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[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

[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

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

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

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

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

[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

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

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

The alpha 1-blocker dapiprazole inhibits diuresis but not drinking and feeding induced by U-50,488H.

To further explore the interaction between opiates and catecholamines in the control of water balance, we studied the effects of the alpha 1-adrenoceptor antagonist dapiprazole on the modifications in drinking and diuresis produced by U-50,488H (a selective kappa-opiate agonist), morphine, naloxone, and amphetamine in rats. Because animals were maintained in a free-feeding paradigm and water intake is also controlled by feeding (prandial drinking), food intake was also measured. At doses administered (3-6 mg/kg, IP), dapiprazole had no effect on basal food and water intake or on diuresis. Nor did it modify changes in feeding and drinking produced by U-50,488H, morphine, naloxone, and amphetamine. It did, however, antagonize the diuretic effect of both U-50,488H and amphetamine. In addition, suppression of diuresis was obtained by combining doses of dapiprazole and morphine or naloxone that were devoid of antidiuretic effects when administered independently. A further experiment showed that diuresis produced by water load was also prevented by dapiprazole. alpha 1-Adrenoceptors thus appear to play a role in the regulation of water balance in a condition of free access to water, inhibiting diuresis without affecting drinking.

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

[Investigations into urea elimination in patients with advanced chronic renal failure during forced diuresis].

Controlled balance studies were performed in 12 oedema-free patients with advanced chronic renal failure with optimal dietary pretreatment. Forced water diuresis did not result in a significantly increased urea excretion as compared with spontaneous diuresis. Furosemide diuresis resulted in a significant increase (P less than 0.05) which was irrelevant therapeutically. The serum urea may even increase slightly under furosemide due to massive fluid loss. During thirst-regulated diuresis of advanced chronic renal failure urea back-diffusion is probably already reduced to a minimum. Normal hydration provided, forced water diuresis (oral or parenteral fluid) is useless and irresponsible as it poses additional risks in such patients. Furosemide in high dosage in over-hydrated patients is an effective diuretic even in advanced renal failure. The slightly significant increase in urea excretion during furosemide treatment does not result in important benefits in dietetically well treated patients.

Adult

Pressure diuresis and autonomic function in conscious dogs.

Pressure diuresis is thought to be a major long-term regulator of arterial blood pressure (AP). Previously, pressure diuresis has been characterized using pharmacological or surgical blockade of other mechanisms known to affect renal function. This study evaluated pressure diuresis in conscious dogs with minimal experimental interference. Dogs were chronically instrumented under pentobarbital anesthesia with aortic and urinary bladder catheters. AP was increased by 10% in resting dogs by exposure to increased light and sound intensity (arousal) for 90 min. During arousal, urine flow (UV) and Na+ excretion (UNa+ V) correlated with AP (UV vs. AP, r = 0.12, P less than 0.05; UNa+ V vs. AP, r = 0.19, P less than 0.005; 17 trials in 7 dogs). Arousal did not affect the plasma concentration of atrial natriuretic factor, suggesting that this hormone did not contribute to the correlations between UV or UNa+ V and AP. Because arousal may induce an autonomically mediated antidiuresis, studies were repeated during autonomic ganglionic blockade with hexamethonium. During autonomic blockade, the correlations between UV or UNa+ V and AP were increased (UV vs. AP, r = 0.72; UNa+ V vs. AP, r = 0.72, P less than 0.001; 6 trials in 4 dogs). We conclude that the effect of pressure diuresis on UV and UNa+ V can be detected in the intact animal, during normal operation of all the mechanisms that control renal function. Furthermore, when autonomic reflexes are blocked, the pressure-diuresis mechanism is a major determinant of UV and UNa+ V.

Animals

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

Diurnal and nocturnal diuresis and natriuresis in obstructive sleep apnea. Effects of nasal continuous positive airway pressure therapy.

Excessive nocturnal diuresis and natriuresis have been reported in patients with sleep apnea. The mechanisms responsible for these alternations in nocturnal renal function have not been clearly identified. To gain further insight into this matter, we studied 12 patients (one woman) with a mean +/- SD age of 50 +/- 9 yr and body mass index of 36.9 +/- 8.6 kg/m2. Polysomnography showed in all a sleep apnea syndrome with an apnea-hyponea index (AHI) of 81.3 +/- 41.7. Treatment with nasal continuous positive airway pressure (nCPAP) resulted in an AHI of 19.4 +/- 13.7 and in normalization of sleep characteristics. Diurnal renal function was normal in all subjects. Although untreated, patients showed an abolition of the well-known decrease in diuresis and natriuresis during the night (diurnal and nocturnal diuresis 56.3 +/- 26.8 and 77.2 +/- 33.4 ml/h, respectively, p = NS; diurnal and nocturnal fractional urinary Na+ excretion 0.42 +/- 0.09 and 0.70 +/- 0.55 ml/100 ml glomerular filtration [GF], respectively, p = NS). Results of nocturnal studies under nCPAP therapy showed a significant decrease in diuresis and natriuresis (nocturnal diuresis before and under nCPAP, respectively: 90.4 +/- 27.3 and 70.6 +/- 25.1 ml/h, p less than 0.02; nocturnal fractional urinary sodium excretion before and under nCPAP, respectively: 0.76 +/- 0.53 and 0.44 +/- 0.37 ml/100 ml GF, p less than 0.03). Morning blood levels of renin, aldosterone, antidiuretic hormone, epinephrine, and atrial natriuretic factor showed no significant difference before and under nCPAP, whereas norepinephrine significantly decreased from 309.5 +/- 104.2 before to 230.4 +/- 88.4 pg/ml under nCPAP (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Circadian Rhythm

The effect of electrophoretic lignocaine blockade in the region of the carotid sinuses on spontaneous and water diuresis.

The effect of electrophoretic lignocaine blockade in the region of the carotid sinuses on changes in the intensity of spontaneous and water diuresis was investigated on anaesthetized dogs. After the blockade a reduction in spontaneous diuresis was observed and a marked and statistically significant restriction of water diuresis was noted as compared with the control experiments. The reduction in diuresis after the blockade was of a brief duration and did not appear to be related to changes in the intensity of the filtration through the kidneys, which was only slightly lower, but to changes in reabsorption. In all probability, the carotid blockade is connected with a dominance of hormonal effects by elimination of the effect of the nervi vagi, osmoreceptors of the carotid arteries and in particular the chemoreceptors of the carotid body.

Animals

Nocturnal diuresis in panhypopituitarism.

Although impaired water diuresis in adrenocortical insufficiency is well-known, little attention has been paid to the diuretic pattern at night. In two cases of panhypopituitarism, the nocturnal diuretic pattern was found to be quite different from that in the morning, and marked diuresis did occur after water loading at night, without any significant change of serum cortisol which remained at a low level throughout the day. At the antidiuretic stage in the morning, urine osmolality continued to rise gradually, in spite of the water loading, to the level of 666 mOsm/liter. At the water restriction test, the urine was concentrated only to the same level of 600-700mOsm/liter. At the ascending stage of urine osmolality, exogenously injected pitressin showed little antidiuretic effect, although the kidney was able concentrate urine to the higher level later. In the morning, 3 liters of 5% glucose infusion failed to produce a marked diuresis in spite of extreme plasma dilution and expansion. Furosemide immediately induced diuresis even in the morning and the kidney recovered its ability to respond to pitressin. Glucocorticoid also improved the diuretic pattern in the morning, but a latent period of about 2 hr was always observed before the appearance of the effect. What happened during this latent period was unclear, but it was interesting to note that a mechanism similar to that which induces diuretic response seemed to occur without glucocorticoid at night.

Betamethasone

Diuresis increases ascitic fluid opsonic activity in patients who survive spontaneous bacterial peritonitis.

Patients with low protein ascites and deficient ascitic fluid opsonic activity have been shown to be unusually predisposed to development of spontaneous bacterial peritonitis. Survivors of spontaneous peritonitis frequently develop recurrent infection. Diuresis has been shown to increase the ascitic fluid opsonic activity of patients who have never had spontaneous bacterial peritonitis. Patients with adequate opsonic activity are protected from ascitic fluid infection. Theoretically, the subset of patients who develop spontaneous peritonitis may have such severe liver disease that (i) their ascites is refractory to diuretic therapy or (ii) their ascitic fluid opsonic activity does not increase in response to diuresis. In this study, opsonic activity and concentrations of total protein and complement components were measured in the ascitic fluid of 11 patients who were hospitalized with spontaneous bacterial peritonitis and who responded to oral diuretics. The mean values of all of these parameters were found to increase significantly comparing the end-of-diuresis samples to the specimens that were diagnostic of ascitic fluid infection. Patients who survive spontaneous bacterial peritonitis are able to increase their ascitic fluid total protein and opsonic activity in response to diuresis. This increase in endogenous antimicrobial activity may help prevent recurrence of ascitic fluid infection.

Amiloride

Post-obstructive diuresis: a varied syndrome.

A prospective study was undertaken to define the clinical features, natural history and etiology of post-obstructive diuresis. Studied in detail were 8 patients with a massive diuresis after relief of urinary tract obstruction. We found that urea mediated osmotic diuresis, natriuresis owing to elimination of retained sodium from the obstructed phase, tubular defects in sodium reabsorption, renal unresponsiveness to antidiuretic hormone and iatrogenic factors may play varying roles in each individual diuresis. Overzealous fluid replacement should be avoided.

Adult