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PubMed1980

Sauvagine, a new polypeptide from Phyllomedusa sauvagei skin. Occurrence in various Phyllomedusa species and pharmacological actions on rat blood pressure and diuresis.

1. The occurrence of sauvagine, a new polypeptide from amphibian skin, and its actions on rat blood pressure and diuresis were studied. 2. Sauvagine was found to be present in the skin of all the 10 Phyllomedusa species so far studied, amounts ranging from a few micrograms to 240 micrograms per g fresh skin. 3. The polypeptide displayed in the rat an intense, long-lasting hypotensive action accompanied by tachycardia. Hypotension was not modified by either atropine or propranolol, excluding the participation of the autonomic nervous system in its production. Tachycardia, on the contrary, was partially inhibited by propranolol. 4. Hypotension is probably the main cause of the intense antidiuresis seen in hydrated rats following sauvagine administration. Reduction in urina volume was accompanied by a decrease in GFR and an increase in tubular NA+ reabsorption.

Amphibian Proteins↗
PubMed1975

Intrarenal distribution of citrate in the dog during antidiuresis and diuresis.

The intrarenal distribution of citrate was evaluated in the dog during antidiuresis and osmotic diuresis, by using the specific citrate assay method of Moellering and Gruber. The measurements were made on tissue samples taken from four different regions throughout the kidney: cortex, outer and inner medulla, and papilla. During antidiuresis, a characteristic distribution of citrate was observed with highest levels in the papilla and lowest ones in the outer medulla. A medullary concentration gradient for citrate was found. Mannitol greatly decreased papillary citrate and sodium, but no changes in outer and inner medullary citrate occured. The results could not be explained by the citrate contained either in the trapped urine or blood in the tissue. It is suggested that citrate accumulation in the inner regions of renal medulla may be accounted for by countercurrent mechanisms or regional differences in renal citrate metabolism.

Animals↗
PubMed1980

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↗
PubMed1977

Acute acetylsalicylic acid poisoning: treatment with forced alkaline diuresis and diuretics.

101 patients were treated for acute acetylsalicylic acid (ASA) poisoning in the Nephrological Unit Trondheim between 1971-1975. On admission 33 of them had a serum salicylic acid (SA) concentration greater than 400 microgram/ml (mean 588 +/- 40 microgram/ml). This group was compared with a group of 11 children less than 5 years old with ASA poisoning and a mean serum SA on admission of 550 +/- 34 microgram/ml. Blood pH on admission was normal or elevated in all patients more than 12 years old (mean 7.43 +/- 0.01), whereas 7 of the 11 children suffered from metabolic acidosis. The results of forced alkaline diuresis produced by loop diuretics (bumetanide, furosemide) in ASA poisoned patients older than 12 years are reported. The mean T 1/2 of SA was 9.6 h in the treated group as compared to 18-22 h in untreated patients. There was no apparent difference between the diuretic effect of bumetanide and furosemide.

Acid-Base Equilibrium↗
PubMedDate not supplied

Mechanism of action of neurohypophyseal hormones on sodium excretion and diuresis.

Administration of pituitrin, vasopressin, and oxytocin to rats during spontaneous micturition increases diuresis and sodium excretion by reducing tubular reabsorption. In adrenalectomized rats these preparations have no diuretic effect and increased sodium excretion is observed only after administration of vasopressin. After hypophysectomy the diuretic effect of the preparations disappears but they still increase sodium excretion. It is postulated that the diuretic effect of the neurohypophyseal hormones is connected with activation of the pituitary-adrenal system, whereas some additional mechanism is involved in their effect on sodium excretion.

Adrenal Glands↗
PubMed1979

Inhibition of saline-induced diuresis in the rat by sulpiride.

Sulpiride (120 mg/kg, i.p.) inhibited saline-induced diuresis in the rat, an effect not observed with haloperidol, clozapine, pimozide or chloromazine. The antidiuretic effect of sulpiride also occurred in hypophysectomized rats suggesting that the response was not prolactin-mediated.

Animals↗
PubMed1975

Determination of the glomerular filtration rate by the minute diuresis at a specific gravity of 1001.

A new method is described for determination of the glomerular filtration rate, based on the fact that at an urinary specific gravity of 1001 the final urine is concentrated 6.67 times, as compared with the primary glomerular filtrate. The glomerular filtration rate is evaluated by multiplication of the minute diuresis at a specific gravity of 1001 by the factor 6.67. In this manner the chemical analysis of urine and blood is avoided. Urine with a specific gravity of 1001 is obtained by water loading much the same as in the dilution test of Volhard. For checking the accuracy of the method, comparative studies were conducted with creatinine clearance in 36 patients and with 51Cr-EDTA clearance in 33 patients. The difference in the values of the glomerular filtration rate, evaluated by the above-mentioned two methods and the new method was statistically not significant (p greater than 0.05). The method is recommended for the early detection of disturbances in the glomerular function prior to the occurrence of azotemia.

Diuresis↗
PubMed2005

Chronic albumin infusions to achieve diuresis in patients with ascites who are not candidates for transjugular intrahepatic portosystemic shunt (TIPS).

While transjugular intrahepatic portosystemic shunt (TIPS) is a common therapy for cirrhotic patients with diuretic-resistant or diuretic-refractory ascites, some patients are unsuitable for the procedure for technical or medical reasons. We report our experience with the use of chronic intravenous albumin infusions to achieve diuresis in this difficult patient population and review the historic experience of chronic albumin infusions as a treatment for ascites. Nineteen patients with cirrhosis and diuretic-resistant or diuretic-refractory ascites who were deemed unsuitable for TIPS received outpatient intravenous albumin infusions (50 g) weekly for at least 4 weeks. The following endpoints were retrospectively recorded: serum sodium, serum creatinine, blood urea nitrogen, hematocrit, bilirubin, albumin, international normalized ratio, body weight, and Model for End-stage Liver Disease (MELD) score. The contraindications for TIPS included the following: portal vein thrombosis, two; advanced age, one; encephalopathy, nine; hyperbilirubinemia, five; and other, two. Compared to pretreatment, posttreatment weight decreased in 17 patients, remained unchanged in 0 patients, and increased in 2 patients. The overall mean change in body weight (before vs. after therapy) was 8 lb (P < 0.05). The only significant change in biochemistry was an increase in serum albumin from 2.5 g/dl before therapy to 3.5 g/dl after therapy (P < 0.05). We conclude that (1) recurrent intravenous weekly albumin infusions resulted in significant loss of edema and ascites as measured by loss of body weight, and (2) clinicians may want to consider chronic albumin infusions for selected patients with refractory ascites who are not candidates for TIPS.

Albumins↗
PubMed1992

Effects of HS-142-1, a novel non-peptide ANP antagonist, on diuresis and natriuresis induced by acute volume expansion in anesthetized rats.

In this study we used HS-142-1, a novel non-peptide antagonist for the atrial natriuretic peptide (ANP) receptor, to clarify the possible physiological significance of ANP in acute hypervolemia. Substantial volume expansion in anesthetized rats induced a strong diuresis and natriuresis. These renal responses were significantly blocked by HS-142-1 at a dose of 3.0 mgkg-1 i.v. This observation suggests that ANP and its guanylyl cyclase-coupled receptor are, under the present conditions, physiologically involved that appears to be responsible for the renal responses in the volume homeostasis.

Animals↗
PubMed1985

Diuresis and reduction of salt appetite by lateral ventricular infusions of atriopeptin II.

Infusions of 60 pmol/h atriopeptin II into the lateral ventricles stimulated urine flow in both normally hydrated and sodium depleted conscious rats without any increase in the excretion of sodium, potassium or total solutes. The urinary sodium concentration and osmolality both declined significantly. In addition to the renal effects, cerebroventricular infusions of 60 pmol/h atropeptin II reduced salt appetite in rats following depletion of sodium by combined treatment with furosemide diuresis and low sodium diet. Neither 60 nor 600 pmol/h doses had any effect on urine volume or concentration during intravenous infusions, so the effects appear to be mediated by the central nervous system (CNS). Atriopeptins may act through the CNS to facilitate reduction of extracellular volume in synergy with peripheral natriuresis: by increasing urine flow independently from natriuresis; and by restricting further expansion of extracellular volume by reducing salt appetite.

Animals↗
PubMed1989

GPC phosphodiesterase and phosphomonoesterase activities of renal cortex and medulla of control, antidiuresis and diuresis rats.

Glycerylphosphorylcholine (GPC) concentration was reported to be elevated in renal medulla of experimental animals deprived of water. The activities of GPC phosphodiesterases were similar in homogenates and membrane subfractions of renal cortex prepared from control, diuresis and antidiuresis rats. There were no differences in these preparations' ability to hydrolyze phosphorylcholine. In contrast, there was a nearly 50% reduction of non-specific phosphomonoesterase activity, using p-nitrophenylphosphate as substrate and membrane subfractions prepared from the antidiuresis animals. It is suggested that as a consequence, a pathway for the formation from L-alpha-glycerylphosphate is activated.

Animals↗
PubMed1988

Intrarenal thromboxane A2 generation reduces the furosemide-induced sodium and water diuresis in cirrhosis with ascites.

To assess the effects of intrarenal thromboxane A2 generation on furosemide-induced sodium and water excretion we administered furosemide (40 mg i.v.) to 8 nonazotemic cirrhotic patients with ascites and 8 healthy subjects before and after the administration of OKY 046 (200 mg twice orally), a powerful thromboxane-synthase inhibitor. Selective thromboxane-synthase inhibition significantly reduced basal and postfurosemide (1 h) urinary thromboxane B2 excretion in healthy subjects (65% before and 62% after furosemide) as well as in cirrhotic patients (52% before and 67% after furosemide) without affecting urinary prostaglandin E2 and 6-keto prostaglandin F1 alpha excretion. During the first hour after furosemide administration, OKY 046 administration significantly enhanced postfurosemide water excretion (milliliters per minute) in both healthy subjects (from 8.5 +/- 2.0 to 11.6 +/- 2.1, p less than 0.001) and cirrhotic patients (from 1.1 +/- 0.8 to 4.2 +/- 0.5, p less than 0.005), whereas furesemide-induced natriuresis (microequivalents per minute) was significantly increased only in the latter group (from 973 +/- 125 to 1405 +/- 121, p less than 0.05). Our data indicate that intrarenal thromboxane A2 generation, elicited by furosemide administration, may reduce the effects of the drug on water and sodium diuresis. Such a reduction seems to be more marked in the presence of an activated intrarenal prostaglandin system, suggesting that renal thromboxane A2 may represent an additional factor in conditioning the impaired responsiveness to furosemide, which is frequently observed in cirrhotic patients with ascites.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

A possible role of atrial natriuretic peptide in ethanol-induced acute diuresis.

The acute effects of ethanol on plasma atrial natriuretic peptide levels were investigated in 4 clinically healthy males, aged 24-26 years, consumed either 750 ml of water as a control study, or the same beverage with 1 ml/kg alcohol added, which increased the plasma alcohol concentration to 99.12 +/- 15.10 mg/dl at 60 min. Plasma atrial natriuretic peptide levels were significantly higher in the alcohol study compared to the control study at each time point (10, 20, 30, 60, 120 min after drinking onset), and with a peak at 10 min. Atrial natriuretic peptide levels showed a positive significant correlation with plasma antidiuretic hormone in the control group, while no relationship was found between the two peptides in the alcohol study. Moreover, a significant correlation exists between plasma atrial natriuretic peptide levels and systolic arterial blood pressure, and heart rate, and between the variations in atrial natriuretic peptide values and the variations in plasma sodium, serum ethanol, and plasma osmolality in the alcohol study. Acute ethanol intake causes an increase in urinary volume, and a decrease in urinary potassium excretion and urinary osmolality, and no change in urinary sodium excretion. These data suggest that acute ethanol administration causes a rapid increase in plasma levels of atrial natriuretic peptide, which could be an important factor of ethanol-induced diuresis. The main mechanisms for increased atrial natriuretic peptide release from atria after acute ethanol ingestion seem to be atrial stretch, due to the increase in arterial blood pressure, in heart rate, in sympathetic tone, and in plasma osmolality, and to a direct secretory effect by antidiuretic hormone.

Adult↗
PubMed1985

Effect of nicotine on drinking and diuresis in septal lesioned rats.

Lesions of septal nuclei in rats enhance water intake and urine outflow. The effects of nicotine tartrate (2.5 mg/kg) on drinking and diuresis were investigated in normal, sham and septal lesioned rats. Nicotine administration resulted in a surprising hyperdipsia and polyuria in lesioned animals, the mean output rose from 38 +/- 1.3 ml (before treatment) to 101.6 +/- 6.1 (during treatment) and water intake increased from 74.2 +/- 1.8 ml to 129.8 +/- 6.4 ml.

Acetylcholine↗
PubMed1995

A computerized system for the continuous recording and analysis of feeding, drinking, diuresis, and locomotor activity.

A system has been designed to study the intake of liquids and solid foods in rats that allows for the analysis of feeding and drinking episodes over time. In addition, it monitors locomotor activity and diuresis. This system is particularly useful for the study of the differential effects of drugs on various parameters of feeding and drinking. Because it allows for the monitoring of all behaviors for periods of 24 consecutive hours without disturbing the animals, it can be applied to the study of light/dark cycles of ingestive behavior. The apparatus consists of rat cages (equipped with photocells, bottles, electronic balances, and a funnel to collect urine), computer interfaces, an AT-compatible microcomputer for data collection, and a VAX system for analysis.

Animals↗
PubMed1981

The effect of prostaglandin synthetase inhibitors on renal function: studies in normal rats during sodium or water diuresis and in rats with chronic renal insufficiency.

The effect of acute infusion of the prostaglandin synthetase inhibitors - meclofenamate or indomethacin - was examined in awake rats. Studies were performed in normal rats undergoing either sodium or water diuresis and in salt-replete rats with chronic renal insufficiency. Prostaglandin synthetase inhibitors had no effect on renal plasma flow, glomerular filtration rate or fractional excretion of sodium in any of the groups. Absolute urinary excretion rates for sodium and potassium decreased only in the normal, salt-replete rats. In contrast, prostaglandin synthetase inhibitors consistently decreased urinary flow and osmolar clearance under all experimental conditions studied. In the normal, salt-replete rats the fall in urine flow was preceded by an increase in urinary excretion of cyclic AMP. These results show that inhibitors of prostaglandin synthesis enhance the ability of the kidney to reabsorb water. This effect may be secondary to increased cyclic AMP generation and to increased urea recirculation resulting in higher urea accumulation in the renal medulla.

Animals↗