[Reversal of hepatorenal syndrome with oral misoprostol. Is the dose the key to the response?].
Explore the source record for details and available documents.
Administration, Oral↗
SEARCH · Search PubMed
Results for “DIURESIS AND DIURETICS”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[Salidiuretic and hypotensive action of Ribes-leaves (author's transl)].
Explore the source record for details and available documents.
Animals↗
Hemodynamic and natriuretic effects of bumetanide and furosemide in the cat.
Renal hemodynamic and natriuretic effects of bumetanide and furosemide were studied by clearance and micropuncture methods in cats. Furosemide (0.04-5.0 mg/kg i.v.) effects increased with increasing doses up to a maximal fractional sodium (FEna) and water (V/GFR) excretion of 23%. GFR and superficial single nephron GFR remained constant. Renal blood flow (RBF) increased up to 45% over control. A preferential increase in outer cortical RBF occurred at 5.0 mg/kg. Bumetanide (0.001-0.14 mg/kg i.v.) raised FEna and V/GFR maximally by 26%. Only at a supramaximal dose (0.69 mg/kg) did bumetanide raise RBF and depress filtration fraction. Probenecid (50 mg/kg i.v.) failed to block the natriuretic effect of bumetanide (0.025 microgram/kg-min) when infused into one renal artery but abolished the natriuretic action of furosemide (1.0 microgram/kg-min). Probenecid failed to displace the dose-response curve for bumetanide.
Animals↗
[Effect of intravenous infusion of polyosm preparation on diuresis and indices of systemic and cerebral hemodynamics].
Explore the source record for details and available documents.
Animals↗
[The role of the natriuretic hormone in the action of nifedipine and verapamil on the kidneys].
It was demonstrated in experiments on albino rats that under the effect of nifedipine and verapamil the increase in the excretion of electrolytes and water by the kidneys is accompanied with a rise in the natriuretic hormone (NUH) content in blood plasma and urine. This causes the renal effects of the drugs under study. The sensitivity of the kidneys to NUH increases in this case.
Animals↗
Influence of renal nerves and sodium balance on the acute antidiuretic effect of bendroflumethiazide in rats with diabetes insipidus.
To examine the role of the renal nerves and sodium depletion for the acute antidiuretic response to bendroflumethiazide (BFTZ; 25 microg/hr) in rats with diabetes insipidus (DI), renal clearance experiments were performed in the following groups of conscious, chronically instrumented male Brattleboro rats with vasopressin-deficient DI: Control (n = 7), BFTZ (n = 9), BFTZ + sodium replacement (n = 7) and BFTZ + chronic bilateral renal denervation (n = 6). Urine flow rate and urinary sodium concentration were measured drop-by-drop with a sodium-sensitive electrode and by collection of urine in vials placed on an electronic balance. This allowed computer driven, servo-controlled, independent i.v. replacement of sodium and fluid losses, respectively. Mean arterial pressure, glomerular filtration rate (GFR) and proximal tubular water and sodium handling, assessed by lithium clearance (C(Li)), were stable in the control group. BFTZ produced a marked antidiuretic response (deltaV = -79%; deltaUrine osmolality = +218%) associated with decreases in GFR (-28%), C(Li) (-62%), free water clearance (-100%) and plasma Na (-5 mM). Fractional water reabsorption was increased by 19% in the proximal tubules and by 7% in segments beyond. Sodium replacement did not modify the fall in GFR or the antidiuresis, but partly prevented the increase in fractional proximal water reabsorption. Bilateral renal denervation did not affect the response to BFTZ. We conclude that the acute antidiuretic effect of BFTZ is independent of sodium balance and renal nerve activity and is elicited by a reduction in GFR accompanied by an increase in fractional water reabsorption in the proximal tubules and in the distal nephron.
Animals↗
Obstruction score of ureteropelvic junction investigated by modified F-15 diuresis renography.
AIM: Introduction and assessment of an obstruction score in patients with obstructive uropathy, based on a diuresis renography time-activity curve. METHODS: Twenty-eight adults with unilateral pelviureteric junction obstruction were assessed by ultrasound scan, furosemide-enhanced intravenous urography and modified (F-15) 99mTc-DTPA diuresis renography. Renal unit drainage pattern was assessed by the obstruction score (sum of the time to peak, the index of excretion, and the tracer washout 40 min after furosemide administration). Renal units were classified as normal (0-3), equivocal (4-7) or obstructed (8-10). Renal function was determined by a split renal function and individual kidney glomerular filtration rate. The whole kidney minimum transit time was assessed as an interval on time scale between tracer input and output curve. RESULTS: After a 28-month mean follow-up, ultrasound findings were improved in 23 and unchanged in 5 patients. Regarding the response to furosemide, intravenous urography showed improvement in 19, no change in 8, and deterioration in 1 patient. The upper urinary tract on the affected side was obstructed in 26 and equivocal in 2 patients. Postpyeloplasty outcome was normal in 12 and equivocal in 16 cases. Overall drainage function was improved in 27 and unchanged in 1 patient. Parenchymal function was improved in 20, unchanged in 2, and deteriorated in 6 patients. Whole kidney minimum transit time was significantly reduced (5.55 +/- 1.56 to 4.41 +/- 0.83 min; p<0.001). CONCLUSION: The F-15 diuresis renography supplemented with the obstruction score system may be used for assessing the upper urinary tract urodynamics as initial diagnosis and in long-term follow-ups.
Adolescent↗
Standardization of diuresis renography techniques.
Explore the source record for details and available documents.
Adolescent↗
The effects of diuresis on the pharmacokinetics of the loop diuretics furosemide and torsemide in patients with heart failure.
PURPOSE: To evaluate the pharmacokinetics of furosemide and torsemide before and after diuresis in patients presenting with marked fluid overload. SUBJECTS AND METHODS: We studied 44 patients with New York Heart Association class III or IV heart failure, ejection fraction < or =40%, and an estimated excess fluid body weight > or =6.8 kg. Oral furosemide or torsemide was administered before and after diuresis. Pharmacokinetic parameters were assessed before and after diuresis. RESULTS: Following diuresis, maximum plasma concentration increased from 11.0+/-5.0 microg/mL to 13.9+/-6.8 with torsemide (P <0.05) and from 3.1< or =1.5 to 3.9+/-1.9 with furosemide (P=0.16). Maximum concentration increased by more than 30% in only one third of the patients. Total absorption (by area under the curve method) increased 6% among patients on torsemide (P=0.38) and 7% among patients on furosemide (P=0.63) and increased >30% in only 1 torsemide and 2 furosemide patients. The time to maximum concentration decreased from 1.40+/-.82 h to 0.81+/-0.36 with torsemide (P <0.01). There were no differences between furosemide and torsemide in the effects of edema on absorption. CONCLUSION: Marked diuresis altered the pharmacokinetics of both furosemide and torsemide in only a small percentage of patients. The use of adequate doses of oral diuretics in edematous patients may be successful, thereby permitting home treatment with oral diuretics and avoiding the cost of hospitalizations or home intravenous administration services.
Aged↗
Studies with the optically active isomers of the new diuretic drug ozolinone. II. Inhibition by d-ozolinone of furosemide-induced diuresis.
The effect of the non-diuretic dextrorotatory isomer of ozolinone on furosemide-induced diuresis was studied by means of clearance and micropuncture techniques in rats. After intravenous injection, d-ozolinone antagonized the furosemide-induced increase in renal fluid and electrolyte excretion in a dose-related manner. Microperfusion experiments of Henle's loop in vivo revealed that d-ozolinone did not interfere with the action of furosemide at this tubular site. However, d-ozolinone markedly decreased the furosemide to inulin clearance ratio, presumably as a consequence of inhibition of furosemide secretion into the proximal tubules. It is assumed that, in consequence of a high affinity for the proximal organic acid transport system, d-ozolinone depresses proximal tubular furosemide secretion and prevents transfer of this diuretic to the tubular fluid. Thus, under the influence of d-ozolinone, furosemide cannot reach the loop of Henle in sufficient amounts and its diuretic effect is blocked.
Animals↗
Effects of chlorothiazide, furosemide and PTH on Na+ and Ca2+ handling in isolated perfused kidneys of the spontaneously hypertensive rat.
The role of the kidney in a disturbed calcium metabolism in spontaneously hypertensive rats (SHR) was investigated. The hemodynamics of isolated perfused SHR kidneys were not basically altered compared to Wistar-Kyoto (WKY) control kidneys. Renal calcium handling by isolated perfused WKY and SHR kidneys at 12 weeks of age was not significantly different. In addition, the effects of chlorothiazide and furosemide on renal calcium handling were studied in isolated perfused kidneys from both rat strains. Both diuretics increased glomerular filtration rate, diuresis and excretion of sodium and calcium. However, both diuretics stimulated diuresis and calcium excretion significantly less in SHR than in WKY kidneys. The calciuric action of chlorothiazide was completely abolished by administration of human-parathyroidhormone (hPTH), while the natriuric effect was unchanged by hPTH. This observation suggests that a hypocalciuric action of chlorothiazide 'in vivo' is possibly mediated by PTH. Our study suggests that the kidney is not responsible for the disturbance in calcium metabolism in SHR. A surprising finding is that the SHR kidney was less responsive to the diuretics furosemide and chlorothiazide than the kidney of the WKY control.
Animals↗
The control of diuresis in the tsetse fly Glossina austeni: a preliminary investigation of the diuretic hormone.
The rate of secretion of the Malpighian tubules of Glossina austeni is controlled by a diuretic hormone. This hormone is present in the nervous tissue of the fly together with a degradative enzyme that can be activated by boiling. It is demonstrated that the Malpighian tubules are able to destroy the diuretic hormone; they may therefore participate in the control of diuresis. The diuretic hormone appears to be a heat-stable, non-dialysable, alcohol-soluble molecule, containing amino acid, glucose and sialic acid residues.
Animals↗
Attenuation of adrenomedullin-induced renal vasodilatation by NG-nitro L-arginine but not glibenclamide.
1. The present study was conducted in order to elucidate the in vivo contribution of nitric oxide (NO) and the glibenclamide-sensitive potassium channel in the renal action of adrenomedullin in anaesthetized dogs. 2. Intrarenal arterial infusion of adrenomedullin (20 ng kg-1 min-1) elicited a pronounced increase in renal blood flow with no changes in systemic blood pressure. The renal vasodilator action of adrenomedullin was markedly attenuated by pretreatment with NG-nitro L-arginine (L-NOARG), but this was reversed by continuous infusion of L-arginine. 3. Pretreatment with glibenclamide almost completely blocked the renal vasodilatation induced by lemakalim, but had no effect on the renal vasodilator and diuretic action of adrenomedullin. 4. Intrarenal arterial infusion of adrenomedullin induced diuresis and natriuresis. Diuretic and natriuretic action of adrenomedullin was also attenuated by L-NOARG. L-Arginine partly reversed the effect of L-NOARG and adrenomedullin-induced diuresis and natriuresis. 5. These data indicate that the in vivo renal vasodilator action of adrenomedullin is mediated by the release of NO. The glibenclamide-sensitive potassium channel is not involved in the renal action of adrenomedullin, at least, not in anaesthetized dogs. Since the inhibition of L-NOARG of adrenomedullin-induced diuresis occurred concomitantly with the attenuation of the renal vasodilator action of adrenomedullin, direct involvement of NO in adrenomedullin-induced diuresis remains to be established.
Adrenomedullin↗
Expression of aldose reductase, sorbitol dehydrogenase and Na+/myo-inositol and Na+/Cl-/betaine transporter mRNAs in individual cells of the kidney during changes in the diuretic state.
The effect of changes in medullary extracellular tonicity on mRNA expression for aldose reductase (AR), sorbitol dehydrogenase (SDH), Na+/Cl-/betaine (BGT) and Na+/myo-inositol (SMIT) cotransporter in different kidney zones was studied using Northern blot analysis and non-radioactive in situ hybridization in four groups of rats: controls, acute diuresis (the loop diuretic furosemide was administered), chronic diuresis (5 days of diuresis), and antidiuresis [5 days of diuresis followed by 24 h deamino-Cys1, d-Arg8 vasopressin (dDAVP)]. Acute administration of the loop diuretic furosemide significantly reduced AR, SMIT and BGT gene expression in the inner and outer medulla compared with controls. Administration of dDAVP to chronically diuretic rats raised the expression of these three mRNAs in the inner but not the outer medulla compared with the chronically diuretic rats. None of these alterations in medullary tonicity significantly changed SDH expression. The in situ hybridization studies showed AR, BGT and SMIT mRNAs to be expressed in both epithelial and non-epithelial cells of the outer and inner medulla. The various cell types (epithelial, endothelial and interstitial cells) differed in their expression pattern and intensity of AR, SDH, BGT and SMIT mRNA, but the inner medullary cells responded uniformly to a decrease in extracellular tonicity with a reduction, and to an increase with enhancement of their AR, BGT and SMIT expression.
Aldehyde Reductase↗
Has the anti-diuretic hormone a role in the diuresis from stimulation of atrial receptors.
Explore the source record for details and available documents.
Animals↗
Diuresis and pulmonary function in premature infants with respiratory distress syndrome.
A prospective study of 99 premature infants with severe respiratory distress syndrome who were randomly assigned to receive diuretic treatment with either furosemide or chlorothiazide was analyzed to examine the relationship of diuretic administration and diuresis to survival and to the duration and degree of mechanical ventilatory support. Subjects were given a diuretic, usually beginning on the second or third day of life, if they had not initiated the expected spontaneous diuresis and did not show pulmonary improvement. Infants given furosemide experienced a postnatal weight loss nearly identical to that in infants who were deemed not to need a diuretic; infants given chlorothiazide lost weight more slowly and had significantly greater body weight on postnatal days 4 and 5. Four factors were independently correlated with improved survival: furosemide usage, high birth weight, low initial mean airway pressure, and the absence of intraventricular hemorrhage. Ventilator mean airway pressure on the seventh day of life and duration of mechanical ventilation were both related to diuresis. These data provide additional evidence for the importance of water homeostasis in determining the course of respiratory distress syndrome in premature infants and indicate that furosemide administration is beneficial when spontaneous diuresis does not occur. Furosemide may be particularly effective if combined with early closure of the ductus arteriosus.
Chlorothiazide↗
[Value of aldosterone receptor blockade in diuretic therapy of patients with chronic heart failure].
PATHOGENESIS: All forms of chronic heart failure (high-output and low-output failure) are accompanied by an "arterial underfilling" inducing the activation of various neurohumoral systems (renin-angiotensin-aldosterone system, sympathic nervous system, non-osmotic stimulation of vasopressin). Elevated levels of those neurohormones detrimentally modulate renal function. Subsequently, renal salt and volume retention occurs leading to the main symptoms of heart failure, edema formation and dyspnea. DIURETIC THERAPY: Diuretics, which have been discovered more than 40 years ago, beneficially influence renal salt- and volume retention by their effects on tubular sodium reabsorption. While thiazides are recommended in mild forms, loop diuretics are used in severe stages of congestive heart failure. The clinician has to consider the changed pharmacokinetic and -dynamic properties during the application of diuretics in patients with chronic heart failure. In addition, increased sodium reabsorption occurs immediately after cessation of diuretic action often nullifying the preceding diuresis. Thus, salt- and volume restriction should be guaranteed, and a regular application of loop diuretics during the day should be preferred due to the short-acting nature of currently available loop diuretics. Sometimes, diuresis does not longer occur during the treatment with one substance (diuretic resistance), although the therapeutic goals of water excretion have not been achieved. After ruling out factors reducing the actions of diuretics (non-compliance, hyponatremia, etc.), a sequential nephron blockade should be initiated (combination of loop diuretics and a thiazide or an aldosterone-receptor antagonist) to increase diuresis and to elevate symptoms of volume overload. SIDE EFFECTS: Loop diuretics and thiazides often induce mild hypokalemia, which has been demonstrated to be not as benign as thought before. Chronic treatment with oral potassium supplements has several drawbacks, as urine excretion of potassium is subsequently increased and supplementation is not as effective as believed. Diuretic-induced hypokalemia seems to be aldosterone dependent. As aldosterone levels increase during diuretic therapy even during chronic treatment with an angiotensin-converting enzyme (aldosterone-escape) a combined treatment including an aldosterone-receptor antagonist has been suggested. Beneficial effects of aldosterone-receptor blockade on mortality (RALES trial) appear to be mediated be extrarenal and renal mechanisms. The suggested beneficial renal mechanisms of aldosterone receptor blockade are discussed in detail in the review. CONCLUSION: In conclusion, diuretic therapy of patients with congestive heart failure is effective to relieve symptoms and, presumably, to prolong life. As renal function and pharmacokinetics and -dynamics of diuretics are changed in heart failure, diuretic treatment has to be adapted to provide optimal treatment. Increased levels of aldosterone appear to play an important role in diuretic-induced hypokalemia, and in the progression of heart and renal failure. Thus, aldosterone receptor antagonists should be used in the treatment of heart failure more frequently.
Benzothiadiazines↗