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PubMed1978

Thallium intoxication treated with long-term hemodialysis, forced diuresis and Prussian blue.

A 56-year-old woman, who ingested 2 g of thallium sulfate, was successfully treated with long-term hemodialysis for 200 hours during ten days, combined with forced diuresis and Prussian blue. The effect of the artificial kidney dialysis was determined by repeated analysis of the thallium concentration in the dialysis bath and in blood samples. During the first 120 hours of hemodialysis, 143 mg of thallium was eliminated via the artificial kidney and 110 mg via the urinary tract. The present case of acute thallium intoxication is the first in which long-term hemodialysis has been used in the acute phase together with forced diuresis and Prussian blue. The data obtained are compared to those obtained from cases treated with hemodialysis in the past. It is concluded that treatment with hemodialysis should be considered as an important supplement to treatment with forced diuresis and Prussian blue in cases of thallium intoxication.

Antidotes↗
PubMed1987

Prolonged administration of human atrial natriuretic peptide in healthy men: evanescent effect on diuresis in spite of simultaneous infusion of norepinephrine.

In healthy, sodium and fluid replete men (n = 6) a transient increase in diuresis is seen during the prolonged infusion of human atrial natriuretic peptide (hANP: 50 micrograms h-1 for 6 h). In order to evaluate whether this evanescent diuretic effect of hANP is due to the peptide's hypotensive action, the latter was compensated for by the concomitant infusion of norepinephrine (NE: 50 ng kg-1 min-1). The decrease in hANP-induced diuresis towards the end of the 6-h infusion was not prevented by the additional infusion of norepinephrine, which also failed to influence hANP-stimulated natriuresis. Plasma concentrations of hANP, which were continuously elevated to about double of basal concentrations during the infusion of hANP, were not affected by exogenous norepinephrine. These data demonstrate that the transient character of hANP-induced diuresis cannot be offset by counterbalancing the peptide's hypotensive effect.

Adult↗
PubMed1985

Comparison of dynamic computed tomography, diuresis renography and DTPA parenchymal transit time in the assessment of dilatation of the upper urinary tract.

Three methods of assessment of upper urinary tract dilatation were compared prospectively. Forty-eight dilated renal units (35 patients) were studied, the majority being idiopathic pelvic hydronephrosis (69%). Dynamic computed tomography (CT) involves rapid sequence CT after injection of contrast medium. The maximum enhancement of a medullary region of interest (MMR) and its rate of enhancement (SMS) were derived from dynamic CT. Dynamic CT was compared with diuresis probe renography and measurement of parenchymal transit time (PTT) from DTPA imaging. The MMR (70.1 +/- 10.6 HU) and SMS (2.0 +/- 0.5 HU/s) in controls were significantly greater than in patients with upper tract dilatation (52.8 +/- 18.5 and 1.43 +/- 0.85 HU/s; both P less than 0.001). A significant association was observed between impairment of renal function in patients with upper tract dilatation and a low SMS and MMR (P less than 0.01). Statistically significant agreement was observed between the results of diuresis renography and PTT (P less than 0.025). However, no significant agreement was found when the results of dynamic CT were compared with either diuresis renography or with PTT. Dynamic CT as performed in the present study has no useful contribution to make in the diagnosis of patients with dilatation of the upper urinary tract.

Adult↗
PubMed1987

Modified method of diuresis renography for the assessment of equivocal pelviureteric junction obstruction.

Thirty-five hydronephrotic kidneys, in which diuresis renography showed either an equivocal (13) or non-obstructive (22) response pattern, were studied by a modified method in which intravenous frusemide was given 15 min before the start of the renogram so as to assess elimination during the period of maximum diuresis. Thirteen kidneys were identified as obstructed, including three in which the standard diuretic renogram appeared to exclude obstruction. These results indicate that the modified method increases the specificity of diuresis renography when used to assess patients with equivocal pelviureteric junction obstruction.

Adolescent↗
PubMedDate not supplied

Noradrenergic mechanisms in ethanol diuresis.

Neurotransmitter mechanisms that mediate the effect of ethanol on urine output were examined in male rats. To establish the neuronal systems involved in the diuretic action of ethanol, urine output was evaluated in animals pretreated with various pharmacological agents. The intraventricular administration of norepinephrine (1.5-12 micrograms) increased the diuresis produced by a 1.25 g/kg dose of ethanol. Clonidine (2.5, 5.0 micrograms), an alpha 2-receptor agonist, also increased ethanol diuresis, while the alpha 1-receptor antagonist phentolamine (14 and 35 micrograms) reduced it. beta 1,2-Adrenergic blocker propranolol (5 and 10 micrograms) significantly depressed ethanol-induced urine output. Conversely the beta 2,2-noradrenergic agonist isoproterenol (5 and 10 micrograms) increased the diuretic action of ethanol. On the other hand dopamine (4-20 micrograms) and serotonin (8 and 20 micrograms) had no effect on ethanol diuresis when given intraventricularly. These results indicate that the diuretic action of ethanol involves noradrenergic mechanisms.

Animals↗
PubMed1994

Renal excretion of endothelin in children is influenced by age and diuresis.

Endothelin is a peptide with vasoactive and diuretic potential. Its release has been demonstrated from endothelial and renal epithelial cells. Urinary excretion of endothelin, as shown by others, is thought to reflect intrarenal production. We measured endothelin by RIA in a population of healthy children from Germany and Hungary (group 1), neonates (group 3) and children before and during forced diuresis (groups 2a and 2b). Group 1 consisted of 24 children living in Germany and 13 children resident in Hungary. The age range in this group was 2.9-17 years. Daily excretion correlated significantly with age (r = 0.48, p < 0.001), but endothelin excretion corrected for body surface area remained constant with regard to the age group studied. This indicates that body or kidney size may influence endothelin excretion, respectively. There was no difference in endothelin excretion between the two countries. In premature infants and neonates (group 3), daily excretion of endothelin was highest in infants with very low gestational ages and decreased in full-term neonates to values not significantly different to the group of older children. The high values in premature infants may have been influenced by mechanical ventilation of physical stress, which cannot be differentiated in this study, however. In contrast to reported results in adults, renal excretion of endothelin was correlated positively to urine flow in all groups. Furthermore, the influence of forced diuresis was evaluated in 10 children with oncological disease before (group 2a) and during (group 2b) forced diuresis with fluid load (3 l/m2; n = 4) and fluid load with furosemide injection (0.3-1.0 mg/kg body weight; n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1981

Diuresis from stimulation of left atrial receptors: ADH and the Malpighian tubules of Rhodnius prolixus.

Stimulation of left atrial receptors causes a diuresis partly through a blood borne agent. Malpighian tubules of Rhodnius prolixus can detect a blood borne agent during the diuresis. It has been suggested that the agent is ADH but this is in dispute. In the present investigation, vasopressin (1-300 mu i.u. cm-3) was found to have no effect on Malpighian tubule secretion when added to plasma, Rhodnius Ringer and Rhodnius Ringer + 5-HT. In addition, it was shown that incubation with sodium thioglycollate of plasma samples obtained from anaesthetized dogs, before and during stimulation of atrial receptors by distension of a balloon in the lumen of the left atrium, did not abolish the differences between test and control plasma samples detected by the Malpighian tubules. It is concluded that differences in plasma detected by the Malpighian tubules and related to the diuresis which results from left atrial stimulation are not attributable to changes in concentration of ADH.

Animals↗
PubMed1983

Abolition of atrial receptor diuresis and of release of humoral agent by cooling the vagal nerves.

Stimulation of atrial receptors in anaesthetized dogs results in a reflex increase in urine flow mediated by vagal myelinated fibres and, in part, by a humoral agent of unknown identity. The humoral agent has been detected by an in vitro preparation of the Malpighian tubules of Rhodnius prolixus. The purpose of this investigation was to determine whether the present extract of plasma purporting to contain the humoral agent is also related to the reflex diuresis. In nine chloralose anaesthetized dogs atrial receptors were stimulated by distension of a balloon in the left atrium. Plasma samples collected before and during distension of the balloon, respectively, were precipitated with acetone, acid-treated and fractionated on Bio-Gel P-2. The purified samples were tested for the activity of the humoral agent on the Malpighian tubule preparation. In each dog, distensions of the balloon were performed with the cervical vagal nerves at 9 and 37 degrees C. Cooling the vagal nerves to 9 degrees C abolished the reflex diuresis and abolished the activity of the humoral agent recovered from a Bio-Gel P-2 fraction (molecular weight range 100-1800) which elutes between the void volume and the salt fraction. It was concluded that the substance recovered from Bio-Gel P-2 is associated with the diuresis in response to stimulation of atrial receptors; it is suggested that its presence is dependent on the integrity of the afferent limb of the atrial receptor reflex.

Animals↗
PubMed2004

Role of nitric oxide in the reflex diuresis in rabbits during pulmonary lymphatic obstruction.

The role of nitric oxide in the reflex diuresis in response to pulmonary lymphatic drainage was examined in anaesthetized, artificially ventilated New Zealand White rabbits. Pulmonary lymphatic drainage was obstructed by raising the pressure in a pouch created from the right external jugular vein. Pulmonary lymphatic obstruction resulted in a significant increase in urine flow from an initial control value of 8.9 +/- 0.5 ml (10 min)(-1) to 12.1 +/- 0.6 ml (10 min)(-1) during lymphatic obstruction (mean +/-s.e.m.; n= 17, P < 0.001). This increase in urine flow was accompanied by a significant increase in the excretion of sodium. Additionally, renal blood flow remained unchanged during the increase in urine flow caused by lymphatic obstruction. Intravenous infusion of L-NAME, a non-selective inhibitor of nitric oxide synthase (NOS), abolished the reflex diuresis. Furthermore, intraperitoneal administration of the relatively selective neuronal NOS blocker, 7-nitroindazole also abolished the response. It was observed that infusion of a more soluble neuronal NOS blocker, 7-nitroindazole sodium salt (7-NINA), into the renal medulla also abolished the reflex diuresis. These findings suggest that the increase in urine flow in rabbits caused by pulmonary lymphatic obstruction is dependent upon the integrity of neuronal NOS activity within the renal medulla.

Animals↗
PubMed2005

Role of adrenergic receptors in the reflex diuresis in rabbits during pulmonary lymphatic obstruction.

The role of adrenergic receptors in the reflex diuresis in response to pulmonary lymphatic drainage was examined in anaesthetized, artificially ventilated New Zealand White rabbits. Pulmonary lymphatic drainage was obstructed by raising the pressure in a pouch created from the right external jugular vein. This pulmonary lymphatic obstruction results in a reflex increase in urine flow and sodium excretion. This reflex is abolished by renal denervation and by administration of L-NAME, a non-selective inhibitor of nitric oxide synthase. Also, infusion of the relatively selective neuronal nitric oxide synthase blocker, 7-nitroindazole sodium salt, into the renal medulla abolished the reflex diuresis. In this study the effects of adrenergic receptor antagonists on the reflex increase in urine were observed. Both ureters were cannulated in order to determine urine flow from both kidneys separately. Prazosin, an alpha1 adrenergic receptor antagonist, was infused into the renal medulla of the right kidney, while the left kidney acted as control. Administration of prazosin in this manner did not block the reflex diuresis in response to pulmonary lymphatic obstruction in either kidney. However, rauwolscine, an alpha2 adrenergic receptor antagonist, abolished the reflex increase in urine and sodium excretion in the ipsilateral kidney while preserving it in the contralateral kidney. These findings suggest that the increase in urine flow in rabbits caused by pulmonary lymphatic obstruction is dependent upon activation of alpha2 adrenergic receptors within the renal medulla.

Animals↗
PubMed1975

Effect of destruction of the posterior pituitary on the diuresis from left atrial receptors.

1. In anaesthetized dogs, stimulation of atrial receptors after destruction of the pituitary gland results in a diuresis. This response was not abolished by the administration of bretylium tosylate and was also observed in a surgically denervated kidney. 2. The diuresis is qualitatively similar to that observed in anaesthetized dogs with intact pituitary glands. 3. It is concluded that the diuresis which results from stimulation of the left atrial receptors is mediated by a blood-borne agent which is not the antidiuretic hormone.

Animals↗
PubMed1987

Plasma atrial natriuretic peptide and spontaneous diuresis in sick neonates.

Plasma concentrations of immunoreactive human atrial natriuretic peptide (human ANP) were sequentially determined in 12 infants with respiratory distress syndrome (RDS) or meconium aspiration syndrome (MAS) during various phases of diuresis to elucidate the role of human ANP in the occurrence of spontaneous diuresis in the newborn. Plasma immunoreactive ANP concentrations during the diuretic as well as the maximum diuretic phase were significantly (p less than 0.001) higher than during the prediuretic phase. A gradual decrease occurred during the post diuretic phase, returning to prediuretic values after one week of life. Significant natriuresis, increased glomerular filtration rate, mild hyponatremia, and decreased blood pressure were observed in the diuretic phase in all the cases studied. These results suggest that hypersecretion of human ANP may play an important part in initiating spontaneous diuresis in sick neonates.

Atrial Natriuretic Factor↗
PubMed1991

'Low sodium' diuresis and ileal loss in patients with ileostomies: effect of desmopressin.

Patients with ileostomies show an early diuresis when sodium restricted; this, together with an obligatory ileal sodium loss, predisposes them to severe salt and water depletion. The role of arginine vasopressin in this circumstance and whether it is natriuretic, or antinatriuretic, is unclear. There is also controversy over its likely effect on small bowel fluid reabsorption. We have examined the effect of the non-pressor (V2) synthetic vasopressin analogue 1-deamino-8-D-arginine (desmopressin) on renal and ileal sodium and water excretion in ileostomy patients during acute adaptation to a low sodium diet. Patients were studied on two separate occasions (nonrandomised) with and without the administration of desmopressin (0.75 micrograms intramuscular, three times a day). In eight subjects without desmopressin there was pronounced diuresis on the first low sodium day, associated with a fall in renal sodium excretion and no change in ileal output or composition. In five (of the original) subjects with desmopressin there was pronounced antidiuresis, no change in renal sodium excretion, and no change in ileal output or composition. In both studies rises in plasma renin activity and salivary aldosterone concentration lagged behind the early decline in renal sodium excretion. We have confirmed the phenomenon of 'low sodium' diuresis after sodium restriction in ileostomy patients and shown that it can be prevented by desmopressin. Desmopressin has no direct or indirect effect on renal sodium excretion or ileal fluid and electrolyte loss in humans.

Aged↗
PubMed2006

Temporal diabetes- and diuresis-induced remodeling of the urinary bladder in the rat.

The natural history of diabetes mellitus-induced remodeling of the urinary bladder is poorly understood. In this study, we examined temporal remodeling of the bladder in diabetic and diuretic rats. Male Sprague-Dawley rats were divided into three groups: streptozotocin-induced diabetic, 5% sucrose-induced diuretic, and age-matched control. Micturition and morphometric characteristics were evaluated using metabolic cages and light-microscopic examination of the bladder 4 days and 1, 2, 3, and 9 wk after induction. Digital image analysis was used to quantify equatorial cross-sectional areas of bladder tissue and lumen, as well as relative content of the three primary tissue components: smooth muscle, urothelium, and collagen. Diabetes and diuresis caused significant increases in fluid intake, urine output, and bladder weight. In both groups, progressive increases were observed in lumen area from 4 days to 3 wk after induction and in wall area from 2 to 3 wk after induction. Wall thickness decreased within the first 2 wk in the diabetic and diuretic rats but returned to control at 3 and 9 wk. As a percentage of total cross-sectional area, smooth muscle area increased, urothelium area was unchanged, and collagen area decreased in diabetic and diuretic rats after 2-3 wk compared with control rats. In conclusion, diabetes and diuresis induced similar bladder remodeling. Diabetes-induced diuresis caused adaptive physical changes in rat bladder by 4 days after induction; remodeling was observed by 2-3 wk after induction and remained stable from 3 to 9 wk.

Animals↗
PubMed1990

Regulation of renal pelvic pressure by diuresis and micturition.

The influence of the voiding cycle and diuresis on the hydrodynamic pressures of the renal pelvis in the multicalyceal kidney of miniature pigs has been examined. Identification of the pressure patterns characteristic of the renal pelvis with an undisturbed pelviureteric and ureterovesical junction was emphasized. The frequency and amplitude of contractions in the renal pelvis were measured bilaterally. The patterns of renal pelvic pressure changes were interpreted during bladder filling and emptying and diuresis to evaluate the mechanisms facilitating the pressure isolation of the upper urinary tract. These studies were undertaken in the awake pig equipped with a long-term radiotelemetry implant transmitting renal pelvic and urinary bladder pressure. The results show that renal pelvic contractions are low-pressure events having an amplitude of 10.3 +/- 4.2 cmH2O and a frequency of 6.6 +/- 0.7 contractions/min. During basal hydration, the process of renal pelvic filling and emptying is active, with rhythmic pelvic contractions. The left and right renal pelvis demonstrate approximately equal frequency, 1.04:1.00, but are not synchronous. Furosemide-stimulated diuresis produces radical changes in the renal pelvis by transforming emptying from an active to passive mode and facilitating the transmission of voiding pressures and spontaneous bladder pressures to the kidney.

Animals↗
PubMed1994

Reflex control of renal sympathetic nerve activity during furosemide diuresis in rats.

To examine the relative role of cardiopulmonary and sinoaortic baroreceptor afferents in reflex changes in efferent renal sympathetic nerve activity (ERSNA) during furosemide diuresis, ERSNA was measured before and after administration of a maximal diuretic dose of furosemide (300 mg/kg iv) in four groups (n = 8 each) of pentobarbital sodium-anesthetized rats: animals with intact baroreflexes, sinoaortic denervation (SAD), bilateral vagotomy, or SAD plus bilateral vagotomy. In addition, measurements of left ventricular end-diastolic pressure (LVEDP), mean arterial pressure (MAP), heart rate, and afferent vagal nerve activity were performed. Furosemide administration produced an early increase in MAP (+40 mmHg) and ERSNA (+50%) that was maintained in rats with SAD plus vagotomy, suggesting that this effect is not of sinoaortic or cardiopulmonary baroreflex origin. The early pressor response was due to the vehicle, 2% ethanolamine, whereas the early renal sympathoexcitation was due to furosemide. Whereas MAP remained unchanged in rats with intact arterial baroreflexes, MAP gradually decreased along with a reduction in LVEDP during progressive diuresis-related volume depletion in animals with SAD. With progressive diuresis-related volume depletion and falling LVEDP, ERSNA increased in intact animals (delta ERSNA/delta LVEDP = 46.0 +/- 1.5%/mmHg). This late increase in ERSNA was inhibited by bilateral vagotomy or SAD, suggesting that vagal and sinoaortic baroreceptor afferents are both essential for expressing the reflex increase in ERSNA observed during furosemide-induced volume depletion. There were no significant differences among furosemide groups in urinary flow rate and sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed2000

Renal blood flow, early distal sodium, and plasma renin concentrations during osmotic diuresis.

Inconsistencies in previous reports regarding changes in early distal NaCl concentration (ED(NaCl)) and renin secretion during osmotic diuresis motivated our reinvestigation. After intravenous infusion of 10% mannitol, ED(NaCl) fell from 42.6 to 34.2 mM. Proximal tubular pressure increased by 12.6 mmHg. Urine flow increased 10-fold, and sodium excretion increased by 177%. Plasma renin concentration (PRC) increased by 58%. Renal blood flow and glomerular filtration rate decreased, however end-proximal flow remained unchanged. After a similar volume of hypotonic glucose (152 mM), ED(NaCl) increased by 3.6 mM, (P < 0.01) without changes in renal hemodynamics, urine flow, sodium excretion rate, or PRC. Infusion of 300 micromol NaCl in a smaller volume caused ED(NaCl) to increase by 6.4 mM without significant changes in PRC. Urine flow and sodium excretion increased significantly. There was a significant inverse relationship between superficial nephron ED(NaCl) and PRC. We conclude that ED(Na) decreases during osmotic diuresis, suggesting that the increase in PRC was mediated by the macula densa. The results suggest that the natriuresis during osmotic diuresis is a result of impaired sodium reabsorption in distal tubules and collecting ducts.

Animals↗
PubMed1978

Mechanism of exaggerated diuresis in spontaneously hypertensive rats.

The mechanism of exaggerated diuresis and natriuresis was studied in spontaneously hypertensive rats (SHR) by renal clearance and micropuncture techniques. Control normotensive rats of the same age and sex [Wistar-Kyoto rats (WKY)] were also studied. During the hydropenic control and the volume-expansion experimental periods absolute and fractional water and sodium excretion were greater in SHR than in WKY. Although fractional and absolute water and sodium reabsorption were similar along the proximal convolution in SHR and WKY, fractional and absolute water reabsorption in Henle's loop was less in SHR than in WKY. Hydrostatic and colloid osmotic pressures in the cortical peritubular microvasculature were similar in WKY and SHR. Acute normalization of renal perfusion pressure by aortic constriction reversed the exaggerated diuresis and natriuresis in SHR by halving the filtered load of water and sodium; whole kidney and single nephron glomerular filtration rates and blood flows decreased by 50%. It is concluded that the exaggerated diuresis and natriuresis of the spontaneously hypertensive rat is caused by a decreased reabsorption in the loop of Henle. The mechanism of this decreased reabsorption in the loop of Henle cannot be explained by alterations in the measured physical forces in the renal cortical microvasculature.

Animals↗