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PubMed1981

Diuretic and cardiovascular effects of furosemide in rats.

Dose-response relationships of furosemide to its diuretic and cardiovascular actions and its effects on plasma renin activity (PRA) were evaluated in unanesthetized rats. A dose of 1 mg'kh-1 i.v. induced a small diuretic effect with no change in PRA. Furosemide at 5 mg'kg-1 provoked a clear diuretic effect (about 75) of the maximal effect) accompanied by a 20-25% plasma volume deficit but by only a twofold rise in PRA. Higher doses (10 and 40 mg.kg-1) induced a somewhat larger diuresis without further increases in plasma volume deficit or in PRA. Compared with the marked diuretic effect and plasma volume deficit, water intake increased only slightly (2 mL compared with the diuresis of 10 mL). Furosemide did not induce significant changes in blood pressure and heart rate, but it did alter the renin dependency of the blood pressure as assessed by Saralasin. These results indicate that furosemide has a steep dose-response curve for its effect on plasma volume and PRA; the relation is somewhat less steep for the diuretic action. Considering the large diuresis and plasma volume deficit, the changes in PRA and water intake induced by furosemide appear inappropriately small and suggest an inhibitory effect of furosemide on these parameters.

Animals↗
PubMed1976

[Haemodynamic changes in acute myocardial infarction following high doses of furosemide (author's transl)].

Haemodynamic measurements were carried out after administration of furosemide to 10 patients suffering from acute myocardial infarction and congestive heart failure. It was observed that a transient deterioration in cardiac function (decreased cardiac output, increased enddiastolic pulmonary arterial pressure and increased pulmonary and systemic resistance) occured in the pre-diuretic stage in these failing hearts. After the onset of diuresis the haemodynamic parameters showed a reversal of the previous trends (increased cardiac output, decreased enddiastolic pulmonary arterial pressure and pulmonary resistance). The consistently lower enddiastolic pulmonary arterial pressure in the diuretic phase as compared with the pre-diuretic value ensured an improvement in cardiac haemodynamics. An attempt was made to interpret the haemodynamic results in the light of the Frank-Starling's curve.

Acute Disease↗
PubMed1987

Modified method of diuresis renography for the assessment of equivocal pelviureteric junction obstruction.

Thirty-five hydronephrotic kidneys, in which diuresis renography showed either an equivocal (13) or non-obstructive (22) response pattern, were studied by a modified method in which intravenous frusemide was given 15 min before the start of the renogram so as to assess elimination during the period of maximum diuresis. Thirteen kidneys were identified as obstructed, including three in which the standard diuretic renogram appeared to exclude obstruction. These results indicate that the modified method increases the specificity of diuresis renography when used to assess patients with equivocal pelviureteric junction obstruction.

Adolescent↗
PubMed1992

Induction of water diuresis by endothelin in rats.

Experiments were performed in anesthetized rats to examine the possibility that endothelin (ET) modifies renal epithelial function in addition to its well-established hemodynamic actions. Infusion of ET-3 at rates between 34 and 178 ng.kg-1.min-1 was in many cases followed by a rise in urine flow and a persistent decrease in urine osmolality, whereas glomerular filtration rate (GFR) did not significantly change. The extent of ET-induced diuresis was dependent on the response of GFR: in rats in which ET-3 infusion caused a marked reduction of GFR (greater than 70%) ET-induced diuresis was not seen, even though urine osmolality still fell significantly. From animal to animal, ET-induced changes of urine flow or GFR did not correlate significantly with the rate of ET-3 infusion. ET-1, another ET isopeptide, also produced water diuresis when administered in GFR-neutral doses. Urinary excretion of total solutes and of sodium was not significantly altered by ET-3. Infusion of vasopressin blunted the diuretic effect of ET-3, whereas ET-3-induced water diuresis was not measurably altered by chronic or acute treatment with a converting enzyme inhibitor or by acute inhibition of prostaglandin synthesis. Induction of water diuresis was not secondary to an inhibition of vasopressin secretion since it could be demonstrated in homozygous Brattleboro rats in which antidiuresis was produced by the infusion of vasopressin at a rate of 200 microU.kg-1.min-1. These data suggest that ET may be an inhibitory modulator of the hydrosmotic action of vasopressin at the level of the renal collecting duct.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Vascular effects of loop diuretics.

Although it is generally believed that the beneficial effect of loop diuretics is the result of a rapid increase in diuresis, substantial evidence, from a large number of in vitro and in vivo experiments, has accumulated showing that administration of furosemide causes direct vascular effects, which probably contribute to its acute clinical effects. Several mechanisms are involved in the vascular response to loop diuretics. The role of the renin-angiotensin-adolsterone axis, prostaglandins and the direct vascular effects of loop diuretics on both the arterial and venous parts of the vasculature are discussed.

Animals↗
PubMedDate not supplied

Effect of inhibitors of prostaglandin synthesis on induced diuresis in cirrhosis.

The effect of inhibitors of prostaglandin synthesis on diuretic action was examined in patients with ascites due to chronic liver disease and in normal subjects. In patients with ascites, natriuresis after 80 mg i.v. furosemide was reduced 82% by pretreatment with indomethacin. Creatinine clearance was reduced only 16%. These effects were likely due to inhibition of renal prostaglandin synthesis, since urinary prostaglandin E2 fell and there was also reduction in natriuresis with naproxen (52%). The effects were not specific for furosemide since spironolactone-induced natriuresis was also reduced by indomethacin (82%), naproxen (52%), and aspirin (33%). In normal subjects, indomethacin reduced furosemide natriuresis by only 14% while creatinine clearance was not affected. The mechanisms of these drug interactions are uncertain but probably involve renal hemodynamics which appear to be supported importantly by renal prostaglandins in patients with ascites due to liver disease.

Adult↗
PubMed1989

Noncyclic vasopressin analogs are effective diuretics in conscious rats.

Linear vasopressin analogs lacking a cyclic hexapeptide ring have recently been reported to possess vasopressin antagonist activity. In conscious, chronically catheterized, euhydrated Sprague-Dawley rats, we have compared the effects of two noncyclic vasopressin analogs, peptide 1 ([1-admantaneacetic acid,2-(O-ethyl)-D-tyr,4-val,6-(2-aminobutyric acid),9-arg]arginine vasopressin) and peptide 2 ([1-propionic acid, 2-(O-ethyl)-D-tyr,4-val,6-(2-aminobutyric acid),9- arg]arginine vasopressin), with a cyclic arginine vasopressin antagonist (SK&F 105494; [1-des cysteine, cyclo(2-O-ethyl-D-tyrosine,6-L-(2-amino-6,6-cyclopentamethylene suberic acid], 4-valine,7-arginine,8-D-arginine, 9-des glycine]-vasopressin). All three analogs caused a dose-dependent increase in urine flow by increasing free-water clearance without significantly changing osmotic clearance or sodium excretion, indicating true functional vasopressin antagonism. Peptides 1 and 2 were as efficacious in inducing a diuresis as SK&F 105494. The order of diuretic potency among the three analogs in vivo was the same as the order of potency determined by in vitro binding to rat renal membrane homogenates, suggesting that the analogs exerted their diuretic effect by acting at renal vasopressin receptors. Thus, noncyclic vasopressin analogs, which are easier to synthesize then cyclic structures, could provide new strategies in the design of drugs for the treatment of water balance disorders.

Animals↗
PubMed1988

Suppression by nor-binaltorphimine of kappa opioid-mediated diuresis in rats.

The effects of nor-binaltorphimine (nor-BNI) and beta-funaltrexamine (beta-FNA) were studied on the diuretic activities in rats of several kappa opioid agonists including ethylketazocine, tifluadom, bremazocine and U50,488H. Nor-BNI suppressed the diuretic activity of all kappa agonists, whereas beta-FNA failed to alter the diuresis. On the other hand, beta-FNA treatment completely blocked the morphine-induced antidiuresis, whereas nor-BNI had no effect. The present data add further evidence that nor-BNI is a highly selective antagonist of kappa opioid agonists.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1988

[Experimental studies on the nephrotoxicity of cisplatin--amelioration of nephrotoxicity by continuous infusion].

To evaluate the preventive effect of continuous infusion on the nephrotoxicity of high-dose cisplatin (CDDP), the renal function was monitored in rabbits treated with this antineoplastic agent in various modes of administration. 131I-hippuran uptake of the renal cortical slices and histopathological examination as well as serum creatinine and BUN levels were used as parameters for assessing renal damage. When CDDP was administered at a dose of 3 mg/kg, continuous infusion showed a similar effect in the reduction of nephrotoxicity to the obtained from rapid infusion with mannitol diuresis. For the large dose of 6 mg/kg, only the combination of continuous infusion and mannitol diuresis significantly reduced the nephrotoxicity. When 3 mg/kg of CDDP was serially given once a week for 5 consecutive weeks, continuous infusion produced a similar or even more beneficial effect compared to rapid infusion with mannitol diuresis and maximum effect was observed in continuous infusion with concomitant mannitol diuresis. In conclusion, continuous infusion produced a similar effect compared to rapid infusion with mannitol diuresis and maximum effect was observed in continuous infusion with concomitant mannitol diuresis.

Animals↗
PubMedDate not supplied

Influence of methyldopa and bromocriptine on negative pressure breathing-induced diuresis.

The effects of methyldopa, a central alpha 2-agonist, and bromocriptine, a dopaminergic drug, on negative pressure breathing-induced diuresis were studied in the dog. Methyldopa (20 mg/kg i.v. during 20 min) or bromocriptine (0.3 mg/kg i.v.) suppressed the diuretic reflex without changing blood pressure. Since negative pressure breathing-induced diuresis is mainly due to an inhibition of vasopressin secretion, it is suggested that central alpha 2-adrenoceptors and dopaminergic receptors play an inhibitory role in mediating vasopressin release to non osmotic stimuli.

Animals↗
PubMed1995

Furosemide renal excretion rate and the effects of the diuretic on different tubular sites are modified by endogenous dopamine in normohydrated rats.

The present study was designed to explore the involvement of endogenous dopamine in furosemide excretion and in the actions of the diuretic on tubular sodium reabsorption. The dose-response relationship for the diuretic effect of furosemide given as i.v. bolus injections (0.2-7.5 mg.kg-1) was studied by clearance technique in pentobarbital-anesthetized rats treated with vehicle, benserazide (BZ) (25 mg.kg-1 i.v.) or SCH 23390 (50 micrograms.kg-1 + 10 micrograms.kg-1.min-1 i.v.). Furosemide induced the maximal diuresis 15 to 30 min after i.v. administration. The diuretic response was dose-dependent and was reduced in the animals treated with BZ and SCH 23390. Fractional sodium excretion was also increased by furosemide from 1.8 to 7.5% during the same period. This effect was reduced by both BZ or SCH 23390 by 35 to 50%. The effects of furosemide on proximal and distal renal tubules were dissected by measuring the renal lithium clearance (CLi+). Furosemide effective on proximal tubular sites (measured by FENa+ prox = CLi+/Cln) were completely abolished by BZ and SCH 23390, whereas both drugs reduced furosemide effects on distal tubular sites (measured by FENa+ distal = CNa+/CLi+) by 20 to 40%. Furosemide excretion rate during the peak response to the diuretic was measured in the urine. BZ and SCH 23390 diminished furosemide excretion by 45 to 80% as compared with vehicle-treated animals. The furosemide tubular effects and the proximal and distal functions measured by CLi+ determined during the peak response were correlated to the maximal excretion rate of furosemide in the urine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Study of the possible interactions of indoprofen on the diuretic effect of furosemide.

Twelve elderly in-patients undergoing chronic furosemide treatment (25 mg/day), with stable diuresis, were admitted to a cross-over, double-blind study to investigate the possible interactions between indoprofen and the diuretic. Indoprofen (200 mg t.i.d.) and identical placebo tablets were administered in randomized sequences for 4 days each. The sequence were preceded by a 4-day run-in observation period and followed by a 4-day follow-up. 24-hour urinary volume and the excretion of Na, K and endogenous creatinine were monitored, with serum Na, K, creatinine and creatinine clearance. Blood pressure and heart rate were measured and routine clinical blood chemistry tests and urinalysis were made for safety. The findings of this pilot study suggest that indoprofen does not alter the natriuretic action of furosemide; a tendency was noted towards a reduction of glomerular filtrate and urine volume, but the values after indoprofen were not significantly different from those after placebo.

Aged↗
PubMed1989

Attenuated diuretic and natriuretic effects of atrial natriuretic peptide in rats with heart failure.

Plasma levels of atrial natriuretic peptide (ANP) and renal responses to ANP were examined in rats with chronic cardiac failure produced by coronary artery ligation and in sham-operated controls. Plasma ANP levels were elevated in the rats with severe cardiac failure as compared with the controls (P less than 0.001). ANP injections at the doses of 1, 5, 25 and 50 micrograms/kg increased water and sodium excretion significantly at all but the lowest dose in the controls; only the two largest doses caused clear diuresis and natriuresis in the heart failure group. The diuretic and natriuretic effects of ANP were significantly weaker at the doses of 5 and 25 micrograms/kg in the rats with heart failure as compared with the controls. We conclude, that natriuretic and diuretic effects of ANP are attenuated in this chronic heart failure mode.

Animals↗
PubMedDate not supplied

Noradrenergic mechanisms in ethanol diuresis.

Neurotransmitter mechanisms that mediate the effect of ethanol on urine output were examined in male rats. To establish the neuronal systems involved in the diuretic action of ethanol, urine output was evaluated in animals pretreated with various pharmacological agents. The intraventricular administration of norepinephrine (1.5-12 micrograms) increased the diuresis produced by a 1.25 g/kg dose of ethanol. Clonidine (2.5, 5.0 micrograms), an alpha 2-receptor agonist, also increased ethanol diuresis, while the alpha 1-receptor antagonist phentolamine (14 and 35 micrograms) reduced it. beta 1,2-Adrenergic blocker propranolol (5 and 10 micrograms) significantly depressed ethanol-induced urine output. Conversely the beta 2,2-noradrenergic agonist isoproterenol (5 and 10 micrograms) increased the diuretic action of ethanol. On the other hand dopamine (4-20 micrograms) and serotonin (8 and 20 micrograms) had no effect on ethanol diuresis when given intraventricularly. These results indicate that the diuretic action of ethanol involves noradrenergic mechanisms.

Animals↗
PubMed2002

Impaired saline-stimulated diuresis and natriuresis in the conscious hypertensive glucose-intolerant rat.

BACKGROUND: A major complication of type 2 diabetes is renal dysfunction, a condition that worsens with coexistence of systemic hypertension. However, less is known regarding the renal impact of the prediabetic condition characterized by glucose intolerance. Therefore, we tested the hypothesis that chronic glucose intolerance leads to abnormal renal function, a condition also exacerbated by concurrent systemic hypertension. METHODS: A rat model of concomitant NaCl-sensitive hypertension and glucose intolerance was used to study renal function. Glucose intolerance was produced by administering streptozotocin to neonatal Wistar-Kyoto rats, and systemic hypertension was induced by combining dietary NaCl excess with unilateral nephrectomy. Hemodynamic and renal excretory responses were determined in conscious animals before and after administration of a 30-min isotonic saline challenge (5% of body weight, intravenously). RESULTS: Nine-month-old glucose-intolerant rats fed a normal NaCl diet did not manifest impairment in saline-stimulated diuresis and natriuresis. By contrast, 3-month-old glucose-intolerant rats fed a high NaCl diet displayed an exaggerated diuretic and natriuretic response to a saline challenge. Although saline-stimulated diuresis and natriuresis were enhanced in the hypertensive rats, they were reduced in the hypertensive glucose-intolerant animals. The reduction in renal excretory function of the latter group was caused by alterations in both glomerular function and tubular reabsorption of fluid and sodium. CONCLUSIONS: The coexistence of systemic hypertension and glucose intolerance result in impaired renal excretory function. This defect could be important, as hypertension can develop before the onset of overt type 2 diabetes.

Animals↗
PubMed1999

Changes of renal resistive index in response to hydration and diuretic administration in normal subjects and in patients with small ureteral stone.

The renal resistive index has been measured before and after hydration and administration of diuretics in persons with normal kidneys and in kidneys with small ureteral stone, either obstructing or nonobstructing, to assess induced flow changes and to identify features differentiating obstructing from nonobstructing stones. In normal kidneys the resistive index was normal (mean, 0.62+/-0.03); no changes in the resistive index occurred within 15 to 60 min after hydration alone, whereas the resistive index rose within 15 min after hydration plus administration of diuretics and then returned to initial values within 30 min. In both cases the resistive index decreased below basal values after 75 to 90 min. Similar changes were observed in kidneys with a nonobstructing ureteral stone. In kidneys with an obstructing ureteral stone the resistive index was higher than in normal subjects (mean, 0.73+/-0.02, P<0.01), increased further within 15 min after hydration and administration of diuretics (P<0.01), and remained higher than basal values during the following 90 min. In conclusion, different resistive index changes have been observed in response to hydration and diuretics in normal and obstructed kidneys. Duplex Doppler sonography and diuresis duplex Doppler sonography seem promising diagnostic tools to identify obstructing stones.

Diuretics↗
PubMed2002

[Urine levels of thiamine and riboflavine in diuretic therapy of patients with cardiovascular diseases].

Diuretic therapy entails decreased plasma concentrations of thiamine and riboflavine. Vitamins eliminated with urine more rapidly when diuresis accelerates. This process is not related to diuresis cause. A linear relationship exists between diuresis intensity and amount of eliminated thiamine and riboflavine. Thus it is shown that diuretic therapy provokes thiamine and riboflavine elimination from the body.

Diuretics↗
PubMed2006

Temporal diabetes- and diuresis-induced remodeling of the urinary bladder in the rat.

The natural history of diabetes mellitus-induced remodeling of the urinary bladder is poorly understood. In this study, we examined temporal remodeling of the bladder in diabetic and diuretic rats. Male Sprague-Dawley rats were divided into three groups: streptozotocin-induced diabetic, 5% sucrose-induced diuretic, and age-matched control. Micturition and morphometric characteristics were evaluated using metabolic cages and light-microscopic examination of the bladder 4 days and 1, 2, 3, and 9 wk after induction. Digital image analysis was used to quantify equatorial cross-sectional areas of bladder tissue and lumen, as well as relative content of the three primary tissue components: smooth muscle, urothelium, and collagen. Diabetes and diuresis caused significant increases in fluid intake, urine output, and bladder weight. In both groups, progressive increases were observed in lumen area from 4 days to 3 wk after induction and in wall area from 2 to 3 wk after induction. Wall thickness decreased within the first 2 wk in the diabetic and diuretic rats but returned to control at 3 and 9 wk. As a percentage of total cross-sectional area, smooth muscle area increased, urothelium area was unchanged, and collagen area decreased in diabetic and diuretic rats after 2-3 wk compared with control rats. In conclusion, diabetes and diuresis induced similar bladder remodeling. Diabetes-induced diuresis caused adaptive physical changes in rat bladder by 4 days after induction; remodeling was observed by 2-3 wk after induction and remained stable from 3 to 9 wk.

Animals↗