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PubMed1991

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↗

PubMed1997

Effect of interactions between nitric oxide and angiotensin II on pressure diuresis and natriuresis.

The present study examined the effect of an angiotensin II AT1 or AT2 receptor antagonist on the impairment of the pressure diuresis and natriuresis response produced by nitric oxide (NO) synthesis blockade. N omega-nitro-L-arginine methyl ester (L-NAME, 37 nmol.kg-1.min-1) lowered renal blood flow and reduced the slopes of the pressure diuresis and natriuresis responses by 44 and 40%, respectively. Blockade of AT1 receptors with valsartan increased slightly sodium and water excretion at low renal perfusion pressure (RPP). Blockade of AT2 receptors with PD-123319 had no effect on renal function. The administration of valsartan or PD-123319 to rats given L-NAME had no effect on the renal vasoconstriction induced by NO synthesis blockade. In addition, in rats given L-NAME, valsartan elevated baseline excretory values at all RPP studied, but it had no effect on the sensitivity of the pressure diuresis and natriuresis response. However, the administration of PD-123319 to L-NAME-pretreated rats shifted the slopes of the pressure diuresis and natriuresis responses toward control values, indicating that the impairment produced by NO synthesis blockade on pressure diuresis is dependent on the activation of AT2 angiotensin receptors.

Angiotensin II↗

PubMed1983

Mechanism of cold diuresis in the rat.

The effect of cold exposure (CE) on renal water excretion has not been clearly delineated. Conscious rats were exposed to decreased ambient temperature (15 degrees C). Forty-five minutes of CE resulted in reversible increases in urine flow and decreases in urine osmolality. The diuresis was not due to a diminished response to vasopressin (VP), as the antidiuresis associated with 500 microU of Pitressin given to water-diuresing rats was comparable at 15 and 30 degrees C. To determine whether the diuresis was due to intrarenal factors, glomerular filtration rate, renal blood flow, sodium excretion, and osmolar clearances were measured and found to be equivalent during control and cold conditions. To determine whether the observed diuresis was due to suppression of endogenous VP, VP-free Brattleboro rats undergoing a constant VP infusion were cold exposed. In these rats, CE was not associated with a change in either urine flow or urinary osmolality. This antidiuretic hormone-mediated mechanism was corroborated by a decrease in immunoassayable VP levels. To determine the mechanism whereby CE suppresses endogenous VP, plasma osmolality and hemodynamic parameters were measured. Although CE was not associated with a change in plasma osmolality, it did result in a significant increase in both mean arterial pressure and cardiac index. Pretreatment of rats with 6-hydroxydopamine prevented both the increase in mean arterial pressure and cold diuresis. We conclude that the diuresis observed upon exposure to 15 degrees C results from nonosmotic suppression of endogenous VP, as a consequence of the increase in mean arterial pressure.

Animals↗

PubMed1985

Effect of sustained water diuresis on prostaglandin E2 excretion in humans.

The relationship of the renal excretion of prostaglandin E2 (PGE2) to urine flow during a water diuresis was examined using radioimmunoassay (RIA) and gas chromatography-mass spectrometry (GC-MS). Seven normal women fasted overnight were water loaded with 20 ml/kg orally, and each hour for 3 h they drank water to replace the urine volume plus 20 ml. The osmolality of the collected urines ranged from 49 to 1,073 mosmol/kg. Assay of urinary PGE2 concentrations by both RIA and GC-MS gave a correlation coefficient of 0.94. Eight normal women were then studied with a water diuresis sustained for 6 h. The excretion of PGE2 (measured with the validated RIA) increased for the 1st 2-3 h (from 1.8 +/- 0.5 to 25.8 +/- 16.6 pg X kg-1 X min-1), but then fell to base-line level by the 5th h (to 2.9 +/- 0.8 pg X kg-1 X min-1) even though the water diuresis was sustained. The urinary concentration vs. time curves for PGE2 and for the freely diffusible solute urea were compared. PGE2 concentration remained elevated for 3 h before falling (from the 100 pg/ml range to 15 pg/ml) while urea concentration decreased steadily from the 1st h. This finding suggests that the early urinary PGE2 excretion was not a washout phenomenon and is consistent with a transient increase in PGE2 synthesis. We conclude that urinary excretion of PGE2 is not a simple function of urine flow after a water load. There is a transient initial increase in urinary PGE2 excretion at the start of a water load that probably reflects an increase in renal PGE2 synthesis. However, with a sustained water diuresis, PGE2 excretion falls, indicating that an enhanced PGE2 synthesis rate is not required to sustain a water diuresis.

Adult↗

PubMed1992

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↗

PubMed1981

Effects of vasopressin administration on diuresis of water immersion in normal humans.

Although previous studies have demonstrated that water immersion to the neck (NI) results in a significant diuresis, the mechanisms are incompletely delineated. Because recent studies in our laboratory have demonstrated that NI is associated with a suppression of antidiuretic hormone (ADH), it is possible that such a suppression mediates the encountered diuresis. The present study was undertaken to assess more directly the relative role of ADH suppression by determining the effects of vasopressin administration. Six hydrated normal subjects were studied on two occasions while undergoing 6 h of NI. During the second NI study, aqueous vasopressin (20 mU/h) was infused for the initial 4 h of study (NI + vasopressin). NI resulted in a significant increase in urinary flow rate beginning during hour 1 and persisting throughout NI. In contrast, during NI + vasopressin, the anticipated diuresis was abolished throughout the 4 h of vasopressin administration. Cessation of vasopressin administration during the final 2 h of NI + vasopressin resulted in a marked and prompt diuresis. The present observations are consistent with the formulation that ADH suppression participates importantly in mediating the diuresis of NI in hydrated normal subjects.

Adult↗

PubMed1993

Evaluation of upper urinary tract dynamics by diuresis renography in patients receiving urinary reservoir operation. Comparison of full and empty reservoir.

Upper urinary tract dynamics was evaluated using diuresis renography during full and empty reservoir in 14 patients (11 men, 3 women, 13-70 years old) with intestinal urinary reservoir or intestinal bladder augmentation. Types of operation were Mainz pouch urinary diversion 5, Mainz neobladder to urethra, 5, Kock pouch urinary diversion 2, and Mainz bladder augmentation 2. Diuresis renography was performed using 99mTc-DTPA and furosemide during full and empty reservoir, and several parameters (Tmax, T75, T50, GFR) in addition to the patterns of renogram were evaluated. In the normal control, none of the parameters of the diuresis renogram with full bladder differed from those with empty bladder. In 5 of 14 patients, abnormal waves on cystometry (CMG) were found, and in 4 of these 5 patients, the patterns of diuresis renogram of full reservoir were worse than those of empty reservoir. However, the patterns of diuresis renogram of full reservoir were not different from those of empty reservoir in 9 patients without abnormal waves on CMG. In conclusion, renal injury may easily occur in patients with intestinal reservoir and abnormal waves on CMG.

Adolescent↗

PubMed1992

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↗

PubMed1969

Effective plasma volume in cirrhosis with ascites. Evidence that a decreased value does not account for renal sodium retention, a sponteneous reduction in glomerular filtration rate (GFR), and a fall in GFR during drug-induced diuresis.

A reduction in effective (nonportal) plasma volume is considered the basis for renal sodium retention, a spontaneous reduction in glomerular filtration rate (GFR), and a fall in GFR occurring during drug-induced diuresis in patients with cirrhosis and ascites. In the present study the concept of a reduced effective plasma volume in cirrhosis is challenged by two lines of evidence, even though effective plasma volume itself could not be measured. (a) Total plasma volume failed to rise in 10 patients with the spontaneous loss of ascites, the appearance of sodium in the urine, and a rise in GFR. Portal pressure remained constant in these patients as ascites left, suggesting that effective plasma volume had not increased while portal plasma volume decreased. (b) Reduction of GFR could not be prevented in five patients with cirrhosis and ascites while total plasma volume was prevented from falling with albumin infusions during drug-induced diuresis. Reduction of GFR during drug-induced diuresis in 15 patients with cirrhosis and ascites was completely reversed with saline infusion despite continued diuresis with the identical drugs, excluding drug nephrotoxicity as the cause for the reduced GFR. The ascites of cirrhosis might no longer be regarded as a cause of effective plasma volume contraction, stimulating renal sodium retention and a reduction in GFR. More likely, this form of ascites is a result of plasma volume expansion and sodium retention. The causes for renal sodium retention and a spontaneous reduction in GFR remain unknown. The cause for a fall in GFR during drug-induced diuresis also remains unknown, but effective plasma volume contraction and drug nephrotoxicity seem excluded.

Alcoholism↗

PubMed1972

A micropuncture study of postobstructive diuresis in the rat.

In order to investigate the syndrome of postobstructive diuresis, clearance and micropuncture studies were carried out in rats after relief of 24 hr of bilateral (BUL) or unilateral (UUL) ureteral ligation. In rats with BUL, a striking diuresis and natriuresis occurred when the obstruction to one kidney (the experimental kidney) was relieved. The results were not influenced by administration of vasopressin or d-aldosterone. Whole kidney clearances of inulin and p-aminohippuric acid (PAH) in the experimental kidney were reduced to 10% and 20% of normal, respectively. Superficial nephron inulin and PAH clearances were also reduced, but only to 40% and 45%, respectively. These findings suggest a heterogeneity of nephron function in which deep nephrons were functioning poorly or not at all. To investigate the site of impaired tubular reabsorption in the surface nephrons, absolute and fractional water reabsorption was measured. Absolute reabsorption was found to be decreased all along the nephron. Fractional reabsorption in proximal tubules was normal, as indicated by an average endproximal tubular fluid per plasma inulin (TF/P(In)) of 2.16 vs. 2.30 in controls. TF/P(In) was markedly decreased in distal tubules (2.91 vs. 8.02) and final urine (5.56 vs. 263). These observations indicate that the major sites of impaired sodium reabsorption leading to the diuresis were beyond the proximal tubule.Rats with 24 hr of UUL did not demonstrate a comparable natriuresis or diuresis either spontaneously when the obstruction was relieved or after i.v. infusion of urea. A major difference between the BUL and UUL rats was that prerelease intrarenal hydrostatic pressure was markedly elevated (30.1 mm Hg) in the former but was below normal free-flow values (9.2 mm Hg) in the latter. Thus, elevation of intrarenal pressure during the period of obstruction may be causally related to the natriuresis and diuresis which occurs after the obstruction is relieved.

Aminohippuric Acids↗

PubMed1996

Distinction between obstructive and nonobstructive hydronephrosis: value of diuresis duplex Doppler sonography.

OBJECTIVE: The purpose of this study was to determine the diagnostic accuracy of diuresis duplex Doppler sonography in distinguishing between obstructive and nonobstructive hydronephrosis by calculating the resistive indexes before and after administration of furosemide. SUBJECTS AND METHODS: We prospectively studied 48 kidneys in 26 patients with suspected chronic renal obstruction. All patients underwent diuretic renography and duplex Doppler sonography before and after administration of furosemide. According to the findings at diuretic renography, kidneys were classified as nonobstructed (n = 12), indeterminate (n =9), obstructed (n = 8), or normal (n = 19). The mean resistive index of each kidney and the difference between the mean resistive indexes of both kidneys were calculated before and after administration of 0.5 mg furosemide per kilogram of body weight. A receiver operating characteristic curve was generated to determine the discriminatory resistive index value for diagnosing obstruction. RESULTS: Resistive indexes were not significantly different between kidneys with nonobstructive dilatation and normal kidneys before and after diuresis. Significant differences in resistive indexes before and after diuresis were seen between kidneys with obstructive dilatation and kidneys with nonobstructive dilatation, and between normal kidneys. Kidneys with obstructive dilatation showed a significant increase in resistive index after administration of furosemide. In the indeterminate kidneys, furosemide had a heterogeneous effect on the resistive indexes, indicating obstructive resistive indexes in five kidneys and nonobstructive resistive indexes in four kidneys. Receiver operating characteristic analysis revealed a diuresis resistive index of 0.75, which resulted in an accuracy rate of 95% in diagnosing renal obstruction. CONCLUSION: Diuresis duplex Doppler sonography is accurate in the differentiation of obstructed from nonobstructed kidneys and may facilitate the distinction between obstructive and nonobstructive hydronephrosis, notably in kidneys classified as indeterminate according to diuretic renography.

Diuresis↗

PubMed2003

Validation and comparison of the use of diuresis cystometry and retrograde filling cystometry at various infusion rates in female Beagle dogs.

OBJECTIVES: To compare retrograde filling cystometry at infusion rates of 5, 10, and 20 mL/min with diuresis cystometry for determination of an appropriate infusion rate and to confirm the reproducibility of measurements obtained by urethral pressure profilometry (UPP) and cystometry in female Beagles. ANIMALS: Adult female Beagles. PROCEDURE: Successive UPP and cystometry were performed by use of a water perfusion catheter on dogs anesthetized with propofol. Dogs randomly underwent each of the following at 1-week intervals: retrograde filling cystometry at 5, 10, and 20 mL/min, and diuresis cystometry. The maximum urethral pressure and closure pressure, functional and anatomic profile lengths, threshold pressure, threshold volume, and compliance were measured. RESULTS: For each UPP variable, significant differences were found among dogs, but no significant differences were found in intra- or interstudy measurements for individual dogs. For retrograde filling cystometry, threshold pressure was not significantly different between a 5 and 10 mL/min infusion rate. Threshold pressure was significantly higher during retrograde filling cystometry at 20 mL/min, compared with 5 and 10 mL/min, and was associated with bladder wall damages. Threshold pressure was significantly lower during diuresis cystometry, compared with retrograde filling cystometries. Threshold volume and compliance were not significantly different among retrograde filling cystometries but were significantly higher during diuresis cystometry. CONCLUSIONS AND CLINICAL RELEVANCE: Retrograde filling cystometry at 20 mL/min leads to unacceptable sudden increase in threshold bladder pressure. Retrograde filling cystometry at 10 mL/min can be recommended in a clinical setting, shortening the anesthesia time. However, diuresis cystometry approximates physiologic bladder filling most accurately.

Animals↗

PubMed1984

Protein intake conditions the diuresis seen after relief of bilateral ureteral obstruction in the rat.

Natriuresis and diuresis occur in experimental animals after release of bilateral ureteral obstruction. Accumulation of urea and/or other natriuretic factors during the interval of complete obstruction may play a role in the ensuing postobstructive diuresis. The present experiments examine the potential role of dietary protein intake in conditioning the magnitude of the postobstructive diuresis after unilateral release of bilateral ureteral obstruction of 24-hr duration in the rat. Rats were fed isocaloric diets containing high (40% casein) or low (6% casein) protein for 4 weeks prior to obstruction. Rats fed a high protein diet had greater urine flows and fractional excretion of sodium and potassium after relief of obstruction than rats fed a low protein diet. Increased excretion of urea accounted for only part of the greater diuresis seen in rats fed a high protein diet. Hence, greater accumulation of other natriuretic factors during the period of obstruction in rats fed a high protein diet must play a role in the increased diuresis seen in this group of animals after release of obstruction.

Animals↗

PubMed1999

Is the Gauer-Henry reflex important for immersion diuresis in men?

BACKGROUND: This study examines the relationship between the threshold for plasma vasopressin concentration [PVP] responses and diuresis (Gauer-Henry reflex), and tests the hypothesis that water intake would not influence diuresis. METHODS: Eight men (19-25 yr) underwent four treatments: euhydration in air (Eu-air), euhydration in water immersion (Eu-H2O), and with prior 3.6% hypohydration in air (Hypo-air), and hypohydration in immersion (Hypo-H2O). Ad libitum drinking was allowed during the 3-h experimental and 1-h recovery periods. RESULTS: Drinking was greatest during the first 10 min: 3.5 ml x kg(-1) with Hypo-air (450 ml x 3 h(-1)) and only 1.7 ml x kg(-1) (p < 0.05) with Hypo-H2O (235 ml x 3 h(-1)). At 1 h, concomitant [PVP] decreased from a control level of 6.6+/-1.5 to 4.0+/-1 .0 pg x ml(-1) (delta = 2.6 pg x ml(-1), p < 0.05) with Hypo-air, and from 5.9+/-0.6 to 2.3+/-0.2 pg x ml(-1) (delta = 3.6 pg x ml(-1), p < 0.05) with Hypo-H2O. Urine flow was unchanged from control level (<1.0 ml x min(-1)) with Hypo-air, Hypo-H2O, and Eu-air, but increased to 4-5 ml x min(-1) with Eu-H2O. Neither water intake volume nor urine flow was related to the magnitude of [PVP] depression. Regression of Uosm/Posm ratio on [PVP] and urine flow indicated that [PVP] above 2 pg x ml(-1) did not affect urine flow. Thus, ad libitum water intake in previously hypohydrated subjects did not affect urine flow or the decrease in [PVP]. The threshold [PVP] to initiate significant diuresis was about 2 pg x ml(-1), and significant diuresis can occur with no change in [PVP] maintained at about 1 pg x ml(-1) during immersion in euhydrated subjects. CONCLUSIONS: Thus, it appears that the Gauer-Henry reflex is not the major mechanism for immersion-induced diuresis. Clearly, other diuretic factors are also involved.

Adult↗

PubMed2006

[Role of V1- and V2-receptors in mechanism of physiological paradox--an increase of reabsorption of the solute free water and simultaneous rise of diuresis].

In experiments on non-anesthetized rats with administration into stomach of water (5 ml/100 g body mass) direct correlation has been found between an increase of diuresis and excretion of solute free water (r = 0.98, p < 0.01), while after injection to these animals of 5 x 10(-11) M arginine-vasotocin - between an increase of diuresis and simultaneous rise reabsorption of solute free water (r = 0.8, p < 0.01). The rise of diuresis after the vasotocin injection is due to inhibition of sodium re- absorption, with the solute excretion fraction increasing from 2.6 +/- 0.2 % to 11.9 +/- 1.2, p < 0.001. A similar physiological paradox - an increase of diuresis with the simultaneous increase of reabsorption of solute free water - has been revealed at night hours in children with tendency for nocturnal enuresis (r = 0.64, p < 0.01). Mechanism responsible for this phenomenon consists in a rise of diuresis due to a decrease of sodium ion reabsorption in the ascending Henle loop limb. A problem is discussed of the homeostatic significance of a decrease of sodium reabsorption combined with an increase of solute-free water reabsorption; it is suggested that this phenomenon is based on a redistribution of reabsorption inside the nephron - a decrease of ion and water reabsorption in the initial parts of the nephron distal segment and an increase of solute free water reabsorption with the antidiuretic hormone-stimulated high osmotic permeability of terminal parts of renal tubules. An intraperitoneal injection of V1-anatagonist (OPC-21268) decreased the natriuretic component of response to arginine-vasotocin, while injection of V2-antagonist (OPC-31260) eliminated the antidiuretic component.

Absorption↗

PubMed1987

Seadragon VI: a 7-day dry saturation dive at 31 ATA. II. Characteristics of diuresis and nocturia.

Four male divers were exposed to a dry, 31 ATA, He-O2 environment for 7 d (Seadragon VI). Urine was collected diurnally (0700-2200 h) and nocturnally (2200-0700 h) before (predive 1 ATA air), during, and after (decompression and postdive 1 ATA air) exposure to 31 ATA. A typical hyperbaric diuresis associated with a reduction in urine osmolality was observed in the face of a constant creatinine clearance. A significant increase (P less than 0.05) in osmolal clearance (COSM) was observed with concomitant decrease (P less than 0.05) in negative free water clearance, indicating that the diuresis has both osmotic and free water components. Although urine flow increased at pressure during both day and night, its magnitude was twofold greater at night as compared to daytime. Moreover, the diurnal diuresis was entirely due to an increase in free water excretion, whereas the nocturnal diuresis was largely due to an increased COSM. These results indicate that hyperbaric diuresis is induced by inhibition of tubular reabsorption of free water during daytime and of certain solutes during the night. Approximately 80% of the nocturnal increase in the excretion of osmotic substances was accounted for by Na, K, Cl, and urea.

Adult↗

PubMed1994

Contribution of alpha-2 adrenoceptors to kappa opioid agonist-induced water diuresis in the rat.

Clearance studies in rats using kappa opioid agonists have demonstrated that agonists that can cross the blood-brain barrier are more potent water diuretics than agonists which have limited access to the brain. The mechanism of kappa agonist-induced water diuresis is unclear but may involve inhibition of vasopressin secretion and/or an adrenomedullary factor. In the present study the effect of an alpha-2 adrenoceptor antagonist (yohimbine, 10 micrograms/kg.min i.v.) on kappa agonist-induced water diuresis was evaluated in conscious chronically instrumented rats. BRL 53117 (1-[(3,4-dichlorophenyl)acetyl]-2-[(3-hydroxy-1-pyrrolidinyl) methyl]4,4-dimethyl piperidine), a kappa agonist that can cross the blood-brain barrier, caused a dose-dependent (1-100 micrograms/kg) water diuresis which was attenuated by yohimbine. The effective dose to cause a free water clearnace of zero for BRL 53117 was 13 +/- 5 micrograms/kg in vehicle-treated rats and 37 +/- 12 micrograms/kg in yohimbine-treated rats. BRL 52974 (5-[(3,4-dichlorophenyl)acetyl]4-(1-pyrrolidinylmethyl)-4,5,6,7-te trahydro- 1H-imidazo[4,5-c]pyridine), a compound with limited ability to cross the blood-brain barrier, also caused a dose-dependent water diuresis, albeit at higher doses (30-3000 micrograms/kg), and thus a higher effective dose to cause a free water clearance of zero (129 +/- 61 micrograms/kg); however, the effect was abolished by yohimbine. The data suggest that kappa agonists cause a water diuresis by both a central mechanism involving inhibition of vasopressin secretion and a peripheral mechanism involving stimulation of renal alpha-2 receptors.

Animals↗

PubMedDate not supplied

Increase in ascites white blood cell and protein concentrations during diuresis in patients with chronic liver disease.

Serum and ascites protein concentration and ascites cell concentration alterations with determined serially during diuresis in 27 patients with uncomplicated liver disease. The total protein concentration in ascites increased from 1.38 +/- 0.96 gm% to 2.86 +/- 1.28 gm% (p less than 0.001); the serum protein concentration from 6.26 +/- 0.81 gm% to 7.24 +/- 0.93 gm% (p less than 0.001), and the ascites to serum ratio of the total protein concentration from 0.21 +/- 0.13 to 0.38 +/- 0.14 (p less than 0.001). The white blood cell (WBC) concentration in ascites increased from 289 +/- 179 cells per mm3 to 1,108 +/- 924 cells per mm3 (p less than 0.001). Despite the increase in WBC concentration, the polymorphonuclear cell concentration remained constant (42 +/- 52 cells per mm3 to 68 +/- 96 cells per mm3). Protein concentration of the ascitic fluid greater than 3.0 gm% was demonstrated in 12 patients before completion of diuresis and ascitic fluid WBC concentration was greater than 750 cells per mm3 in 17 patients. Ten of 27 patients eventually developed ascites which had a combination of more than 3.0 gm% total protein concentration and greater than 750 cells per mm3. Ascitic fluid protein and WBC concentrations are not "fixed" at a low level in chronic liver disease since each rose during diuresis. Thus, the interpretation of these parameters must be made with caution in patients following significant diuresis.

Ascitic Fluid↗