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At least 1,765 records · Page 98Linked to original sources
PubMed1978

Effects of intracerebroventricular prostaglandins E2 and F2alpha on the urine outflow, and a possible role of pgE2 as a modulator.

Effects of intracerebroventricularly (i.c.v.) injected PGE2 and PGF2alpha on the urine outflow were studied in ethanol-anesthetized rats. PGE2 and PGF2alpha, when injected i.c.v., caused diuresis which was followed by antidiuresis. Phentolamine, when perfused i.c.v., was an antidiuretic and inhibited the diuretic and antidiuretic effects of PGE2. Diphloretin phosphate inhibited both effects of PGE2. Polyphloretin phosphate (PPP) and propranolol blocked completely the PGE2-induced diuresis and consequently remarkable antidiuresis was observed after the combined treatments with PGE2 and PPP or propranolol. When PGE2 was perfused i.c.v., a sustained diuresis was obtained and antidiuretic effects of noradrenaline, gamma-aminobutyric acid and L-glutamate were potentiated, inhibited and unaffected by the perfusion with PGE2, respectively. It was indicated that the antidiuretic effect of PGE2 could be dissociated from the diuretic effect and that both effects were mediated through adrenergic mechanisms. The present result also suggested that central PGE2 might act as a modulator of some neurotransmitters involved in water metabolism.

Animals↗
PubMed1987

Blockade of the response to volume expansion by monoclonal antibodies against atrial natriuretic peptides.

It is known that plasma levels of atrial natriuretic peptides (ANP) increase in response to volume expansion. However, the extent to which these increased levels of ANP participate in the renal response to volume expansion remained unknown. This question can be answered with the aid of a monoclonal antibody that binds specifically to the biologically active forms of ANP: Ascitic fluid containing this monoclonal antibody dose-dependently and specifically blocks the natriuretic, diuretic and hypotensive effects of synthetic atriopeptin II given intravenously in rats. Volume expansion induced by injection of 20 ml/kg homologous blood in anaesthetized rats evokes massive diuresis and natriuresis. Pretreatment with ascitic fluid containing monoclonal antibody completely blocks this diuretic and natriuretic response during the first 20 min after volume expansion. Thus the initial renal response to volume expansion is due to the increase in endogenous ANP. Similar results were obtained for volume expansion with isotonic saline in conscious rats. It is supposed that the effects of ANP are mediated through particulate guanylate cyclase activation and intracellular cyclic guanosine-monophosphate (cGMP) accumulation in target tissues including renal and vascular smooth muscles cells. Besides increasing plasma ANP levels (measured by radioimmunoassay) volume expansion also induces an increase of cGMP levels both in plasma, urine and in renal tissue. This increase is ANP-dependent as it can be blocked by the monoclonal antibody.

Animals↗
PubMed1955

Diuretics in therapy of epilepsy; their use for the potentiation of anticonvulsant drugs.

Animal experiments having indicated a nearly twofold increase in anticonvulsant protection with the use of diuretics which increase blood-brain barrier permeability, the principle was applied to treatment of humans with epilepsy. The addition of diuretics to anticonvulsant medication permitted a decrease of previously toxic dosages in ten epileptics, followed for six months, without lessening (and in some cases improving) the control of seizures. In three cases excessive diuresis and gastric distress necessitated discontinuance or decrease in dosage of the diuretic used.

Animals↗
PubMed1977

Clearance and micropuncture studies of the effects of a new indanyloxyacetic acid diuretic on segmental nephron function in rats.

The renal effects of a new, substituted indanyloxyacetic acid diuretic agent were evaluated in 16 anesthetized rats using micropuncture and clearance techniques. Glomerular filtration rate, mean arterial pressure and hematocrit remained unchanged. Urine flow increased 13 times after i.v. administration of 50 mg/kg b.wt. of the diuretic. Sodium excretion increased from 0.4 +/- 0.05% of the amount filtered to 6.62+/-0.87%. Potassium urine/plasma concentration ratio declined 6-fold while potassium excretion nearly doubled. Proximal tubular reabsorption was not altered significantly by this indanone diuretic. Reabsorption was markedly inhibited between late proximal and early distal micropuncture sites, that is, in the loop of Henle. The diuretic did not appear to interfere with normal distal tubular function. In the collecting tubules, reabsorption was markedly reduced from 41+/-0.2 mul/min/100 g b.wt. to 26+/-5 (with P less than .005). This new indanone compound appears to be a potent, specific natriuretic diuretic agent which inhibits tubular reabsorption primarily in the loop of Henle and collecting tubules, that is, in distal nephron segments located deep within the kidney. It produces a somewhat delayed but prolonged diuresis in the rat.

Animals↗
PubMed1996

Neuropeptides implicated in the control of diuresis in insects.

Primary urine production in insect Malpighian tubules is stimulated by two classes of neuropeptides, CRF-related diuretic peptides and insect kinins. The CRF-related peptide of the locust, Locusta migratoria, has a hormonal role in the control of postfeeding diuresis, but the functional role of the kinins has yet to be defined. The two classes of peptide act synergistically to stimulate tubule secretion, and the kinins may therefore have a modulatory action in the control of diuresis. The peptides differ in their effects on Malpighian tubule ion transport, and this could be important for the regulation of hemolymph volume and composition.

Amino Acid Sequence↗
PubMed1999

The contribution of nitric oxide to diuretic and natriuretic effects of renal kinins in normotensive rats.

We have reported that diuresis and natriuresis due to increase in renal kinins induced by the neutral endopeptidase 24.11 (NEP) inhibitor were attenuated by nitric oxide (NO) synthase inhibitor. To further clarify the water-sodium excretory mechanism of renal kinins, we estimated NO2+NO3 (NOx) and cGMP in plasma and urine with and without a specific NEP inhibitor, thiorphan. P-aminohippuric acid (PAH) and inulin were injected into male Sprague-Dawley rats. Vehicle (n = 8) or thiorphan (30 mg/kg, n = 10) was injected after the control period. Mean blood pressure (MBP), plasma and urinary PAH, inulin, NOx and cGMP, urinary volume (UV) and urinary sodium excretion (UNaV) were measured before and after injection of the reagents. MBP, renal plasma flow and glomerular filtration rate were not affected by thiorphan. Plasma NOx and cGMP with thiorphan did not differ from the vehicle, while urinary NOx and cGMP increased. None of the variables were affected by vehicle. UV and UNaV were higher with thiorphan than with vehicle. Positive correlation was found between urinary deltaNOx and deltacGMP. Each urinary deltaNOx and deltacGMP was significantly correlated to both deltaUV and deltaUNaV. Urinary NOx and cGMP were increased while maintaining correlations to UV and UNaV, but plasma NOx and cGMP were not affected by thiorphan. This implies that the mechanism of water-sodium excretion induced by NEP inhibitor is mediated by renal NO. Therefore, renal NO may contribute to the diuretic and natriuretic effects of renal kinins.

Animals↗
PubMed1989

Lower than conventional doses of captopril in the initiation of converting enzyme inhibition in patients with severe congestive heart failure.

Angiotensin converting enzyme (ACE) inhibitors are effective long-term therapy for congestive heart failure, improving symptoms, exercise tolerance, biochemical anomalies, and mortality. Captopril, in doses of up to 150 mg daily is relatively free of serious adverse effects. A test dose of 6.25 mg normally precedes regular therapy in an attempt to avoid first-dose hypotension, which may also be prevented by reduction in diuretic dosage and by the avoidance of over-diuresis leading to volume depletion. We report two patients who, despite the above precautions developed symptomatic first-dose hypotension with 6.25 mg, but were subsequently able to recommence captopril therapy by the initial oral administration of doses as low as 1 mg.

Aged↗
PubMed1983

Diuretic radionuclide urography.

Diuretic radionuclide urography is a modification of conventional renography which utilizes the administration of intravenous furosemide to distinguish dilated, non-obstructed, hydronephrotic systems from those with significant mechanical obstruction. Diagnostic patterns are derived from computer generated time-activity histograms that depict the accumulation and washout of radiotracer before and after diuretic injection. In dilated but non-obstructed systems, diuresis produces a decline in activity. In obstructed systems, there is a failure of radiotracer washout in response to diuresis and no decline in activity is observed. The procedure is applicable to patients of all ages with suspected upper urinary tract obstruction. Clinical and experimental data support the accuracy and utility of this methodology and define its limitations and pitfalls.

Animals↗
PubMed2001

[Treatment of lithiasis in horseshoe kidney with extracorporeal shock-wave lithotripsy].

UNLABELLED: The horseshoe kidney is the most frequent renal anomaly. As a consequence of impaired urinary drainage, urolithiasis is present in 20% of the cases. Indications for extracorporeal shock wave lithotripsy (ESWL) in the treatment of patients with anomalous kidneys is still the subject of controversy. OBJECTIVE: To evaluate ESWL efficacy in the treatment for lithiasis in horseshoe kidney. MATERIAL AND METHODS: Between april 1988 and december 1999 a total of 32 symptomatic lithiasis in 30 patients with horseshoe kidneys were managed by 65 sessions with ESWL. Until march 1999 a Dornier HM-4 electrohydraulic lithotripter was used. Posteriorly, two treatments was performed with an electromagnetic Dornier Lithotripter S. These procedures have been performed without anaesthesia or sedation for the Dornier HM-4 equipment. Analgesia with Meperidine was used for the Dornier Lithotripter S. Diuresis was not forced during or after treatment with diuretics or serotherapy. Treatments was conducted in an outpatient clinic in all cases. RESULTS: Treatment/lithiasis rate was 2.03. Following treatment 16 patients (54%) were stone-free by X-ray, 9 patients (30%) had residual fragments and in 5 patients (16%) no sign of stone disintegration was observed. Open surgery was performed in three of this patients. Better results was achieved in stones located in the renal pelvis and stone size is 10 mm or less. Clinical evolution: free of symptoms in 20 patients; chronic vague flank pain in 5 patients and acute renal colic with or without hematuria in 5 patients. No major complication was observed in our compilation. CONCLUSIONS: These results suggest that ESWL is the method of primary choice in the treatment for small lithiasis (10 mm or less) in horseshoe kidney.

Adult↗
PubMed1990

Kappa-opioid-receptor agonists modulate the renal excretion of water and electrolytes in anaesthetized rats.

1. Subcutaneous injection of the kappa-opioid agonists U50,488 (10 mg kg-1) and tifluadom (3.5 mg kg-1) into Inactin-anaesthetized, saline-infused rats was associated with a diuresis, antinatriuresis and antikaliuresis which lasted for up to 2 h. A high (5 mg kg-1), but not low (0.1 mg kg-1), dose of naloxone blocked the renal effects of U50,488. 2. U50,488 administration in anaesthetized, vasopressin-deficient Brattleboro DI rats was associated with an attenuated diuresis, though the antinatriuretic response remained intact. 3. The diuretic action of U50,488 was associated with an increase in glomerular filtration rate while fractional fluid reabsorption remained steady. In contrast, fractional sodium and potassium reabsorption were increased. 4. These data suggest that kappa-opioid agonists alter renal handling of both water and electrolytes. This appears to be mediated by two separate mechanisms: increased fluid loss largely reflects altered glomerular events while the fall in electrolyte excretion results from altered tubular handling.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1979

Changes of electrolyte excretion, renin activity, angiotensin-II and aldosterone concentrations during administration of 3-amino-1-(3,4-dichloro-a-methyl-benzyl)-2-pyrazolin-5-one (Bay g 2821).

After the administration of 40 mg Bay g 2821, a new potent diuretic substance, a significant increase of sodium and water diuresis occurred. There was only a short rise in potassium excretion. In contrast to the sodium and water diuresis no significant increase of renin-activity, angiotensin-II or aldosterone concentration was seen. In spite of the insignificant stimulation of the renin-angiotensin-aldosterone system, a significant increase of correlation occurred between the three components of the renin-angiotensin-aldosterone system.

Adult↗
PubMed1981

Treatment of massive phenobarbital overdose with dopamine diuresis.

We report a case of severe phenobarbital sodium overdose with a peak plasma concentration of 253 microgram/mL, normally considered fatal. The patient was successfully treated with forced alkaline diuresis. Treatment was unusual in that dopamine hydrochloride was used to sustain the diuresis.

Diuretics↗
PubMed2006

Practical applications of intravenous diuretic therapy in decompensated heart failure.

Intravenous (IV) loop diuretics play an important role in the treatment of decompensated heart failure (DHF). They inhibit the Na(+)-K(+)-2Cl(-) reabsorptive pump in the thick ascending limb of the loop of Henle, and the resultant natriuresis and diuresis decreases volume load, improves hemodynamics, and reduces DHF symptoms. However, loop diuretics have a short half-life and their efficacy may be limited by postdiuretic sodium rebound during the period between doses in which the tubular diuretic concentration is subtherapeutic. Moreover, they can produce electrolyte abnormalities, neurohormonal activation, intravascular volume depletion, and renal dysfunction. Several studies have reported an association between diuretic therapy and increased morbidity and mortality. In addition, many patients, especially those with more advanced forms of heart failure (HF), are resistant to standard doses of loop diuretics. These high-risk, resistant patients may benefit from pharmacologic and/or nonpharmacologic interventions to improve hemodynamic performance, treatment of renovascular disease, discontinuation of aspirin and other sodium-retaining drugs, manipulation of the route of delivery or combination of diuretic classes, or hemofiltration. Despite >50 years of use, many questions regarding the use of intravenous diuretic agents in patients with DHF are still unanswered, and there remains a compelling need for well-designed randomized, controlled clinical trials to establish appropriate treatment regimens that maximize therapeutic benefit while minimizing morbidity and mortality.

Diuretics↗
PubMed1998

Principles of diuretic therapy.

This section discusses the reasons different diuretic agents inhibit salt reabsorption at specific sites within the renal tubule. It also includes a brief review of how diuretics reach their target site of action along the nephron, together with a discussion of how disease states may affect the delivery of diuretics to those sites. When diuretics are administered to edematous patients, the natriuretic response is often blunted. In addition, increased renal tubular salt avidity is observed after administration of loop diuretics. The elements required to successfully achieve adequate natriuresis under such conditions are analyzed. Because achieving diuresis may result in significant hypokalemia, hyponatremia, metabolic alkalosis, and worsening prerenal azotemia, the prevention and management of these complications of diuretic therapy are also reviewed. A description of successful use of diuretics in specific edematous states, such as congestive heart failure, chronic renal failure, nephrotic syndrome, and liver disease, is followed by a brief discussion of the management of resistant edema and the use of diuretics in nonedematous states, including essential hypertension and other conditions.

Diuretics↗
PubMed1991

Interaction of ketoprofen and frusemide in man.

The effects of ketoprofen on frusemide-induced diuresis, natriuresis and renin release were studied in 12 healthy male volunteers. Each received frusemide 40 mg once daily with either ketoprofen 100 mg twice daily or placebo for two periods of 5 days separated by a treatment-free period according to a randomized, double-blind, cross-over study design. Ketoprofen significantly reduced frusemide-induced diuresis on Day 1 but not on Day 5 of treatment. The natriuresis induced by frusemide on Day 1 or Day 5 of treatment did not differ significantly whether ketoprofen or placebo was administered, although the mean urinary sodium excretion values were consistently lower following ketoprofen. Ketoprofen did not affect the kaliuretic response to frusemide on Day 1 or Day 5 of treatment. The increase in plasma renin activity after frusemide was inhibited by ketoprofen on both Day 1 and Day 5. These results suggest that ketoprofen reduces the diuresis and renin release induced by frusemide, but that the reduction in diuretic response may become less important after their repeated coadministration.

Adult↗
PubMed1994

Effects of glucagon on diuresis, renal plasma flow and glomerular filtration in sheep.

The effects of intravenous infusion of glucagon (100 ng.kg-1.min-1) on diuresis, renal plasma flow and glomerular filtration rate were studied in conscious sheep. Diuresis began to decrease upon initiation of glucagon infusion, down to 50% of its baseline value at the end of glucagon infusion. Glomerular filtration rate was also decreased by 75%. With regard to renal plasma flow, the decrease started at the beginning of glucagon infusion, but remained restricted. It was not possible, from these results, to explain the reduced diuresis by a decrease in renal plasma flow; the observed anti-diuretic effect could be the consequence of a modification of either the filtration coefficient or water tubular reabsorption.

Animals↗
PubMedDate not supplied

Norepinephrine-induced diuresis in chronically ethanol-treated rats.

Previous research from this laboratory indicated that noradrenergic mechanisms mediate ethanol diuresis. Experiments described here examined changes in sensitivity of these noradrenergic mechanisms in animals chronically treated with ethanol. Norepinephrine hydrochloride (0-12 micrograms intraventricularly) produced dose-dependent diuresis in control (dextrin maltose)- and ethanol (8-11 g/kg/day)-treated rats on the first day of treatment. Tolerance to ethanol diuresis was present after 10 days of ethanol treatment. Lack of responsiveness to norepinephrine-induced diuresis was evident only on the 20th day of treatment in both ethanol and dextrin-maltose groups of rats. These results suggest that norepinephrine does not play a primary role in the development of tolerance to the diuretic action of ethanol.

Animals↗
PubMed2006

An integrated model of thermodynamic-hemodynamic-pharmacokinetic system and its application on decoupling control of intracranial temperature and pressure in brain hypothermia treatment.

Brain hypothermia treatment (BHT) is an intensive care characterized by simultaneous managements of various vital signs, such as intracranial temperature (ICT) and pressure (ICP), of the severe neuropatient. Medical treatments including therapeutic ambient cooling and diuresis are separately carried out based on the experience of the medical staff involved in the clinical management of various pathophysiological processes, such as thermodynamics, hemodynamics and pharmacokinetics. However, no special attention has been paid to the interactions among these subsystems in therapeutic hypothermia because of the lack of theoretical knowledge. Therefore, quantitative analyses using an integrated model of various physiological processes and their interactions are of pressing need. In the present paper, we propose a general compartmental model to describe the pathophysiological processes of the three aforementioned dynamics, on account of the dynamical analogy of temperature, pressure and concentration. The model is verified by the agreement of model-based simulation results with clinical evidence. Based on responses of the integrated model to various stimuli, a transfer function matrix is identified to linearly approximate the characteristic interrelationships between medical treatments (ambient cooling and diuresis) and the vital signs (ICT and ICP). Then a controller that decouples ambient cooling and diuresis is proposed for efficient management of ICT and ICP, enhancement of hypothermic decompression and reduction of diuretic dosage. Decoupling control simulation indicates that ICT and ICP of the integrated model, representing a patient under BHT, can be simultaneously regulated by a single PID controller for ambient cooling and another for diuresis. The proposed decoupler effectively establishes hypothermic decompression, reduces the dosage of diuretic and improves ICP management. Theoretical analyses of the integrated model and decoupling control of ICT and ICP provide insights into the intensive care of various pathophysiological processes in patients undergoing BHT.

Brain↗