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PubMed1984

Renal PGs in essential hypertension; the role of water-electrolyte shifts in their metabolism.

Reduced PG formation in the renal vascular bed and urinary tract with increased PGF2 alpha/PGE2 ratio and altered PG response to acute and chronic salt loads were revealed in 100 patients with EH of different severity. The experiment on 70 rats has shown that the above changes in renal PG can be related to the increased Na concentration in the renal parenchyma resulting in decreased biosynthesis of both PGs in the kidneys and increased PGE2 transformation into PGF2 alpha. Renal PG changes are reversible after sodiumuresis and diuresis induced by various diuretics and other agents. The role of renal prostaglandins (PG) in the pathogenesis of essential hypertension (EH) and regulation of water-electrolyte metabolism has been studied for many years (B. Scherer et al., B. Lee et al., K. Abe et al., J.C. McGiff et al.). Reduced urinary PGE2 excretion was observed in patients with elevated blood pressure, while normotensive rats and healthy subjects on a low salt diet, treated by furosemide, showed PGE2 excretion increase. Salt loads, according to different authors, reduced, increased or caused no changes in urinary PGE2 excretion, with PGE2-9-ketoreductase activity increased. The aim of the present paper was the study of PGE2 and PGF2 alpha content in renal veins, their urinary excretion, biosynthesis and renal metabolism. The study was performed on patients with EH and on experimental rats at different salt loads.

Adult↗
PubMed1998

Local and systemic consequences of severe ischemia and reperfusion of the skeletal muscle. Physiopathology and prevention.

Revascularization of a limb after a severe and prolonged period of ischemia may be associated with high rates of mortality and amputation, because of the development of a postrevascularization syndrome, regardless the cause of occlusion (ischemia, trauma, iatrogenic) or the methods used to achieve reperfusion (fibrinolysis, surgery, resuscitative therapy). This "revascularization" syndrome includes several complications, both local (explosive swelling of the limb, compartment syndrome and skeletal muscle infarction (rhabdomyolysis) and general (acidosis, hypercalcemia, hypovolaemic shock, renal, hepatointestinal and pulmonary failures, arrhythmias and cardiac arrest (multiple organ dysfunction). Current therapies are directed against complications after they occurred, once revascularization is completed: fasciotomy, mannitol and diuretics administration for forced diuresis, fluid administration to correct hypovolaemia, use of resins, insulin and glucose or haemodialysis to deal with hypercalcemia, administration of buffers (THAM, bicarbonate) to correct acidosis, control of hypercalcaemia with orthophosphates and calcitonin.... Nevertheless, a substantial percentage of the injury is generated upon reperfusion and the muscle may remain viable after prolonged period of ischemia. Intra and extraacellular swelling, tissue acidosis, free radical mediated damage, loss of adenine nucleotide precursors, and intracellular calcium overload have been suggested to be the mechanisms responsible for reperfusion injury. Careful control of both the composition and the physical conditions of the initial reperfusion (controlled reperfusion) may result, in selected cases, in improvements in the metabolism, structure and function of the limb after reperfusion.

Acute Kidney Injury↗
PubMedDate not supplied

[Tolerance of chest-to-back [+Gx] and head-to-feet [+Gx] acceleration in drug-induced hypohydration].

The effect of drug-induced hypohydration (furosemide, 40 mg per os) on the tolerance of chest-to-back (+Gx) and head-to-feet (+Gz) acceleration was investigated in 9 healthy male test subjects, aged 25-45 years. The test subjects were rotated in a 7.5 m arm centrifuge. The first exposure during which they were centrifuged at 4 G (+Gx and +Gz) served as a control. The second time they were exposed to centrifugation after diuretic administration. Prior to second exposure, the subjects showed increased diuresis (5.7 +/- 0.7 ml/min) and increased excretion of osmotically active compounds, including electrolytes. This led to a decrease of the circulating blood volume by 7.0 +/- 1.8% on an average. During centrifugation the following parameters were recorded: electrocardiogram, blood pressure in the arm and ear lobe vessels, ear pulsogram, and pneumogram. After diuretic intake +Gx tolerance remained essentially unchanged whereas +Gz tolerance was good but required greater efforts. It is concluded that moderate diuretic-induced hypohydration did not result in a drastic deterioration of acceleration tolerance.

Acceleration↗
PubMed1986

Morphological changes in the renal macula densa during natriuresis and diuresis.

Morphological changes in the macula densa have been studied during the infusion of diuretic agents into the renal artery of anesthetized dogs. The kidneys were fixed by rapid high pressure perfusion with glutaraldehyde. Large basolateral intercellular spaces were seen between macula densa cells in control kidneys, but the number and extent of these spaces were strikingly reduced during the natriuresis and diuresis induced by the infusion of frusemide, ethacrynic acid or mannitol. Natriuresis and diuresis produced by the intravenous infusion of large volumes of 0.9% NaCl solution also resulted in closure of these spaces. No simple relationship existed between changes in plasma renin activity and closure of the spaces between macula densa cells during these procedures. A distinctive, membrane-bound, vesicle-containing structure was identified between the basolateral processes of the cells of each macula densa; the function of this structure awaits elucidation. We suggest that changes in the size of the basolateral intercellular spaces of the macula densa reflect changes in fluid flux between the distal tubule and the interstitium of the juxtaglomerular apparatus.

Animals↗
PubMed2004

[Role of prostaglandin E2 in regulation of urine excretion in saluresis, water and osmotic diuresis in rat].

In the saluresis, water and osmotic diuresis were indicating an increase of prostaglandin E2 excretion and a correlation between this index and diuresis. Unselective blockade of cyclooxygenase by diclofenac-natrium leads to a decrease of diuresis in the observed types of urine-production in rats. Inhibition of inducible cyclooxygenase by celebrex didn't change the value of diuresis after water load or administration of osmotic agent, but decreased the diuretic effect of furosemide.

Animals↗
PubMed1991

Renal dynamics after pyeloplasty.

Dismembered pyeloplasty was done on 12 renal units for ureteropelvic junction obstruction. Postoperatively, response of repaired kidney to standard diuretic dose of furosemide (0.3 mg/kg) was evaluated. Also renal pelvic pressures at rest and during diuresis were measured. All renal units responded to the diuretic by increasing their urine output an average of three times over baseline value. Renal pelvic pressure registration revealed no significant change after diuresis over baseline values. Diuretic technetium-99 DTPA renal scans were obtained two to six months postoperatively and compared with preoperative scans; the best results were obtained in renal units whose intrapelvic pressures did not exceed 10 cm of water in the immediate postoperative period.

Female↗
PubMed1991

[Effect of flavonoid fractions of Solidago virgaurea L on diuresis and levels of electrolytes].

The flavonoid fractions of Solidago virgaurea L.S. gigantea Ait., S. canadensis var. canadensis and S. canadensis var. "scabra" flowers were administrated p.o. to rats and showed diuretic activity. Increase in overnight diuresis reached 57-88%. Decrease of overnight excretion of potassium and sodium also occurred after administration of form examined fractions. The flavonoids from S. virgaurea and S. canadensis var. canadensis caused increased excretion of calcium with urine.

Administration, Oral↗
PubMed2006

Distribution, activity and evidence for the release of an anti-diuretic peptide in the kissing bug Rhodnius prolixus.

In the haematophagous insect Rhodnius prolixus, diuresis is accomplished through the combined actions of peptidergic diuretic hormones and 5-HT released from neurohaemal sites on the abdominal nerves. Preliminary work on anti-diuresis in this blood-feeder, previously believed to occur through a decrease in the levels of the diuretic factors, indicates that an anti-diuretic hormone, with properties similar to CAP2b (pELYAFPRVamide; recently renamed Mas-CAPA-1), might also be present in R. prolixus. Here, we present evidence from immunohistochemical analysis that suggests a PRXamide-like neuropeptide may be released from the abdominal neurohaemal sites beginning 3-4 h following feeding; a time that coincides with the cessation of diuresis. We also show evidence for an endogenous factor, isolated from the central nervous system using reversed-phase high performance liquid chromatography, which mimics the effects of Mas-CAPA-1. Specifically, this endogenous anti-diuretic factor inhibits rates of 5-HT-stimulated secretion in a dose-dependent manner and elevates intracellular cGMP levels of Malpighian tubules stimulated with 5-HT.

Animals↗
PubMed1961

Diuresis in rats: effects of sympathomimetic and sympathetic blocking agents.

Dopamine and tyramine possess diuretic properties resembling but weaker than those of noradrenaline in the rat. These three amines produce a relatively smaller loss of sodium than does adrenaline. Bretylium shows a diuretic action which is apparently associated with its sympathomimetic properties and which is antagonized by phenoxybenzamine. However, bretylium causes a relatively greater loss of potassium and chloride than do the sympathomimetic amines. A slight antidiuretic action is shown by bretylium after its diuretic effect has subsided and a similar effect is produced by BW 172C58, which has relatively weak sympathomimetic properties. In contrast to these adrenergic neurone blocking agents, phenoxybenzamine and a ganglion blocking agent (pentacynium) show powerful antidiuretic effects. These observations are consistent with the view that the adrenal medulla has an important role in facilitating water diuresis in rats.

Adrenergic Agents↗
PubMed1993

Diuretic action of potassium channel blockers.

The availability of specific potassium channel blockers has made it possible to examine their effects along the nephron on fluid and electrolyte excretion. Recent experiments indicate that they modulate transepithelial sodium and potassium transport. In the thick ascending limb, potassium channel blockers, by interfering with potassium recycling across the apical cell membrane, reduce the activity of the sodium-2chloride-potassium cotransporter. In the initial and cortical collecting duct their inhibitory action on ATP-sensitive potassium channels reduces potassium secretion. Accordingly, tissue-specific potassium channel blockers are promising diuretic agents that may induce diuresis by inhibiting tubular sodium transport with only minimal loss of potassium.

Animals↗
PubMed1963

EFFECT OF AN ALDOSTERONE ANTAGONIST (SPIRONOLACTONE) ON PATIENTS WITH SEVERE CONGESTIVE HEART FAILURE.

Spironolactone was evaluated as a diuretic in the therapy of six patients with chronic severe congestive heart failure, during which metabolic balance studies were performed. Two of the patients showed a clear-cut although moderate diuresis and natriuresis in response to spironolactone in the presence of other diuretics. Two patients had slight unsustained responses and two showed no response. No significant change in potassium excretion was observed. A decrease in the serum sodium level was noted in four patients, associated with a rise in serum potassium. Urinary aldosterone excretion was normal or low in all patients and showed no correlation with the diuretic response to spironolactone.It is concluded that spironolactone has definite but limited usefulness in the therapy of some but not all patients with chronic congestive heart failure.

Aldosterone↗
PubMed1986

Guidelines for rational diuretic use in the elderly.

The elderly not only have lower body stores of potassium, but also tend to eat a diet relatively low in potassium content. Loss of muscle strength, constipation and mental apathy are all features of potassium deficiency. In addition, serious arrhythmias have been attributed to hypokalaemia and must therefore be prevented. While potassium supplements may replete body potassium stores, they often require large amounts and may still be ineffective in preventing diuretic-induced hypokalaemia. Thus, several guidelines for the rational and safe use of diuretics in the elderly have been proposed including in addition to potassium supplementation, the determination of dietary and total body potassium sources, dosage of the diuretic and intensity of the diuresis, and the relationship between potassium and calcium and magnesium.

Aged↗
PubMed1986

The adenosine receptor antagonist, 8-phenyltheophylline, causes diuresis and saliuresis in the rat.

The diuretic and adenosine antagonist actions of two alkylxanthines have been compared in the conscious rat. 8-Phenyltheophylline (10 mg kg-1) antagonized adenosine-induced bradycardia in the rat for at least 3 h whereas enprofylline (10 mg kg-1) had no effect on this response. 8-Phenyltheophylline (10 mg kg-1) evoked diuresis and saliuresis in the rat whereas enprofylline (10 mg kg-1) had no effect on excretory parameters. These results indicate that the diuretic action of some alkylxanthines may be related to adenosine antagonism.

Adenosine↗
PubMed1964

RESPONSE OF THE INFANT KIDNEY TO DIURETIC DRUGS.

The diuretic response of normal infants, 6 to 47 days of age, to single doses of mercaptomerin, chlorothiazide, acetazolamide, triamterene and spironolactone was studied by following urinary electrolytes, pH and osmolality. Peak diuresis occured two to four hours after drug administration, and because of compensatory mechanisms little change in urinary excretion was found if only 24-hour urines were studied. Mercaptomerin increased sodium excretion seven-fold, compared to three- to four-fold increases for the other diuretics. Control urinary Na:K ratios averaged 0.68 in infants compared to 2.8 for adults, and mercaptomerin produced the largest increase in this ratio. Qualitatively the response to diuretics is the same in newborn in the ages studied as it is reported to be for adults; no immaturity of the infant kidney in this regard was demonstrated.

Acetazolamide↗
PubMed1999

Clinical consequences of the biphasic elimination kinetics for the diuretic effect of furosemide and its acyl glucuronide in humans.

This review discusses the possibility of whether furosemide acyl glucuronide, a metabolite of furosemide, contributes to the clinical effect of diuresis. First an analytical method (e.g. HPLC) must be available to measure both parent drug and furosemide acyl glucuronide. Then, with correctly treated plasma and urine samples (light protected, pH 5) from volunteers and furosemide-treated patients, the kinetic curves of both furosemide as well as its acyl glucuronide can be measured. The acyl glucuronide is formed in part by the kidney tubules and it is possible that the compound is pharmacologically active through inhibition of the Na+/2Cl-/K+ co-transport system; up to now the mechanism of action has been solely attributed to furosemide. The total body clearance of furosemide occurs by hepatic and renal glucuronidation (50%) and by renal excretion (50%). Enterohepatic cycling of furosemide acyl glucuronide, followed by hydrolysis, results in a second and slow elimination phase with a half-life of 20-30 h. This slow elimination phase coincides with a pharmacodynamic rebound phase of urine retention. After each dosage of furosemide, there is first a short stimulation of urine flow (4 h), which is followed by a 3-day recovery period of the body. The following clinical implications arise from study of the elimination kinetics of furosemide. Repetitive dosing must result in accumulation of the recovery period. Accumulation of furosemide and its acyl glucuronide in patients with end-stage renal failure results from infinite hepatic cycling. Impaired kidney function may result in impaired glucuronidation and diuresis. While kidney impairment normally requires a dose reduction for those compounds which are mainly eliminated by renal excretion, for diuretics, a dose increment is required in order to maintain a required level of diuresis. The full clinical impact of the accumulation of furosemide and its acyl glucuronide in patients with end-stage renal failure has to be determined.

Chromatography, High Pressure Liquid↗
PubMed1976

Effect of chlorothiazide and furosemide diuresis on in vivo growth of Staphylococcus aureus in kidneys of mice.

In mice subcutaneous administration of the diuretics chlorothiazide or furosemide resulted in a prompt diuresis characterized by production of dilute urine within 30 min and lasting for 6 hr. In vivo proliferation or clearance of Staphylococcus aureus from the kidneys was only temporarily impaired during the time of maximum diuresis. When treatment was delayed until after phagocytosis was initiated, there was no effect on clearance. Clinically it would appear that bacterial proliferations in the renal parenchyma would not be promoted as a consequence of diuretic treatment.

Animals↗
PubMed1981

Human plasma vasopressin response to potent loop-diuretic drugs.

To investigate the effect of potent loop diuretic drugs on the factors that control water excretion, immunoreactive plasma arginine vasopressin was measured at regular intervals for 6 h after intravenous administration of frusemide (40 mg) and piretanide (12 mg) in healthy adults. Despite a large diuresis there was no significant rise in plasma vasopressin compared to controls. Diuretic drug treatment caused small increases in plasma osmolality comparable to the control group, but no change in mean arterial blood pressure. The fall in blood volume of 7% within 1 h of frusemide administration was insufficient to stimulate vasopressin secretion. We conclude that loop diuretic drugs in the dose given have little effect on plasma vasopressin and osmolality but cause a small fall in blood volume in healthy adults.

Adult↗