Prostaglandin-dependent polyuria in hypercalcemia

1981 ◽  
Vol 241 (3) ◽  
pp. F224-F230 ◽  
Author(s):  
E. R. Serros ◽  
M. A. Kirschenbaum
Keyword(s):  
Flow Rate ◽  
Plasma Osmolality ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Prostaglandin E ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Final Group ◽  
Thirst Mechanism

The present experiments examined the role of prostaglandin biosynthesis in the increase in urine flow rate seen in rats with hypercalcemia induced by the administration of 1,25-dihydroxycholecalciferol. In a first group, rats receiving the vitamin D metabolite developed hypercalcemia, polyuria, and increased urine prostaglandin E excretion. Indomethacin resulted in a fall in urine prostaglandin E excretion. A second group was fluid restricted to ascertain whether increased thirst could be an etiologic mechanism of the polyuria. This resulted in a trivial fall in urine flow rate despite a fall in body weight and a rise in both urine and plasma osmolality. In a final group, prostaglandin inhibition restored the vasopressin sensitivity of the hypercalcemic kidney. Accordingly, the polyuria seen in hypercalcemic rats after the administration of 1,25-dihydroxycholecalciferol is associated with an increase in urine prostaglandin E excretion and can be reversed by inhibition of prostaglandin synthesis. In addition, this polyuria can occur independent of the thirst mechanism. Finally, there is evidence that the vasopressin resistance of the hypercalcemic kidney could be reversed by prostaglandin inhibition.

Effects of alterations in urine flow rate on prostaglandin E excretion in conscious dogs

1980 ◽  
Vol 238 (2) ◽  
pp. F107-F111 ◽  
Author(s):  
M. A. Kirschenbaum ◽  
E. R. Serros
Keyword(s):  
Flow Rate ◽  
Plasma Osmolality ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Prostaglandin E ◽  
Flow Rates ◽  
Water Loading ◽  
Receptor Assay ◽  
Excretion Rates ◽  
Previous Group

The relationships between urinary prostaglandin E excretion and urine flow rate were evaluated in 11 conscious mongrel dogs during antidiuresis, maximal water loading, vasopressin administration during maximal water loading, and mannitol infusion. Urine flow rates between 0.21 and 15.1 ml/min were achieved. Urinary prostaglandin E excretion rates, determined by a membrane receptor assay, varied directly with urine flow rates (r = 0.908). Vasopressin administration (34--540 microU . kg-1 . min-1) resulted in a fall, rather than the expected rise, in urinary prostaglandin E excretion. When the concentration of prostaglandin E in the urine was plotted against urine flow rate, the demonstrated relationship appeared most consistent with passive diffusion. Mannitol infusion increased urine flow rates to levels comparable to the levels seen with maximal water loading but did not result in a fall in plasma osmolality. Urinary prostaglandin E excretion rates, however, were not distinguishable from those in the previous group. These data demonstrate that urinary prostaglandin E excretion rates are determined, to a great extent, by urine flow rate and that the significance of the interpretation of elevated excretion levels of these lipids in diuretic states may have to be reevaluated.

The Role of Prostaglandins in Glucagon-Induced Natriuresis

1980 ◽  
Vol 58 (5) ◽  
pp. 393-401 ◽  
Author(s):  
M. A. Kirschenbaum ◽  
E. T. Zawada
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Flow Rate ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Prostaglandin E ◽  
Excretion Rates

1. Three groups of anaesthetized dogs were studied to determine the role of renal prostaglandins in glucagon-induced natriuresis. 2. Urine flow, sodium and prostaglandin E excretion rates increased significantly in the experimental kidney with glucagon infusion (0.20 μg/min) into the renal artery. These changes were completely reversed after the administration of either of two inhibitors of prostaglandin synthesis. 3. Infusion of glucagon (0.20 μg/min) after the administration of either of the prostaglandin synthetase inhibitors failed to increase either urine flow rate or sodium excretion above control values and failed to elevate urine prostaglandin E excretion rates. 4. Infusion of glucagon (0.75–1.25 μg/min) resulted in significant elevations in urine flow rate, glomerular filtration rate, renal plasma flow, urine sodium and prostaglandin E excretion rates. 5. The data presented indicate that the diuresis and natriuresis seen with the infusion of glucagon (0.20 μg/min) are accompanied by an increase in urine prostaglandin E excretion and are reversed by the administration of inhibitors of prostaglandin synthesis, suggesting that the increased urine flow and sodium excretion rates are dependent on prostaglandin-mediated mechanisms. The administration of glucagon in higher doses appears to be associated with alterations in electrolyte excretion and glomerular filtration rate, which presumably is related to factors other than prostaglandin synthesis and release.

Urine Reinfusion Diuresis and Natriuresis in Rats: Role of Water, Electrolytes and Urea

1979 ◽  
Vol 57 (2) ◽  
pp. 187-193
Author(s):  
R. A. Norman ◽  
T. G. Coleman ◽  
P. R. Kastner
Keyword(s):  
Flow Rate ◽  
Sodium Excretion ◽  
Infusion Rate ◽  
Ringer Solution ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Urinary Volume ◽  
Natriuretic Factors

1. The purpose of this study was to determine the role of reinfused water, electrolytes and urea in the diuresis and natriuresis of urine reinfusion. 2. Three groups of rats underwent 5 h of urine reinfusion. The first group served as a control, and during urine reinfusion the urinary volume and sodium excretion increased to 10 or 12 times control values. 3. In a second group, urine reinfusion was followed by 2 h of infusion of Ringer solution at a rate equal to the urine flow rate; 71% of the diuresis and 75% of the natriuresis resulting from urine reinfusion were maintained. 4. In a third group, urine reinfusion was followed by infusion of Ringer solution with urea added. The infusion rate was equal to urine flow rate and the concentration of urea was equal to that in the urine; 98% of the diuresis and 102% of the natriuresis were maintained. 5. These results indicate that the majority of urine-reinfusion diuresis and natriuresis is due to reinfused volume and electrolytes, and the remainder, in these experiments at least, could be explained by the reinfused urea. Therefore there was no need to postulate additional urinary natriuretic factors to explain the results of urine reinfusion.

Renal melatonin excretion in sheep is enhanced by water diuresis

1993 ◽  
Vol 138 (3) ◽  
pp. 445-450 ◽  
Author(s):  
M. Valtonen ◽  
J. T. Laitinen ◽  
L. Eriksson
Keyword(s):  
Water Balance ◽  
Flow Rate ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Urine Collection ◽  
Pineal Function ◽  
Fluid Load ◽  
Normal Water

ABSTRACT Diurnal variation in blood melatonin levels and renal melatonin excretion was monitored in five ewes by blood sampling and quantitative urine collection at 2-h intervals. A typical secretory pattern of melatonin was seen both in blood and urine levels and in the renal excretion of melatonin. Serum melatonin levels increased from daytime values of approximately 200 pmol/l to a mean of 800 pmol/l during darkness. Urine flow rate and urine osmolality did not show any clear diurnal rhythm. To examine whether urine flow rate affects renal melatonin excretion at night, urine was collected in three consecutive 30-min fractions, and blood was sampled in the middle of each urine collection period when the sheep were in normal water balance or after hydration. Hydration increased urine flow rate over sixfold and decreased urine osmolality well below plasma osmolality. Glomerular filtration rate, measured as creatinine clearance, did not change. Serum melatonin concentrations did not differ between hydrated and non-hydrated sheep. However, urinary melatonin excretion was 1·1 ± 0·3 (s.e.m.) pmol/min at midnight in normal water balance, and significantly higher (2·6 ± 0·4 pmol/min) in the hydrated state. In this study, the validity of urinary melatonin determinations as an indicator of pineal function was confirmed in normal water balance. In addition, our results suggest that a high tubular fluid load during diuresis increases urinary melatonin excretion because of decreased tubular reabsorption. This means that urine flow rate should be taken into consideration in studies where urinary melatonin levels are used as an index of production of the indole by the pineal gland. Journal of Endocrinology (1993) 138, 445–450

High urine flow rate increases prostaglandin E excretion in the conscious dog

1981 ◽  
Vol 22 (1) ◽  
pp. 21-34 ◽  
Author(s):  
Lucius F. Wright ◽  
Steven G. Rosenblatt ◽  
Meyer D. Lifschitz
Keyword(s):  
Flow Rate ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Prostaglandin E ◽  
Conscious Dog

Influence of serotonergic mechanisms on the urine flow rate in male rats

2014 ◽  
Vol 307 (10) ◽  
pp. R1239-R1250 ◽  
Author(s):  
Wen-Jia Fan ◽  
Shih-Ching Chen ◽  
Tsung-Hsun Hsieh ◽  
Chien-Hung Lai ◽  
You Shuei Lin ◽  
...  
Keyword(s):  
Flow Rate ◽  
Silent Period ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Male Rats ◽  
External Urethral Sphincter ◽  
Voiding Function ◽  
Pressure Threshold ◽  
Burst Period

This study extensively examined the role of a 5-HT1A receptor in controlling voiding function in anesthetized male rats. A simultaneous recording of the intravesical pressure (IVP), external urethral sphincter (EUS)-electromyography (EMG), and urine flow rate (UFR) during continuous cystometry was used. 8-Hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), a 5-HT1A receptor agonist, significantly improved the voiding efficiency, as detected by increases in the evoked contraction amplitude, EUS burst period, and silent period, and decreases in the volume threshold, pressure threshold, and residual volume. Interestingly, the UFR during voiding was reduced by 8-OH-DPAT, as evidenced by decreases in the maximal UFR and mean UFRs of the voiding period, spike duration, and interspike interval. Conversely, treating rats with WAY-100635, a 5-HT1A antagonist, produced effects opposite to those produced by 8-OH-DPAT. These findings suggest that 8-OH-DPAT improved the voiding efficiency by enhancing the detrusor contractile ability and prolonging EUS burst period, which would compensate for the lower UFR, resulting from urethral smooth muscle contractions and longer EUS silent periods during voiding. The present study contributes to our understanding of the role of 5-HT1A receptors in controlling the urine flow rate in male rats.

Does pharmacological activation of 5-HT1A receptors improve urine flow rate in female rats?

2016 ◽  
Vol 311 (1) ◽  
pp. F166-F175 ◽  
Author(s):  
Shih-Ching Chen ◽  
Tsung-Hsun Hsieh ◽  
Wen-Jia Fan ◽  
Chien-Hung Lai ◽  
Chih-Wei Peng
Keyword(s):  
Flow Rate ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Female Rats ◽  
Smooth Muscle Relaxation ◽  
External Urethral Sphincter ◽  
Zero Level ◽  
Flow Duration ◽  
The Mean

The role of 5-HT1A receptors in regulating voiding functions remains unclear, particularly regarding the urine flow rate (UFR) during voiding. This study examined the effects of 5-HT1A receptors on regulating urethral functions in female rats and investigated underlying modulatory mechanisms. Intravesical pressure (IVP), external urethral sphincter-electromyography (EUS-EMG), and UFR were simultaneously recorded during continuous transvesical infusion to examine the effects of a 5-HT1A receptor agonist (8-OH-DPAT) and antagonist (WAY-100635) on bladder and urethral functions. In addition, this study evaluated the independent roles of urethral striated and smooth muscles in the UFR in rats after a neuromuscular blockade (NMB) treatment and bilateral hypogastric nerve transection. Our results revealed that 8-OH-DPAT significantly increased the maximal UFR but reduced the mean UFR. This discrepancy may be because 8-OH-DPAT markedly increased the maximal UFR during the initial segment of the flow duration and subsequently induced an approximately zero level of long oscillatory waves during the remaining flow duration. Thus the mean UFR was reduced because of the prolonged approximately zero level of the UFR. However, paralyzing the EUS with an NMB agent, 8-OH-DPAT, significantly increased the maximal and mean UFRs because the prolonged zero level of the oscillatory UFR did not continue. These results support the hypothesis that the increased UFR in female rats during voiding is due to the induction of urethral smooth muscle relaxation by 8-OH-DPAT. This paper provides a detailed understanding of the role of 5-HT1A receptors in controlling the UFR in female rats.

Effect of urine flow rate on uric acid excretion in man

1972 ◽  
Vol 15 (4) ◽  
pp. 338-346 ◽  
Author(s):  
Herbert S. Diamond ◽  
Robert Lazarus ◽  
David Kaplan ◽  
David Halberstam
Keyword(s):  
Uric Acid ◽  
Flow Rate ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Acid Excretion ◽  
Uric Acid Excretion

Homeostatic potassium excretion in fed and fasted sheep

1988 ◽  
Vol 254 (2) ◽  
pp. R357-R380 ◽  
Author(s):  
L. Rabinowitz ◽  
D. M. Green ◽  
R. L. Sarason ◽  
H. Yamauchi
Keyword(s):  
Flow Rate ◽  
Urine Flow ◽  
Plasma Aldosterone ◽  
Urine Flow Rate ◽  
Potassium Excretion ◽  
Adult Sheep ◽  
Blood Ph ◽  
Low Levels ◽  
K Concentration ◽  
Filtered Load

In unanesthetized adult sheep, following intake of a daily meal, there was a peak in K excretion. The maximum and minimum rates of K excretion following meals were directly related to meal K content. On days without meals, no peak in K excretion occurred. Changes in K excretion on fed and fast days occurred without changes in the low levels of plasma aldosterone and were poorly correlated with urine or blood pH, urine flow rate, Na excretion, or the filtered load of K, but they correlated well with fractional K excretion. Plasma K did not change on fast days. Plasma K increased on some, but not all, fed days. Increases in plasma K that occurred on fed days were insufficient to account for the concurrent kaliuresis. Infusion of aldosterone or isotonic NaCl failed to alter K excretion in fed or fasted sheep. Infusion of isotonic NaCl + aldosterone hypertonic Na2SO4 + aldosterone increased K excretion in fasted but not fed sheep. Infusion of K in the rumen of fed and fasted sheep elevated rumen K concentration and led to increases in K excretion that could not be explained by increases in plasma K. The mechanisms responsible for the homeostatic changes in K excretion on fed and fast days were not ascertained but may importantly depend on sensors of enteric K content.

Urine Quantification Following Furosemide for Severe Acute Kidney Injury Prediction in Critically Ill Children

2021 ◽  
Author(s):  
Katja M. Gist ◽  
Jamie Penk ◽  
Eric L. Wald ◽  
Laura Kitzmiller ◽  
Tennille N. Webb ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Critically Ill ◽  
Flow Rate ◽  
Kidney Injury ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Critically Ill Children ◽  
Prospective Assessment ◽  
Critically Ill Adults

AbstractA standardized, quantified assessment of furosemide responsiveness predicts acute kidney injury (AKI) in children after cardiac surgery and AKI progression in critically ill adults. The purpose of this study was to determine if response to furosemide is predictive of severe AKI in critically ill children outside of cardiac surgery. We performed a multicenter retrospective study of critically ill children. Quantification of furosemide response was based on urine flow rate (normalized for weight) measurement 0 to 6 hours after the dose. The primary outcome was presence of creatinine defined severe AKI (Kidney Disease Improving Global Outcomes stage 2 or greater) within 7 days of furosemide administration. Secondary outcomes included mortality, duration of mechanical ventilation and length of stay. A total of 110 patients were analyzed. Severe AKI occurred in 20% (n = 22). Both 2- and 6-hour urine flow rate were significantly lower in those with severe AKI compared with no AKI (p = 0.002 and p < 0.001). Cutoffs for 2- and 6-hour urine flow rate for prediction of severe AKI were <4 and <3 mL/kg/hour, respectively. The adjusted odds of developing severe AKI for 2-hour urine flow rate of <4 mL/kg/hour was 4.3 (95% confidence interval [CI]: 1.33–14.15; p = 0.02). The adjusted odds of developing severe AKI for 6-hour urine flow rate of <3 mL/kg/hour was 6.19 (95% CI: 1.85–20.70; p = 0.003). Urine flow rate in response to furosemide is predictive of severe AKI in critically ill children. A prospective assessment of urine flow rate in response to furosemide for predicting subsequent severe AKI is warranted.

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