflammatory drug naproxen using lysozyme results in an inhibitory effect on renal prostaglandin E2 synthesis but does not affect the excretion of sodium and water, in contrast to free naproxen.

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42

Camuglia, Anthony, Darren Walters, and John Holmes. "Frusemide in the doctor’s bag." Australian Prescriber 35, no. 6 (December 1, 2012): 176–79. http://dx.doi.org/10.18773/austprescr.2012.082.

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43

Jennings, M., J. R. Shortland, and J. L. Maddocks. "Interstitial Nephritis Associated with Frusemide." Journal of the Royal Society of Medicine 79, no. 4 (April 1986): 239–40. http://dx.doi.org/10.1177/014107688607900416.

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Martin, P., V. Shah, and AJ Petros. "Aminophylline Increases Frusemide Induced Diuresis." Clinical Science 87, s31 (December 1, 1994): 10P. http://dx.doi.org/10.1042/cs045010pb_pt2.

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45

Lloyd, E. L. "FRUSEMIDE AND PREVENTION OF BRONCHOCONSTRICTION." Lancet 332, no. 8610 (September 1988): 564. http://dx.doi.org/10.1016/s0140-6736(88)92678-5.

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Canton, Antonio Dal, Giorgio Fuiano, Giuseppe Conte, Maurizio Terribile, Massimo Sabbatini, Bruno Cianciaruso, and Vittorio E. Andreucci. "Mechanism of increased plasma urea after diuretic therapy in uraemic patients." Clinical Science 68, no. 3 (March 1, 1985): 255–61. http://dx.doi.org/10.1042/cs0680255.

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1. To clarify why diuretic therapy raises plasma urea in patients with chronic renal failure, three groups of uraemic subjects were treated with frusemide for 6 days. 2. In group 1 (n = 9), frusemide significantly decreased body weight and increased average plasma urea from 18.7 mmol/l to 28.8 mmol/l (P<0.001). this rise in plasma urea was secondary to reduced urea excretion, which occurred in spite of an increase in urea filtration. 3. In group 2 (n = 7), frusemide was associated with salt replacement, in order to prevent salt depletion; in these patients neither reduction in urea excretion nor increase in plasma urea occurred. 4. In group 3 (n = 10), the marked diuretic-induced fall in urea clearance was found to be independent of enhanced proximal tubular re-absorption (measured in water diuresis). 5. These results show that the rise in plasma urea is due to increased tubular reabsorption of urea, presumably in the distal part of the nephron, secondary to extracellular fluid (ECF) volume depletion.

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Baldwin, DR, KL Grange, I. Pavord, and AJ Knox. "The effect of amiloride on the airway response to metabisulphite in asthma: a negative report." European Respiratory Journal 5, no. 10 (November 1, 1992): 1189–92. http://dx.doi.org/10.1183/09031936.93.05101189.

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Frusemide, a loop diuretic, has been shown to potently inhibit several indirect bronchoconstrictor challenges in asthma. The mechanism by which nebulized frusemide protects against indirect bronchoconstrictor stimuli in asthma is not known. One mechanism could be related to inhibition of sodium transport. If this is the case, then amiloride, another inhibitor of sodium transport, should also protect against indirect bronchoconstrictor challenges. Ten subjects with mild asthma were administered either 10(-2) M amiloride or placebo, by nebulizer, in a double-blind crossover fashion. After each inhalation, forced expiratory volume in one second (FEV1) was recorded at 10 min intervals for 30 min, after which a metabisulphite challenge was performed. No significant difference in the response to metabisulphite was seen between placebo and amiloride treatment. The mean difference in provocative dose of metabisulphite producing a 20% fall in FEV1 (PD20) between placebo and amiloride was 1.015 doubling doses, 95% confidence interval (95% CI) -0.201 to 2.231, (p = 0.09). This result does not support the hypothesis that frusemide is acting to protect against bronchoconstrictor challenges in asthma by an effect on sodium transport.

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UNWIN, R. J., S. J. WALTER, G. GIEBISCH, G. CAPASSO, and D. G. SHIRLEY. "Localization of diuretic effects along the loop of Henle: an in vivo microperfusion study in rats." Clinical Science 98, no. 4 (March 22, 2000): 481–88. http://dx.doi.org/10.1042/cs0980481.

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In order to clarify the effects on sodium reabsorption in the loop of Henle of methazolamide (a carbonic anhydrase inhibitor), chlorothiazide and the loop diuretics frusemide and bumetanide, superficial loops were perfused in vivo in anaesthetized rats and the individual diuretics were included in the perfusate. Differentiation between effects in the pars recta and in the thick ascending limb of Henle (TALH) was achieved by comparing responses to the diuretics when using a standard perfusate, designed to mimic native late proximal tubular fluid, and a low-sodium perfusate, designed to block net sodium reabsorption in the pars recta. With the standard perfusate, methazolamide caused decreases in sodium reabsorption (JNa) and water reabsorption (JV); with the low-sodium perfusate, a modest effect on JNa persisted, suggesting that carbonic anhydrase inhibition reduces sodium reabsorption in both the pars recta and the TALH. The effects of chlorothiazide were very similar to those of methazolamide with both the standard and low-sodium perfusates, suggesting that chlorothiazide also inhibits sodium reabsorption in the pars recta and TALH, perhaps through inhibition of carbonic anhydrase. With the standard perfusate, both frusemide and bumetanide produced the expected large decreases in JNa, but JV was also lowered. With the low-sodium perfusate, the inhibitory effects of the loop diuretics, particularly those of frusemide, were substantially reduced, while net potassium secretion was found. These observations indicate that a significant component of the effect of frusemide (and possibly of bumetanide) on overall sodium reabsorption is located in the pars recta, and that loop diuretics induce potassium secretion in the TALH.

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Higaki, Jitsuo, Toshio Ogihara, and Yuichi Kumahara. "Effects of frusemide and captopril on the relationship between biologically and immunologically active renin in human plasma." Clinical Science 75, no. 6 (December 1, 1988): 669–72. http://dx.doi.org/10.1042/cs0750669.

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1. The plasma renin concentration (PRC) and active renin concentration determined by radioimmunometric assay (ARC) were measured before and after administration of frusemide or captopril to normal volunteers. 2. Injection of 40 mg of frusemide followed by 1 h in the upright position significantly increased both PRC (P < 0.001) and ARC (P < 0.001). Oral administration of 50 mg of captopril also increased PRC (P < 0.05) and ARC (P < 0.05). 3. ARC and PRC were linearly correlated in the basal supine position [y = 0.635 x − 0.048 (y = PRC, x = ARC), r = 0.958, P < 0.001], after frusemide injection and standing (y = 0.800x + 0.359, r = 0.793,P < 0.02) and after captopril administration in the supine position (y = 0.938x − 0.555, r = 0.998,P < 0.001). 4. A cross-calibration study in which pure human renin was added to pooled plasma and PRC and ARC were measured showed linearity between the values obtained by the two methods. 5. The regression line for values of PRC and ARC in the supine position after captopril administration had a significantly greater slope (P < 0.001) and that for values after frusemide injection and standing was significantly elevated (P < 0.001) compared with the regression line for basal values in the supine position. 6. These results show that the biological activity of renin may be increased by various acute stimulations of renin to inappropriately high levels compared with the immunological activity. This implies that the mode of processing of human plasma renin may be altered by acute stimulation of renin. Furthermore, current methods for assay of plasma active renin may give erroneous values in various pathophysiological conditions.

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Ghosh, Amitava, and Prithviraj Chakraborty. "Formulation and Mathematical Optimization of Controlled Release Calcium Alginate Micro Pellets of Frusemide." BioMed Research International 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/819674.

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Objective. Frusemide loaded calcium alginate micropellets, an oral microparticulate delivery system, was statistically optimized exhibiting prolonged therapeutic action minimizing its adverse effects.Methods. Ionotropic Gelation technique was adopted employing 32Factorial designs and keeping the entire process free from organic solvents. Physicochemical and the release characteristics of the prepared formulations were studied, keeping variations only in sodium alginate (primary polymer) and Acrycoat E30D (copolymer) dispersion.Result. Sodium alginate was predominant over Acrycoat E30D in all batches. Nonadditives or interaction was observed to be insignificant. Multiple regressions produced second-order polynomial equation, and the predictive results obtained were validated with high degree of correlation. Thein vivostudy applauded that optimized calcium alginate micropellets of frusemide can produce a much greater diuretic effect over an extended period of 24 hours.Conclusion. This study reveals that the potential of a single dose of the mathematically optimized micro pellets of frusemide formulation is sufficient in the management of peripheral edema and ascites in congestive heart failure and as well in the treatment of chronic hypertension, leading to better patient compliance, and can be produced with minimum experimentation and time, proving far more cost-effective formulation than the conventional methods of formulating dosage forms.

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Journal articles on the topic 'Frusemide'

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