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At least 19 recordsLinked to original sources
PubMed1979

[Studies of the induction of diuresis increase and water intoxication induced diuresis inhibition by oxytocin and vasopressin in lactating cattle].

Intravenous injection of 20 International Units (IU) of oxytocin in the form of synthetic oxytocin or neurohypophyseal extract preparations to dehydrated cows that had already undergone twelve hours of water withdrawal did not produce antidiuresis but rather rise of diuresis accompanied by saluretic effects. Increase in diuresis occurred also in hyperhydrated cows, following water application, provided that oxytocin or vasopressin preparations had caused antidiuresis and saluresis and, consequently, changed urine composition to osmotic pressures beyond the limit values between 650 and 750 mosmol/kg. Rehydration of cow may be associated with retardation of diuresis by four hours or more. If oxytocin or vasopressin are given in the phase of such rehydration, the period between water application and the onset of water diuresis may be defined as "blocked water diuresis". Continuous infusion of 0.34 or 0.8 IU of oxytocin per minute up to 3.5 hours did not cause water intoxication in hyperhydrated cows, though blood plasma values for osmotic pressure had dropped to 244 mosmol/kg, while Na+ concentration had gone down to 116 mmol/l.

Animals↗
PubMed1992

[Ureteropelvic stenosis in infancy. The value of diuresis sonography compared with diuresis excretory urography].

Examinations under conditions of diuresis produced by drugs can be useful to differentiate pyelo-ureteric obstruction from a dilated collecting system with normal flow. 22 infants with 42 kidneys showing moderate dilatation of one of both renal collecting systems were examined by sonography and excretory urography under conditions of diuresis and the results were compared. Depending on the radiological appearances and contrast clearance rates, four diagnostic groups could be identified; these also differed significantly on the sonographic examinations. In general, there was good agreement between the two methods. Carefully performed, diuresis sonography will clearly distinguish between urodynamically significant obstruction from a wide but non-obstructive collecting system. The number of radiographic examinations can therefore be reduced in these patients.

Diagnosis, Differential↗
PubMed1976

The role of the medullary collecting ducts in postobstructive diuresis.

Medullary collecting duct function was studied by direct microcatheterization techniques in rats undergoing postobstructive diuresis. Significant net addition of water and sodium to the duct was demonstrated during postobstructive diuresis after relief of 24-h bilateral ureteral ligation. This striking abnormality in function was associated with reduced delivery of sodium and water to the collecting duct compared to sham-operated controls. To examine the role of circulating factors in this phenomenon, another group of rats was studied that underwent 24 h of total urine reinfusion into the femoral vein. Natriuresis and diuresis were similar to the postobstructive group, but absolute collecting duct reabsorption of sodium and water was normal. The natriuresis and diuresis in rats with urine reinfusion resulted from increased delivery of fluid and sodium to the medullary collecting duct. A third group of rats was studied with 24-h unilateral ureteral ligation as well as urine reinfusion from the contralateral normal kidney. Without urine reinfusion there was no diuresis-natriuresis but with urine reinfusion the diuresis and natriuresis after relief of unilateral obstruction was similar to that after relief of bilateral obstruction. Moreover, net addition of sodium and no significant water reabsorption were demonstrated in the medullary collecting duct of such animals. The results indicate that (a) the medullary collecting duct is the critical nephron segment affected by ureteral obstruction, since postobstructive diuresis occurred despite reduced delivery of fluid from the more proximal nephron; (b) the net addition of sodium to the medullary collecting duct observed during postobstructive diuresis is probably a direct effect of obstruction, since it was found during postobstructive diuresis after relief of bilateral or unilateral ureteral ligation, but not with urine reinfusion alone; and (c) blood-borne factors are important in the development of postobstructive natriuresis and diuresis, and probably act by increasing the fraction of filtered sodium and water delivered from the proximal and distal tubule to the collecting duct.

Absorption↗
PubMed1990

Effects of diuresis on the characteristics of pleural fluid in patients with congestive heart failure.

PURPOSE: The pleural fluid that accumulates secondary to congestive heart failure is almost always a transudate based upon its level of protein and lactic acid dehydrogenase (LDH). Previous work has suggested that the characteristics of the fluid may change into those of an exudate with diuresis. The purpose of the present study was to determine whether aggressive diuresis does result in this change in pleural fluid characteristics. PATIENTS AND METHODS: Twelve patients with severe congestive heart failure (ejection fraction 23.9 +/- 9.6%) and pleural effusions were studied serially as they underwent diuresis. After an initial thoracentesis was performed, the patients then underwent aggressive diuresis for 12 to 48 hours with one or two follow-up thoracentesis. RESULTS: The mean weight loss during the study period was 4.5 +/- 2.8 kg. With diuresis the LDH level, LDH ratio, protein level, and protein ratio all increased significantly (p less than 0.05). All 12 patients had transudative pleural effusions at the onset of diuresis. However, despite the increases in the levels of protein and LDH with diuresis, only one patient's pleural fluid attained values compatible with an exudate. CONCLUSION: From this study we conclude that it is uncommon for a transudative pleural effusion due to congestive heart failure to develop the characteristics of an exudative pleural effusion with rapid diuresis.

Aged↗
PubMed1988

Paradoxical relationship between atriopeptin plasma levels and diuresis-natriuresis induced by acute volume expansion.

Surgical removal of one or both atrial appendages was employed in rats to reduce the intrinsic stores of atriopeptin (AP). In conscious rats (with intact baroreceptor reflexes), bilateral or unilateral atrial appendectomy suppressed the diuresis and natriuresis produced by acute volume expansion. Surprisingly, volume expansion (with 4% bovine serum albumin in saline at 1.5 ml/kg per min for 15 min) did not result in an increase in plasma AP immunoreactivity (APir) in control or atrial-appendectomized conscious rats. Previous studies demonstrated that acute volume expansion in anesthetized animals caused increased plasma APir. Indeed, we found that volume expansion causes comparable diuresis-natriuresis in conscious and chloral hydrate-anesthetized rats, but only the latter group exhibits an increase in plasma APir. Brattleboro rats, which are deficient in vasopressin, exhibit the same response as Long-Evans controls in that acute volume expansion in conscious animals produces a pronounced diuresis and natriuresis but no APir release, but when these same animals are anesthetized, there is a simultaneous induction of diuresis-natriuresis and APir release by volume expansion. Plasma AP does not increase in conscious rats despite a large volume load, 30-40% of the total blood volume given in 15 min, and the natriuresis-diuresis appears to also be independent of vasopressin. On the other hand, the diuresis induced by acute volume expansion in anesthetized rats seems dependent on the elevated APir, since rats made autoimmune to AP (which are nonresponsive to exogenous AP infusions) exhibit a diuresis in conscious but not anesthetized rats. We therefore conclude that the participation of AP in volume homeostasis is more likely in pathophysiological states and that another mechanism or possibly another atrial factor mediates the diuresis-natriuresis induced by volume expansion in conscious rats.

Anesthesia↗
PubMed1977

Immersion diuresis in dogs.

The mechanism of diuresis during the 1st h of immersion was investigated using anesthetized dogs. Four different experiments were carried out. First, left atrial transmural pressure was measured before, during, and after immersion. The data suggest that, although the left atrium may or may not be stretched depending on the conditions of immersion, the amount of diuresis is independent of the amount of left atrial stretch, and therefore a causal relationship between diuresis and left atrial stretch could not be established. Second, bilateral cervical vagotomy was carried out. Immersion diuresis sometimes occurred despite this vagotomy, suggesting that the left atrial stretch reflex was not participating in those cases. Third, negative-pressure breathing was carried out to simulate the negative transthoracic pressure associated with uncompensated immersion. The average left atrial transmural pressure did not change. A slight hemodilution and a moderate diuresis occurred. There was no correlation between changes in left atrial transmural pressure and changes in urine ouput. Fourth, blood studies were done on splenectomized dogs subjected to immersion. Hemodilution occurred and was most marked in dogs which had had their kidneys removed. The hemodilution is sufficient to explain the early phase of the immersion diuresis. The data suggest that, in anesthetized dogs, hemodilution is the probable initiator of diuresis upon immersion and that, in dogs, left atrial stretch is unrelated to diuresis during immersion or negative-pressure breathing.

Animals↗
PubMed1976

Cross-circulation study of natriuretic factors in postobstructive diuresis.

To study the role of circulating natriuretic factors in the postobstructive diuresis that occurs after relief of bilateral, but not unilateral ureteral ligation, cross-circulation was carried out between normal recipient rats and donor rats have either 24-h bilateral (BUL) or unilateral (UUL) ureteral ligation. With BUL donors, there was a rapid marked increase in sodium and water excretion in the recipient rats, sustained for 80-140 min, with a peak approximately 10 times control values. With UUL donors, no significant natriuretic response occurred. Changes in glomerular filtration rate, renal plasma flow, blood pressure, hematocrit, or circulating levels of aldosterone or Pitressin did not explain the diuresis-natriuresis produced by cross-circulation with BUL donors. Differences in the intrinsic renal damage produced by bilateral as compared to unilateral ureteral obstruction did not appear to account for this response, since UUL donors given an acute urea load and urine reinfusion caused a similar diuresis-natriuresis. Moreover, normal donor rats given a urea load also caused a diuresis-natriuresis nearly equal to that produced by BUL rats, and the relationship between increased urea excretion and sodium excretion or urine flow in the recipients was not different in the two groups. Total urine reinfusion for 3 h in donor rats produced a significant, although less marked, diuresis-natriuresis in recipient animals, with only a slight elevation of the blood urea nitrogen level, much less increase in urea excretion rate, and no significant relationship between urea excretion and sodium excretion or urine flow. The results indicate that potent natriuretic factors, which act by decreasing the tubular reabsorption of sodium and water, are present in the blood of rats with bilateral, but not unilateral, ureteral ligation. High blood and urine urea levels appear to be the factors responsible for the marked natriuresis-diuresis occurring in normal rats during cross-circulation with BUL donors, although suggestive evidence of other natriuretic factors in urine reinfused intravenously was also obtained. The data suggest that urea osmotic diuresis is an important mechanism for determining the striking difference between the postobstructive diuresis observed after relief of bilateral as compared to unilateral ureteral ligation.

Adenosine Triphosphatases↗
PubMed1975

Mechanisms of post-obstructive diuresis in the solitary hydronephrotic kidney of the rat.

1. In order to clarify further the phenomenon of post-obstructive diuresis, clearance and micropuncture experiments were done before and after relief of partial ureteral obstruction in rats with a solitary hydronephrotic kidney. 2. Glomerular filtration rate, urine flow and sodium excretion increased markedly, whereas surface nephron glomerular filtration rate increased only slightly and intratubular pressure, proximal and distal tubular water reabsorption did not change significantly. Decreased tubular reabsorption in deeper nephrons and collecting ducts appeared to be of major importance in the post-obstructive diuresis after relief of chronic obstruction. 3. In order to examine further the distinctive functional characteristics of the chronically hydro-nephrotic kidney, the results were compared with control rats having a solitary normal kidney or a solitary remnant kidney with an intact renal medulla. Urine flow rate and sodium excretion were higher and urine osmolality was lower (P less than 0-01) in post-obstructive kidneys when compared with either control group. There were no differences in glomerular filtration rate or surface nephron function which could account for the greater diuresis and natriuresis from the hydronephrotic kidney, thus confirming the importance of an abnormality in deep nephron or medullary function in post-obstructive diuresis. 4. There was a greater diuresis in post-obstructive rats with a marked increase in blood urea concentration. Water reabsorption in the distal nephron was decreased in such animals, as well as in urea-loaded rats with a remnant kidney, indicating the probable mechanism by which urea diuresis potentiates the phenomenon of post-obstructive diuresis.

Animals↗
PubMed1989

Studies on the adrenomedullary dependence of kappa-opioid agonist-induced diuresis in conscious rats.

1. The dependence of kappa-opioid agonist-induced diuresis, upon an intact and functional adrenal medulla in conscious rats, was investigated in order to test the hypothesis that the diuresis is mediated by a blood-borne 'diuretic factor', of adrenomedullary origin, released by kappa-opioid receptor stimulation. 2. Confirming previous observations, adrenal demedullation significantly attenuated diuretic responses to the kappa-opioid agonists U50488H, ethylketocyclazocine (EKC) and tifluadom, but did not affect basal urine output, furosemide-induced diuresis or the antidiuretic response to the mu-opioid agonist, buprenorphine. Naloxone abolished U50488H-induced diuresis, confirming an involvement of opioid receptors. 3. Transfusion studies established that blood, from intact rats treated with U50488H, induced diuresis in intact and demedullated recipient rats, whether or not the recipients had been pretreated with naloxone. However, blood from demedullated rats treated with U50448H was unable to induce diuresis when administered to intact or demedullated recipients. 4. It is concluded that kappa-opioid agonist-induced diuresis is dependent upon an intact and functional adrenal medulla and appears to be mediated by a blood-borne 'diuretic factor' of adrenomedullary origin.

Adrenal Medulla↗
PubMed1988

Diuresis from atrial receptors after hypophysectomy and local ablation with no changes in plasma vasopressin.

Stimulation of the left atrial receptors in dogs anaesthetized with chloralose results in a reflex diuresis and natriuresis. The efferent limb of this reflex is though to have at least three components: nervous, haemodynamic and humoral. The present study was designed to investigate the humoral component in dogs anaesthetized with chloralose; to determine whether a humoral agent, other than vasopressin, might be causative in this reflex diuresis. The nervous and haemodynamic components were prevented by pharmacological denervation. Any possible contribution to the diuresis by a decrease in the plasma concentration of vasopressin was prevented by the removal of the pituitary gland. In animals in which a spontaneous diuresis followed hypophysectomy, an infusion of arginine vasopressin sufficient to maintain urine flow in the normal range for these dogs anaesthetized with chloralose was given. Distension of small balloons at the pulmonary vein-atrial junctions and in the left atrial appendage discretely to stimulate the atrial receptors in eleven dogs anaesthetized with chloralose resulted in a significant diuresis. It was concluded that a blood-borne agent other than vasopressin was responsible for the observed diuresis. At the moment it is not known whether vasopressin or the diuretic agent, or both, are involved in the diuresis accompanying the stimulation of atrial receptors.

Animals↗
PubMed1979

[Studies of the effect of synthetic oxytocin and neurohypophyseal extract on diuresis of water-laden cattle].

The action of synthetic oxytocin and Glanduphen, a neurohypophyseal extract preparation, on the diuresis of six heads of cattle in lactation was studied, following intraruminal application of water. Intravenous injection of something between 10 and 30 I.U. of oxytocin reduced diuresis by 54 per cent on average, within 30 minutes from treatment. Urine-borne Cl- -concentrations went up by 315 per cent on average and quantitative Cl- -secretion by 87 per cent. The values recorded in response to the administration of doses between 10 and 40 I.U. of Glanduphen were 44, 785, and 344 per cent. Additional application of Glanduphen within 30 minutes from oxytocin injection caused less pronounced inhibition of diuresis or even some activation of diuresis. Literature on renal effects of vasopressin and of oxytocin was analysed, in that context, and the conclusion was drawn that antidiuretic effects were recordable neither from man nor from animals unless they were exposed to excessive application of water. The same hormone preparations, however, caused increase of diuresis in thirty animals with low rates of diuresis and higher osmotic urine pressure. Rise in saluresis was a most common result of vasopressin or oxytocin administration and did in no way depend on the diuresis level.

Animals↗
PubMed1986

The effects of peripherally administered monoaminergic drugs on ethanol diuresis in rats.

The effect of peripherally administered drugs that modify monoaminergic function, on ethanol (2.0 g kg-1, intragastrically)-induced changes in urine output has been examined in rats. The alpha-noradrenoceptor agonist, clonidine (0.05-0.15 mg kg-1) produced marked urine output and potentiated slightly the diuretic effect of ethanol. The alpha-noradrenoceptor antagonist, phentolamine (1-5 mg kg-1) dose-dependently decreased ethanol-induced diuresis. p-Chloroamphetamine (0.8-2.0 mg kg-1) produced significant diuresis and potentiated the diuresis produced by ethanol. Methysergide (1.25, 2.5 mg kg-1), a 5-hydroxytryptamine receptor antagonist, had no effect on urine output while it depressed the ethanol-induced increase in urine output. Apomorphine (0.8, 1.5 mg kg-1), a dopamine receptor agonist, did not modify urine output in either control or ethanol-treated animals, while the dopamine receptor antagonist, pimozide (0.75-3.0 mg kg-1), dose-dependently decreased ethanol-induced diuresis, but had no effect on urine output in control animals. Since our previous research indicates that the intraventricular administration of drugs that alter dopaminergic and 5-HT function does not alter ethanol-induced diuresis, the interaction of these types of agents with ethanol-induced diuresis in the present study suggests that the interaction was mediated peripherally.

Animals↗
PubMed1989

Role of atrial peptide in the natriuresis and diuresis that follows relief of obstruction in rat.

The present studies demonstrate that endogenous levels of atrial peptide are significantly elevated in the plasma of rats with bilateral ureteral obstruction (BUO) compared with control rats or rats with unilateral ureteral obstruction. The contribution of endogenous atrial peptide to the natriuresis and diuresis that follows release of BUO was examined by the intravenous infusion of heparin with or without the exogenous administration of atrial peptide. Infusion of heparin, which binds atrial peptide and interferes with its biological effect, decreased the natriuresis and diuresis observed after release of BUO. Heparin administration also markedly blunted the natriuresis and diuresis observed after exogenous administration of atrial peptide following release of BUO in rats. In contrast, heparin administration did not decrease the natriuresis and diuresis seen in the experimental kidney after relief of unilateral ureteral obstruction. The finding of increased plasma levels of atrial peptide in rats with bilateral ureteral obstruction together with the decrease in diuresis and natriuresis observed with the administration of heparin after release of BUO in these animals indicate that endogenous levels of atrial peptide contribute to the natriuresis and diuresis that occur after release of BUO in rats.

Animals↗
PubMed1990

A micropuncture study of proximal tubular transport of lithium during osmotic diuresis.

Lithium and sodium are normally reabsorbed in parallel with water by the renal proximal tubule whereby their tubular fluid-to-plasma concentration ratios (TF/P) remain close to unity throughout the proximal convoluted segment. During osmotic diuresis, the late proximal (TF/P)Na is known to decrease. The present experiments were undertaken to study whether the late proximal TF/P for Li decreases like that of Na during osmotic diuresis. Data were obtained in a control period (C) and in two successive periods during mannitol diuresis (P1, P2). Glomerular filtration rate decreased gradually during osmotic diuresis [1,147 +/- 32 (C) to 950 +/- 22 (P2) microliters.min-1.g kidney wt (KW)-1, P less than 0.01), whereas Li clearance (CLi) increased [377 +/- 21 (C) to 469 +/- 28 (P1, P less than 0.01) and 408 +/- 25 (P2, NS) microliters.min-1.gKW-1, respectively]. (TF/P)Na decreased from 0.98 +/- 0.02 (C) to 0.89 +/- 0.02 (P less than 0.01) and 0.90 +/- 0.04 (P less than 0.05) (P1 and P2, respectively). (TF/P)Li was close to, but significantly higher than, unity during control (1.09 +/- 0.02), but, in contrast to (TF/P)Na, it did not decrease significantly during osmotic diuresis. Delivery of water from the proximal straight segment, as estimated from CLi/CIn, increased in proportion to the delivery from the convoluted segment, as estimated from 1/(TF/P)In. It is concluded that the proximal net Li reabsorption follows more closely the net water reabsorption than the net Na reabsorption during osmotic diuresis.

Absorption↗
PubMed1975

The pathogenesis of post-obstructive diuresis. The role of circulating natriuretic and diuretic factors, including urea.

To investigate the pathogenesis of post-obstructive diuresis, a state of functional "anuria" during ureteral obstruction was created in awake rats by (a) bilateral obstruction (BO); (b) unilateral obstruction and contralateral nephrectomy (UO-Nx); or (c) unilateral obstruction and continuous i.v. reinfusion of urine from the intact contralateral kidney (UO-reinf). These groups were compared with unilaterally obstructed (UO) and sham-operated control (sham) rats. After release of obstruction of 24 h duration, mean urine flows (V) and sodium excretion rates (UNaV) were significantly elevated above those of sham rats in BO, UO-Nx, and UO-reinf animals, but slightly decreased in UO rats. Glomerular filtration rates were comparably depressed in UO, BO, UO-Nx, and UO-reinf rats. These results suggest that post-obstructive diuresis is due to one or more circulating diuretic factors that are normally excreted in the urine, and which, when retained )as in BO or UO-Nx rats) or returned to the circulation (as in UO-reinf rats), exert a diuretic affect. In additional experiments, UO rats infused with urea exhibited post-obstructive diuresis, if extracellular volume contraction was prevented. This result suggests that urea may be an important diuretic factor in post-obstructive diuresis, but does not exclude possible roles for other humoral factors. The intact kidney of UO-reinf rats displayed a massive unilateral diuresis and natriuresis, further suggesting the presence of potent diuretic factors in the urine. A marked increase in the fractional excretion of glomerular filtrate (V/GFR) by the intact kidney suggests that this diuresis may be attributable, in part, to impaired proximal reabsorption.

Aminohippuric Acids↗
PubMedDate not supplied

Diuresis during fluid infusion : buffer nerve and spinal influences on it.

The rate and cumulative volume of diuresis were measured sequentially for each incremental infusion dose of 5 ml/kg body weight till a 100 ml/kg or more dose was reached. Normal saline (NS), Ringer-Locke (RL) and tender coconut water (TCW) were infused in three groups each of paraldehyde (PLD), and chloralose and urethane (C & U) anaesthetised dogs. The slow infusion rate of about 0.5 ml/kg/min was used. The RL infusion was repeated in vagotomised and/or carotid sinus (CS) denervated dogs and spinal dogs with or without intact vagi. During the NS and RL infusion schedules in PLD anaesthetised dogs produced much less urine than C & U groups. The order of minimum to maximum diuretic effect caused by these fluids were RL, NA and TCW in PLD groups and NA, TCW and RL in C & U groups. The study indicates that the type of anaesthesia and the composition of infusion fluid determines the rate of infusion induced diuresis. PLD anaesthesia has antidiuretic effect, which is not overcome by vagotomy. In C & U anaesthetised dogs the vagotomy and CS denervation performed separately greatly increased the rate of infusion induced diuresis but the diuresis largely decreased when combined surgery was performed. The diuresis in spinal dogs was very low, though in the vagotomised-spinal dogs, the rate of diuresis was more than in the spinal dogs.

Animals↗
PubMed1989

Effect of diuresis versus therapeutic paracentesis on ascitic fluid opsonic activity and serum complement.

Therapeutic paracentesis has recently been reported to eliminate ascites in patients with cirrhosis more rapidly than diuresis. However, diuresis has been shown to increase ascitic fluid opsonic activity. Patients with adequate ascitic fluid opsonic activity have been reported to be protected from spontaneous bacterial peritonitis. In this randomized controlled trial, 19 patients with cirrhotic ascites were treated with diuresis versus daily therapeutic paracenteses during 20 hospitalizations. Serum and ascitic fluid complement concentrations and ascitic fluid opsonic activity were measured at the beginning and end of treatment. Although opsonic activity increased significantly (p less than 0.01) in patients treated with diuresis, this parameter was stable in the paracentesis group. The stability of the ascitic fluid opsonic activity and complement concentration in the paracentesis group were maintained at the expense of a decrease in serum complement, whereas serum and ascitic fluid complement increased in the diuresis group. Diuresis may have the advantage over therapeutic paracentesis of providing better protection from spontaneous bacterial peritonitis. Study of larger numbers of patients will determine if these changes in complement concentrations and opsonic activity translate into an increased risk of spontaneous bacterial peritonitis in vivo.

Ascites↗