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PubMed1982

Studies on the nature and mechanism of the diuretic activity of the opioid analgesic ethylketocyclazocine.

Subcutaneous injection (0.1 - 3.0 mg/kg) of ethylketocyclazocine (EKC; a prototype kappa agonist) resulted in a dose-dependent increase in urine formation in conscious rats. The increase in urine volume was unaccompanied by a corresponding increase in electrolyte excretion; thus, EKC behaved like a "water diuretic." The diuretic activity was completely abolished by naltrexone, an opiate antagonist. Water loading (10 ml/kg) and EKC (0.5 mg/kg) diminished plasma vasopressin levels equally 60 min after treatment. However, urine formation during the 1 st hr was greater in EKC-treated rats than in water-loaded rats. These results suggested that more than one component was responsible for the diuretic activity of EKC. A central effect of EKC on plasma vasopressin and urine volume was not evident. EKC (10 micrograms/rat) when injected s.c. caused diuresis, but was ineffective as a diuretic when injected into the lateral ventricle. EKC was effective in blocking stimulation of vasopressin secretion caused by volume contraction. EKC also blocked vasopressin-stimulated water flow in the toad bladder, a model of the renal distal tubule and collecting duct. We propose that EKC is diuretic by virtue of inhibition of vasopressin secretion and attenuation of the ADH response in the kidney. Both of these actions may be mediated via opioid receptors responsive to kappa agonists and inaccessible from the cerebroventricle.

Analgesics, Opioid↗
PubMed1992

A novel quinolinone diuretic, M12285, and its activation mechanism through sulfate conjugation.

The diuretic activity of a quinolinone oxime diuretic, M12285, was examined after renal arterial, i.v. and portal injection in rats. M12285 injected into the renal artery at a dose of 1 mg/kg caused no diuretic effect, whereas i.v. and portal injections induced marked diuresis dose dependently. The minimum effective dose with portal injection was lower (1 mg/kg) than that with i.v. injection (3 mg/kg) and the start of the effect was faster with portal injection. These results indicated that some metabolic modification in the liver is necessary for the diuretic activity to appear. Accordingly, we performed in situ rat liver perfusion with M12285 and obtained several metabolites. Renal arterial injection of each fractionated metabolite of M12285 revealed that all the diuretic activity derived from one of these metabolites. From IR and 1H-nuclear magnetic resonance (1HNMR) measurements, the chemical structure of this active metabolite was assumed to be a sulfate-conjugated form of M12285 at the oxime moiety. Based on this tentative chemical structure, we synthesized the oxime sulfate of M12285 (potassium salt, M17000) and confirmed the identity of IR and 1HNMR spectra. Administration of M17000 into the renal artery induced apparent diuresis in a dose-dependent manner in both rats and dogs. These results indicate that the oxime sulfate of M12285 is responsible for the diuretic activity of M12285. Therefore, we synthesized several derivatives of M17000 and confirmed their possible therapeutic value as a novel family of diuretics, namely quinolinone oxime sulfonic acids.

Animals↗
PubMed1986

On the mechanisms of kappa-opioid-induced diuresis.

In conscious saline loaded rats, the kappa-opioid agonists tifluadom, U50488, and ethylketocyclazocine, given subcutaneously, induced a characteristic diuresis which could be antagonized by naloxone. Bilateral adrenal demedullation significantly reduced adrenal gland catecholamine content and plasma adrenaline levels, but did not significantly affect plasma corticosterone levels, indicating that the adrenal cortex remained both intact and functional. Seven days following bilateral adrenal demedullation, the subcutaneous administration of the kappa-agonists no longer induced diuresis. However, demedullation did not affect the diuretic response to frusemide or clonidine, nor did it affect the antidiuretic response induced by the mu-opioid agonists morphine and buprenorphine. Adrenal catecholamines do not appear to be involved in kappa-opioid-induced diuresis, since pretreatment with propranolol, prazosin and idazoxan did not affect the diuretic response in intact animals. The results indicate a link between the adrenal medulla and kappa-opioid-induced diuresis and suggest that a peripheral mechanism may also be involved in mediating this effect.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1990

Intestinal fluid transport in the small intestine of normotensive and spontaneously hypertensive rats: the importance of enteric nerves, chloride and bicarbonate secretion.

Fluid transport was studied in periarterially denervated jejunal segments of spontaneously hypertensive rats (SHR) of the Okamoto strain and as a control also in Wistar-Kyoto rats (WKR). In agreement with the findings of an earlier report a 'spontaneous' fluid secretion was observed in SHR whereas the intestinal segments of WKR absorbed fluid. The fluid secretion in SHR was inhibited by tetrodotoxin or lidocaine placed on the serosal surface of the intestinal segment under study. These observations confirm our earlier proposal that secretory nervous pathways in the enteric nervous system evoke the fluid secretion in SHR. In an attempt to analyse the cellular mechanisms that underlie the fluid secretion in SHR the animals were given loop diuretics in doses that evoked diuresis. No effect on intestinal fluid transport was seen in SHR or WKR. Furthermore, to study the importance of bicarbonate transport alkaline secretion was monitored with a pH-stat technique. In the initial part of the experiments the alkaline secretion in SHR and WKR was similar. In half of the SHR experiments alkaline secretion increased with time. This increase could be completely reversed with hexamethonium and atropine (only tested in three experiments). The time course of the alkaline and fluid secretion in SHR did not coincide, indicating that bicarbonate ion transport was not the major cause of fluid secretion in SHR. In agreement with this conclusion it was observed that acetazolamide (a blocker of carbonic anhydrase) did not influence rate of fluid transport in SHR or WKR.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Radiochromium conservation and distribution in diuretic states.

The effect of free water diuresis by three different modalities on body 51Cr conservation and distribution was studied in adult male rats. Despite massive diuresis, ADH deficiency had little effect on body 51Cr retention or relative tissue distribution of 51Cr but did induce 25-40% increases in serum 51C concentrations which were reversible by pitressin administration. Glucose feeding produced copious diuresis but no change in body 51Cr retention or relative tissue distribution of 51Cr. The serum 51Cr concentration decreased 23% in association with small increases in serum glucose and insulin concentrations. LiCl administration produced moderate diuresis with little change in body 51Cr retention and inconsistent changes in serum and tissue 51Cr distribution. These data indicate normal body retention of 51Cr despite body water pool turnovers of up to 100% per day. Hence, renal handling of Cr is flow-independent, presumably due to Cr reabsorption at a proximal site within the nephron. However, a marked restriction of Cr filtration by the glomerulus due to protein binding of Cr cannot be ruled out by these data. Differences in body weight, even if assumed to be due to altered extracellular fluid volume, are insufficient to account for the serum 51Cr data. Previous observations in adrenalectomized rats also do not support a role for aldosterone secretion secondary to extracellular fluid volume shifts. Therefore, the increase in serum 51Cr concentration in ADH deficiency may be due to an effect of ADH to promote cellular transport of Cr whereas the decrease in serum 51Cr concentration during glucose feeding is probably due to increased cellular penetration of Cr secondary to insulin action.

Animals↗
PubMed1992

Pseudo-Bartter's syndrome from surreptitious diuretic intake: differential diagnosis with true Bartter's syndrome.

Five patients with pseudo-Bartter's syndrome from surreptitious diuretic abuse were compared with six patients with true Bartter's syndrome, diagnosed as a normotensive, hyperreninaemic, hypokalaemic metabolic alkalosis with normal urine chloride excretion, low CH2O/(CH2O+CCl) ratio during maximal water diuresis and negative urine screen for diuretics. The latter was positive for frusemide in four and for hydrochlorothiazide in the remaining pseudo-Bartter's patients. The two groups of patients did not differ as for plasma Na+, Cl-, K+, HCO3-, renin, and aldosterone, while uric acid and Mg2+ were greater in pseudo-Bartter's patients. Daily and fasting urine Na+, Cl- and K+ excretion were less in pseudo-Bartter's patients; however, there was substantial overlap of values between the two groups. Fractional distal solute reabsorption during maximal water diuresis was low in the six patients with Bartter's syndrome and in two pseudo-Bartter's patients; thus, this parameter could not be taken as a specific diagnostic marker of Bartter's syndrome. Frusemide administration, 40 mg i.v., induced a brisk increase of urine flow (11.7-21.8 ml/min), UOsm (148-186 mOsm/kg H2O) and FENa (14.6-24%) in Bartter's syndrome, but not pseudo-Bartter's patients; in all pseudo-Bartter's patients frusemide-induced changes of UOsm (13-97) and FENa (-0.5 to 10.2) were markedly less than in Bartter's syndrome patients. Frusemide resistance in pseudo-Bartter's patients was most probably related to diuretic-induced ECF volume contraction and increased proximal tubule solute reabsorption; in fact fractional lithium clearance (FELi, a marker of post-proximal solute delivery) was low in pseudo-Bartter's, but not in Bartter's syndrome patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1982

Tracheal relaxant and cardiostimulant actions of xanthines can be differentiated from diuretic and CNS-stimulant effects. Role of adenosine antagonism?

Theophylline (1, 3-dimethylxanthine) and enprofylline (3-propylxanthine) have been examined for effects in the rat. Enprofylline was 3.8 times as potent as theophylline as a tracheal relaxant in vitro, and 1.3 times as potent as theophylline to increase the rate of isolated perfused hearts. An oral dose (5 mg/kg) of enprofylline to rats was almost completely recovered in the urine as unchanged drug, showing that this xanthine is well absorbed and negligibly metabolised. Theophylline (10 and 30 mg/kg p.o.) significantly and dose-dependently increased locomotor activity in rats whereas the same doses of enprofylline were without effect on behaviour. Theophylline ( 5-20 mg/kg p.o.) produced significant and dose-dependent natriuretic and volume diuretic effect with little augmentation of potassium excretion. Enprofylline up to 10 mg/kg was without diuretic effects. At the large dose of 20 mg/kg enprofylline decreased sodium excretion and produced some volume diuresis. It is suggested that lack of diuretic and CNS-stimulant behavioural effects by enprofylline is due to its low ability to antagonise adenosine receptor stimulation. Pharmacodynamic differences between enprofylline and the potent adenosine antagonist theophylline may indicate a functional importance of endogenous adenosine.

Adenosine↗
PubMed1981

Role of dopamine in the diuresis caused by stimulation of atrial receptors.

The diuretic response to stimulation of left atrial receptors, by distending balloons located either at the pulmonary vein-left atrial junctions or in the body of the left atrium was studied during blockade of dopamine receptors using a continuous infusion o sulpiride in doses ranging from 0.632 to 5.153 mumol . kg-1 . min-1, in anaesthetized dogs. A diuretic response was obtained in each experiment of distension of the balloons: the response was similar to that observed in dogs without blockade of dopamine receptors and was not significantly related to the dose os sulpiride used. It is concluded that the diuretic response to stimulation of atrial receptors, known to be mediated by a blood-borne agent, is unlikely to be caused by dopamine.

Animals↗
PubMed1990

Atrial natriuretic polypeptide after burn injury: blood levels and physiological role in rats.

To define the relationship between atrial natriuretic polypeptide and the physiological changes of water and electrolytes after burns, the changes in plasma hormonal levels, including atrial natriuretic polypeptide, and urinary water and sodium excretions were examined in burned rats. Further, to elucidate the physiological significance of atrial natriuretic polypeptide after burns, the effects of a specific antiserum against atrial natriuretic polypeptide were determined in burned rats. Plasma atrial natriuretic polypeptide levels in rats following 30 per cent BSA full skin thickness burns were elevated for sustained periods (432.3 +/- 156.5 pg/ml, P less than 0.01 on day 1 postburn, 244.5 +/- 73.7 pg/ml, P less than 0.05 on day 3 postburn). Urine volume and sodium excretion decreased significantly during the first 72 h after burns. On day 3 postburn, urine volume and sodium excretion began to increase significantly. Specific rabbit antiserum against atrial natriuretic polypeptide was injected into the burned rats during this diuretic phase. Significant inhibition of diuresis and natriuresis was observed after the injection of antiserum (27.5 +/- 2.4 per cen decrease in urine volume, 57.1 +/- 10.4 per cent decrease in sodium excretion). These results suggest that atrial natriuretic polypeptide plays a physiological role in the regulation of urinary water and sodium excretion after burns.

Aldosterone↗
PubMed1987

Negative inotropic effects of furosemide in the isolated rabbit heart: a prostaglandin-mediated event.

Furosemide is an effective diuretic that initiates a rapid diuresis and peripheral vasodilatation through renal adenylate cyclase inhibition and prostaglandin synthesis. Recently, it has been shown to be associated with activation of the neurohumoral vasoconstrictor mechanism and a further compromise of left ventricular function in patients with heart failure. The present study was performed to investigate the direct effects of furosemide on myocardial performance in the isolated perfused rabbit heart. Furosemide (10(-3) M) caused a significant decrease in developed pressure as well as a similar fall in coronary perfusion pressure. Furosemide also decreased myocardial contractility when the coronary perfusion pressure was kept constant. The change in developed pressure but not the decrease in coronary perfusion pressure could be blocked by treatment with indomethacin. Furosemide did not antagonize rabbit cardiac membrane adenylate cyclase. Therefore, furosemide has a direct inhibitory effect on cardiac contractility that is related to prostaglandin synthesis.

Adenylyl Cyclases↗
PubMed1993

Successful use of continuous veno-venous haemofiltration to treat profound fluid retention in severe peripartum cardiomyopathy.

The use of continuous veno-venous haemofiltration after failure of conventional treatment in a patient with severe peripartum cardiomyopathy is described. Treatment with inotropes and diuretics failed to produce a diuresis despite the presence of severe fluid overload. Haemofiltration over a 9-day period allowed removal of 171 of fluid with a concomitant improvement in haemodynamic function and a spontaneous diuresis.

Adult↗
PubMed1987

Refractory ascites precipitated by obstructive uropathy.

A case is presented where a patient's cirrhotic ascites was refractory to conventional treatment and where the usual factors which precipitate refractory ascites were excluded. We believe that this patient's apparently refractory ascites was precipitated by an obstructive uropathy, as evidenced by dramatic diuresis, natriuresis, and return to diuretic sensitivity following relief of the obstruction.

Ascites↗
PubMed2006

Is there a competition between urine volume and peritoneal ultrafiltration in peritoneal dialysis patients?

Many peritoneal dialysis patients are overhydrated. Overhydration may lead to hypertension and left ventricular hypertrophy, and may be related to inflammation and malnutrition. The presence of overhydration is not always detected by clinical examination. Especially patients with peritoneal ultrafiltration failure and/or negligible residual renal function are prone to overhydration. Treatment consists of a combination of sodium and fluid restriction, in combination with increased peritoneal ultrafiltration and loop diuretics in patients with residual diuresis. Peritoneal ultrafiltration can be enhanced by the use of hypertonic glucose solutions or icodextrin. In some, but not all, studies, residual renal function or diuresis declined with an increase in peritoneal ultrafiltration. At least in a subset of patients, underhydration might have played a role in this phenomenon. We propose to treat overhydration using both clinical criteria and objective techniques such as vena cava echography or bioimpedance measurements.

Body Water↗
PubMed1967

The effects of infusion of water on renal hemodynamics and the tubular reabsorption of sodium.

Anesthetized dogs receiving an infusion of chlorothiazide and ethacrynic acid were given 600-ml infusions of distilled water or dilute dextrose solutions. The absolute rate of tubular sodium reabsorption was depressed, and the glomerular filtration rate was increased during the water loading, despite the associated decreases in plasma sodium concentration and decreases in the filtered load of sodium. The extent to which fractional sodium reabsorption decreased and the excretion of sodium increased was inversely related to the degree to which the filtered load of sodium was depressed as a result of the decreased plasma sodium concentration. We conclude that, in the presence of the diuretic blockade of distal tubular sodium reabsorption, infusion of water depresses proximal tubular reabsorption of sodium and that these changes are qualitatively similar to those previously observed during infusions of saline. Similar depression of tubular reabsorption of sodium and increased excretion of sodium occurred during water loading in the absence of diuretics in dogs undergoing saline diuresis, which presumably provided a high rate of distal sodium reabsorption before water loading. We suggest that volume expansion with water depresses proximal tubular reabsorption of sodium in a manner qualitatively similar to infusions of saline and that the extent to which sodium excretion is increased during water loading is dependent upon 1) the absolute extent to which proximal reabsorption is depressed, 2) the extent to which the filtered load of sodium is maintained in the presence of a falling concentration of sodium in plasma, and 3) the extent to which increased distal reabsorption compensates for the depressed proximal reabsorption of sodium. Mechanisms are suggested whereby the previously reported inverse relationship between plasma concentration of sodium and over-all tubular reabsorption of sodium may be only apparent, and could be the result of physiologic "glomerulotubular balance" during the specific experimental maneuvers.

Animals↗
PubMed1992

[Idiopathic hypercalciuria and bone density].

A decrease in bone density of the spine has been reported in individuals with hypercalciuria and the finding of the latter in osteoporosis patients is not uncommon. We studied 21 men and 8 women (mean age 47 +/- 13) with idiopathic hypercalciuria (IHCU) defined by an urinary calcium of more than 7.5 mmol/24 h in men and 6.25 mmol/24 h in women. The duration of IHCU was 10 (+/-) 8 years. Among the 29 patients, 24 had one or more renal calculi. Twenty one had been treated, by low calcium diet only (and diuresis), combined with a thiazide diuretic, or sodium phytate, or phosphorus. Bone mineral content (BMC) was measured in the lumbar spine and the upper end of the femur using an ORIS ODC 200 densitometer and compared with 29 control subjects paired for age and sex. No difference was found between the two groups concerning BMC values in either the spine or the 3 femoral sites (neck, Ward, trochanter). BMC was not correlated with urinary calcium. Thus individuals with IHCU showed no decrease in their bone mass, among this group seen in a department of nephrology. The influence of the treatment of IHCU remains to be defined.

Adult↗
PubMed1983

A-V block by an overdose of Clonidine.

The case of a young addict woman, chronically treated with Clonidine, in whom an overdose of the drug determined transient S-A and A-V conduction disturbances is reported. Such effects have been attributed to vagal hyperactivity and must be kept in mind when the drug is administered to patient of old age, with cardiac disease, or in association with digitalis. The treatment of choice is represented by forced diuresis induced either by osmotic diuretics of furosemide.

Adult↗
PubMed1994

Osmotic diuresis before Homer W. Smith: a winding path to renal physiology.

It was towards the end of the 18th century that a curiosity arose about what controlled the flow of urine. It was noted that though a patient's kidneys might be destroyed, the flow of urine continued until death. This puzzling phenomenon might have been understood had Ségalas's and Wöhler's observations been properly appreciated, that an extra load of urea, or any other substance that is excreted by the kidney, causes a diuresis. Nevertheless, these experiments were forgotten, and because of Bowman's and Ludwig's studies fluctuations in urine flow were ascribed to changes in blood pressure. It was not until 1870 to 1880 that Ustimowitsch, Falck and Richet stressed the role of urinary solutes on urine flow. Around 1900, Cushny also studied the diuretic effect of different solutes excreted in the urine and actually described what is now called an osmotic diuresis, though he did not use the term. These studies enabled him to deliver his "modern view" of the Secretion of the Urine. This was the first coherent concept which attempted to explain the formation of the urine and the regulation of its composition according to a pressure of a selective tubular reabsorption controlled by the needs of the "Milieu Intérieur." When glomerular and tubular functions became quantifiable, Homer W. Smith's disciples were able to define the exact nature of an osmotic diuresis and that explained the paradox of polyuria and renal failure.

Animals↗
PubMed1986

CHF: reflections on current management of the older patient.

The deleterious effects of prolonged bedrest on aerobic capacity, mineral balance, and various metabolic processes have been amply demonstrated. Since these functions are already compromised by aging per se, complete or prolonged bedrest should be avoided in geriatric cardiac patients if at all possible, regardless of their specific diagnosis. Diuretics are still the mainstay therapy for CHF. For elderly patients with mild CHF and preserved renal function, a thiazide rather than a loop diuretic appears preferable, due to more gentle diuresis and lower frequency of side effects.

Aged↗