Search PubMed⌕ Search

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.

At least 631 records · Page 35Linked to original sources
PubMed1997

Sequential nephron blockade breaks resistance to diuretics in edematous states.

Diuretic therapy in edematous diseases often yields an inadequate natriuretic response ("diuretic resistance"). To study the functional changes in patients with congestive heart failure, liver cirrhosis with ascites, and nephrotic syndrome, characterized by a reduced effective arterial blood volume (EABV), different diuretic strategies were studied. It was shown that monotherapy with hydrochlorothiazide or furosemide was followed by an inadequate natriuretic response. Correlation of diuretic response with pretreatment fractional sodium excretion of the patient revealed a clear-cut interdependency: Those patients were resistant whose FENa+ was greatly below normal (<0.2%). In addition, it was found that the coadministration of the carboanhydrase inhibitor acetazolamide to diuretic therapy was very effective. We therefore conclude that an increase in proximal-tubular Na+ reabsorption is the major ("pharmacodynamic") determinant for diuretic resistance in edematous diseases with functional "underfilling" of the vascular tree. This alteration of the kidney can easily be overcome by coadministration of a carboanhydrase inhibitor (e.g., acetazolamide).

Acetazolamide↗
PubMed2005

Dominant role of prostaglandin E2 EP4 receptor in furosemide-induced salt-losing tubulopathy: a model for hyperprostaglandin E syndrome/antenatal Bartter syndrome.

Increased formation of prostaglandin E2 (PGE2) is a key part of hyperprostaglandin E syndrome/antenatal Bartter syndrome (HPS/aBS), a renal disease characterized by NaCl wasting, water loss, and hyperreninism. Inhibition of PGE2 formation by cyclo-oxygenase inhibitors significantly lowers patient mortality and morbidity. However, the pathogenic role of PGE2 in HPS/aBS awaits clarification. Chronic blockade of the Na-K-2Cl co-transporter NKCC2 by diuretics causes symptoms similar to HPS/aBS and provides a useful animal model. In wild-type (WT) mice and in mice lacking distinct PGE2 receptors (EP1-/-, EP2-/-, EP3-/-, and EP4-/-), the effect of chronic furosemide administration (7 d) on urine output, sodium and potassium excretion, and renin secretion was determined. Furthermore, furosemide-induced diuresis and renin activity were analyzed in mice with defective PGI2 receptors (IP-/-). In all animals studied, furosemide stimulated a rise in diuresis and electrolyte excretion. However, this effect was blunted in EP1-/-, EP3-/-, and EP4-/- mice. Compared with WT mice, no difference was observed in EP2-/- and IP-/- mice. The furosemide-induced increase in plasma renin concentration was significantly decreased in EP4-/- mice and to a lesser degree also in IP-/- mice. Pharmacologic inhibition of EP4 receptors in furosemide-treated WT mice with the specific antagonist ONO-AE3-208 mimicked the changes in renin mRNA expression, plasma renin concentration, diuresis, and sodium excretion seen in EP4-/- mice. The GFR in EP4-/- mice was not changed compared with that in WT mice, which indicated that blunted diuresis and salt loss seen in EP4-/- mice were not a consequence of lower GFR. In summary, these findings demonstrate that the EP4 receptor mediates PGE2-induced renin secretion and that EP1, EP3, and EP4 receptors all contribute to enhanced PGE2-mediated salt and water excretion in the HPS/aBS model.

Actins↗
PubMed1989

Diuretics in congestive heart failure.

Congestive heart failure (CHF) is a condition characterized by a number of hormonal and renal adaptations which together conspire to salt and water retention. Diuretic therapy has been, and continues to be, a cornerstone to therapy for CHF. The rational use of diuretics, or diuretic combination such as metolazone-furosemide, can both effectively administer to the congestive symptoms seen in heart failure as well as temper many of the complications of this therapeutic modality.

Diuresis↗
PubMedDate not supplied

[The hypoazotemic and diuretic action of lespeflan in acute kidney failure].

Hypoazotemic and diuretic effects of a new bioflavonoid drug lespephlan made in Russia have been tested in a dose 2 ml/kg to treat acute renal failure induced by mercury bichloride solution (a dose 2 mg/kg). The data were obtained on lespephlan ability to reduce blood levels of urea, creatinine and activate their renal elimination, to enhance diuresis, sodium clearance, glomerular filtration. Water and electrolyte release were also changeable by angiotensin aldosterone system. Mechanism of lespephlan hypoazotemic action is related to hepatic arginase inhibited activity as this enzyme plays a key role in detoxication of nitrous products urea and creatinine.

Acute Kidney Injury↗
PubMed1977

[Finding the effective dose of diuretics in man (author's transl)].

After a short survey of the classes of diuretics the procedures are described which are available to find effective doses of newly synthetized compounds in animal experiments. The method of Lipschitz and its modifications used for screening in rats are discussed in more detail. From the practical view of the clinical pharmacologist an explanation is given of the problems encountered in planning a study, balancing fluid- and electrolyte intake and in the suggestions for dose extrapolations to man. The experimental development in animals and healthy humans is demonstrated by means of the new diuretic compound Hoe 747. A synoptic graph showing the estimated dose-response curves emphazises the fact that it is possible to extrapolate the first dose in man from animal data with sufficient precision.

Animals↗
PubMed1983

[Various principles of treatment of hypertension with diuretics].

A scheme of prolonged continuous treatment has been developed for patients with essential hypertension (EH). It is based on the principle of differentiated application of the drug in individualized doses, and furosemide testing with subsequent switching to small doses of hypothiazide or some other diuretic agent conducive to the maintenance of the daily natriuresis/mean AP ratio at 1.9-2.0. A series of procedures are also proposed which prevent the development of refractory reaction to the drug or side-effects. The scheme was tested in the course of diuretic treatment of 110 in-patients with EH, stage IIA and IIB, of which 23 were subsequently treated for 6-12 months on an out-patient basis. It was noted that 22% of EH patients were highly sensitive to diuretics, 40-43% showed moderate sensitivity, so that 2-3 weeks' courses of small doses of beta-blockers or corinfar were needed 4-5 times a year to provide a good hypotensive effect, and 38-35% of patients showed poor sensitivity to diuretics and should preferably be treated with other hypotensive agents. The diuretic treatment according to the new regimen was associated with a reduced rate of side-effects.

Adult↗
PubMed1995

Central mu opioids mediate differential control of urine flow rate and urinary sodium excretion in conscious rats.

Central administration of the selective mu opioid agonist, dermorphin, produces a concurrent diuretic and antinatriuretic response in conscious rats. To determine whether central mu opioids differentially affect the renal excretion of water and sodium, we examined changes in renal function produced by intracerebroventricular (i.c.v.) administration of dermorphin during continuous intravenous (i.v.) infusion of a synthetic ADH analogue in conscious Sprague-Dawley rats. During ADH infusion the typical diuresis produced by i.c.v. dermorphin was abolished although the antinatriuresis remained intact. Alone, i.v. ADH produced a decrease in urine flow rate without significantly altering urinary sodium excretion. In other studies, the effects of i.c.v. dermorphin were examined on the renal responses produced by i.v. infusion of a V2-ADH receptor antagonist. In these studies the magnitude of the V2 antagonist-induced diuresis was not altered by i.c.v. dermorphin but the increase in urinary sodium excretion produced by this antagonist was converted to an antinatriuresis. Central dermorphin did not alter heart rate or mean arterial pressure in either study. These findings suggest that the effects of central dermorphin on renal sodium and water handling are mediated by separate mechanisms; the effects on water involving changes in circulating ADH levels and the effects on sodium independent of the action of this hormone.

Amino Acid Sequence↗
PubMedDate not supplied

Ultrasound-guided percutaneous nephrostomy in non-dilated pelvicaliceal system.

Percutaneous placement of nephrostomy catheters in patients with non-dilated pelvicaliceal systems remains problematic. We successfully performed ultrasound-guided percutaneous nephrostomies in 5 such patients after intravenous administration of a diuretic agent. Diuresis resulted in transient dilatation of the calyces, facilitating the procedures, which were performed under real-time sonographic guidance using the Seldinger technique. No complications were encountered.

Child↗
PubMed1995

Stereoselective renal effects of the loop diuretic ozolinone in the anesthetized dog.

The renal effects of i.v. injections of (+/-)-ozolinone, its enantiomers (-)-ozolinone and (+)-ozolinone and its prodrug (+/-)-etozoline, were compared with those of furosemide, in pentobarbital anesthetized dogs. Renal blood flow (electromagnetic flow-meter) and glomerular filtration rate (polyfructosan clearance) were assessed on the left denervated kidney together with renin secretion and urinary electrolyte excretion. (-)-Ozolinone (15.5 mg/kg i.v.) behaves as a stereoselective loop diuretic equipotent to 20 mg/kg of furosemide and 45 mg/kg of (+/-)-ozolinone; (+)-ozolinone induced only minor salidiuretic effects. Both ozolinone enantiomers markedly increased the renal blood flow and decreased the filtration fraction, suggesting that the vosodilating effect predominates on the efferent glomerular arterioles. (-)-Ozolinone also induced an acute rise in renin secretion. The inhibition of prostaglandin synthesis (indomethacin or meclofenamate) prevented renin hypersecretion in response to (-)-ozolinone and modified its salidiuretic effects but had no effect on the vascular response. The inhibition of the kallikrein-kinin system by aprotinin had no effect on the overall renal response to (-)-ozolinone. The inhibition of the renin-angiotensin system by captopril decreased blood pressure, prolonged the (-)-ozolinone-induced decrease in renal vascular resistance and increased renin secretion. Our results demonstrate that the loop diuretic, ozolinone, induces stereoselective and prostaglandin-dependent renin secretion, which is involved in the regulation of intra-renal hemodynamics.

Analysis of Variance↗
PubMed1962

Metabolic studies on patients with resistant heart failure treated by spironolactone.

Metabolic balance studies were carried out on five patients with resistant heart failure treated with spironolactone and other diuretics. Spironolactone alone had little effect. When it was used in a daily dose of 400-600 mg. in combination with hydrochlorothiazide 100 mg. daily, the results were excellent in two patients. One of these was still free of failure after 12 months on combined therapy. In the other patient the serum potassium became elevated after a good diuresis, though on subsequent intermittent therapy with the drug the patient remained well for 12 months. In two other patients administration of spironolactone had to be discontinued because of elevation of the serum potassium before a good diuresis could take place. The fifth patient died.Spironolactone can be a useful adjunct to the therapy of resistant heart failure, but there appears to be a real danger of causing the serum potassium to rise to toxic levels in patients so treated.

Diuresis↗
PubMed1986

Failure of indomethacin to impair the diuretic and natriuretic effects of the loop diuretic torasemide in healthy volunteers.

The effects of torasemide, a new potent loop diuretic, on renin release, water and sodium excretion were investigated in young healthy volunteers before and after 3 days of treatment with indomethacin. Torasemide 20 mg i.v. induced a rapid and biphasic increase both in plasma renin activity and plasma angiotensin II levels, which was almost completely abolished by pretreatment with indomethacin. Torasemide also increased urine volume, sodium excretion and, during the first hour after dosing, the creatinine clearance. None of the latter effects was impaired by indomethacin pretreatment. It is concluded that, like other loop diuretics, torasemide stimulates renin release by increasing renal prostaglandin production. However, at variance with what is observed with other loop diuretics, the diuretic and natriuretic effects of torasemide as well as the change in creatinine clearance do not appear to be inhibited by indomethacin.

Adult↗
PubMed1983

The possible mode of action of indapamide: a review.

It is not clear whether indapamide reduces blood pressure by a vasodilator or a diuretic action. This review attempts to answer this fundamental question. Cardiovascular studies show small increases in cardiac output, heart rate and stroke volume with a significant reduction in peripheral resistance. Indapamide, in vitro, directly inhibits pressor stimuli probably through a reduction of calcium flux in vascular smooth muscle, whilst diuretics are inactive. In vivo studies in man also show a reduction in sensitivity to pressor doses of noradrenaline and angiotensin without an increase in adrenergic sensitivity. However, indapamide does have mild diuretic activity at therapeutic doses, as shown by changes in plasma sodium, potassium, urea, uric acid and a reduction in body weight, but the changes are appreciably less than with thiazides. These results would suggest that indapamide has both diuretic and vasodilator properties. A low urinary excretion and specific accumulation into arterial smooth muscle of this lipophilic molecule may provide a rationale for this dual activity.

Benzothiadiazines↗
PubMedDate not supplied

[Mechanism of the diuretic action of epiphyseal extracts].

Experiments on dogs demonstrated that intravenous administration of the epiphysis extracts prevented the antidiuretic action of both the endogenous (traumatic stress) and exogenous (pituitrin) antidiuretic hormone (ADH). Injection of the extract into the renal artery gave a unilateral diuretic effect. The diuretic action of the preparation was eliminated by the block of the alpha-adrenergic receptors, whereas beta-adrenoblockers were ineffective. A conclusion was drawn that the mechanism of the diuretic action of the epiphysis extracts consisted in the competitive suppression of the ADH action at the renal tubules level on account of excitation of the alpha-adrenoceptors and inhibition of the adenylcyclase activity.

Animals↗
PubMed1988

Evidence for diabetogenic action of bumetanide in mice.

The effect of bumetanide on carbohydrate metabolism was studied in mice. Intraperitoneal injection of 50 or 100 mg bumetanide/kg body weight resulted in an acute and transient hyperglycaemia. Pretreatment with 240 mg probenecid/kg body weight reduced the diuretic effect but potentiated the hyperglycaemic effect of bumetanide (50 mg/kg body weight). The glucose tolerance was impaired, and there was an elevated serum glucose and glucose/insulin ratio 2 h after a single injection of bumetanide (100 mg/kg body weight). It is suggested that bumetanide has an acute effect on carbohydrate metabolism in mice that is not secondary to diuresis and that the reduced glucose tolerance may, at least in part, be due to a reduced capacity to secrete insulin.

Animals↗
PubMed2005

[Mechanism of action of xipamide and its classification as a "low ceiling diuretic". Pharmacodynamic-pharmacokinetic studies in healthy volunteers and in kidney and liver patients].

Xipamide (CAS 14293-44-8) shows structural features comparable with the thiazide- as well as the class of loop diuretics. According to earlier findings this diuretic, in contrast to the thiazides, should not decrease the glomerular filtration rate (GFR) and be effective even in patients with advanced renal failure. Therefore recently the question, which class of diuretics xipamide should be related to, has been increasingly discussed. In order to solve this issue, the diuretic effect of xipamide was assessed in healthy volunteers once without and once under strict water and salt restriction. Additionally, changes in GFR were monitored by means of measurement of the creatinine clearance. Kinetic parameters were determined in plasma and urine; further, in patients with liver cirrhosis, renal elimination kinetics of the diuretic were correlated with the concentration of direct plasma bilirubin, as a marker of cholestasis, at the beginning of a treatment with xipamide, 40 mg qd. The investigations proved that xipamide, like a typical thiazide diuretic, gives rise to a temporary decrease in GFR of about 30 %, provided the renin-angiotensin-aldosterone system of the volunteer is activated by previous salt and water restriction. Xipamide leads to an increase of K+ and Mg2+ excretion, but to a decrease of Ca2+ excretion in urine, a charactaristical feature of the thiazide-like diuretics. The correlation between Na+ excretion and drug excreted in urine over time showed a functional graph that is characteristic for a "low ceiling" thiazide diuretic. In patients with renal failure FE(Na) was increased when related to the GFR-adjusted drug excretion rate, whereas it was diminished in conditions with decreased effective circulating volume like in liver cirrhosis with ascites. It could be shown that the elimination kinetics of xipamide are determined by renal drug clearance, which proportionally decreases with GFR. In patients with liver failure, a decrease of non-renal drug clearance went along with an increase in urinary drug excretion. The amount of drug excreted in urine (Ae) proportionally increased with the concentration of the patients' direct plasma bilirubin. Thus, from a pharmacological as well as clinical point of view xipamide acts like a thiazide diuretic. As could be shown for other thiazides some time ago, xipamide is effective not only in patients with cardiovascular diseases, but also in those with advanced renal failure.

Bilirubin↗