scholarly journals Prostaglandin E2 excretion, urine flow and papillary osmolality during saline or dextrose infusion in the conscious rat.

1983 ◽  
Vol 336 (1) ◽  
pp. 39-46 ◽  
Author(s):  
C J Lote ◽  
A J McVicar ◽  
A Thewles
Keyword(s):  
Prostaglandin E2 ◽  
Urine Flow ◽  
Conscious Rat ◽  
Dextrose Infusion

Urinary pH as a determinant of prostaglandin E2 excretion by the conscious rat

1984 ◽  
Vol 66 (6) ◽  
pp. 675-681 ◽  
Author(s):  
J. Haylor ◽  
C. J. Lote ◽  
A. Thewles
Keyword(s):  
Prostaglandin E2 ◽  
Isotonic Saline ◽  
Tubular Secretion ◽  
Urine Flow ◽  
Urine Ph ◽  
Conscious Rat ◽  
Conscious Rats ◽  
Positive Linear Correlation ◽  
Solute Excretion ◽  
Oral Sodium

1. The urinary excretion of prostaglandin E2 (PGE2) was measured in conscious rats under conditions which produced either acid or alkaline urine, but similar change in fluid and solute excretion. 2. Oral isotonic saline increased both urine flow and sodium excretion but did not alter urinary PGE2 output (which remained constant at 80 pmol/3 h per rat) or urine pH (6.2). 3. When the urine was made alkaline (pH 7.8) by oral sodium bicarbonate or carbonate, urinary PGE2 was approximately 3-fold greater (P<0.00l) than the control (pH6.2). The urine flow and sodium output were also increased. 4. When the urine was made acidic (pH 5.7) by oral ammonium chloride, urinary PGE, excretion was reduced (P<0.01) to approximately half the control output. The urine flow and sodium output increased. 5. Within a group of 12 rats receiving oral isotonic saline a positive linear correlation coefficient (P<0.002) was established between urine pH and PGE2 excretion. 6. The results indicate that urine pH may be a determinant of PGE2 excretion in unrestrained, conscious rats. It seems likely that this effect of pH is mediated by a change in the passive reabsorption of PGE, in the distal nephron, although alternative explanations such as altered tubular secretion or synthesis cannot be categorically excluded.

Intravital microscopical studies of the tubular urine flow in the conscious rat

1976 ◽  
Vol 362 (3) ◽  
pp. 261-264 ◽  
Author(s):  
M. Steinhausen ◽  
E. Hill ◽  
N. Parekh
Keyword(s):  
Urine Flow ◽  
Conscious Rat

Study of the Role of Prostaglandin E2 in Urine Flow Regulation in Chronic Renal Failure

2000 ◽  
Vol 34 (5) ◽  
pp. 327-330 ◽  
Author(s):  
Yuri V. Natochin ◽  
Anastasia E. Bogolepova ◽  
Alla A. Kuznetsova ◽  
Elena I. Shakhmatova
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Prostaglandin E2 ◽  
Flow Regulation ◽  
Urine Flow

Renal effects of acute endothelial-derived relaxing factor blockade are not mediated by angiotensin II

1993 ◽  
Vol 264 (1) ◽  
pp. F74-F78 ◽  
Author(s):  
C. Baylis ◽  
K. Engels ◽  
L. Samsell ◽  
P. Harton
Keyword(s):  
Angiotensin Ii ◽  
Sodium Excretion ◽  
Renal Plasma Flow ◽  
Urine Flow ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Conscious Rat ◽  
Relaxing Factor ◽  
Renal Hemodynamic ◽  
Renal Vascular

The renal responses to acute blockade of the endothelial-derived relaxing factor (EDRF) resemble the renal actions of angiotensin II (ANG II), and the present studies were conducted to establish what role, if any, the endogenous renin-angiotensin system plays in mediating the renal response to acute EDRF blockade. These studies were conducted in the conscious chronically catheterized rat. In control experiments we observed that acute blockade of ANG II synthesis with converting-enzyme inhibition (CEI) led to a fall in blood pressure (BP) and a slight renal vasodilation but no significant change in glomerular filtration rate (GFR) or renal plasma flow (RPF). Urine flow and sodium excretion were unchanged by CEI. Use of the nonpeptide ANG II receptor antagonist losartan had no effect on BP, renal vascular resistance (RVR), GFR, or RPF; however, urine flow and sodium excretion did rise significantly. Because of the high specificity of losartan, this suggests that, in the normal conscious rat, endogenous ANG II does not control renal vascular tone but does enhance renal sodium reabsorption. ANG II blockade with either CEI or losartan had little effect on BP and no effect on the renal hemodynamic responses to acute EDRF blockade. The marked natriuretic and diuretic response to acute EDRF blockade persists during concomitant losartan but is abolished by CEI. These studies suggest that in the conscious rat the renal hemodynamic response to EDRF blockade is not mediated by endogenous ANG II.

scholarly journals Dual modulation of urinary bladder activity and urine flow by prostanoid EP3receptors in the conscious rat

2009 ◽  
Vol 158 (1) ◽  
pp. 372-381 ◽  
Author(s):  
MJ Jugus ◽  
JP Jaworski ◽  
PB Patra ◽  
J Jin ◽  
DM Morrow ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Urine Flow ◽  
Conscious Rat ◽  
Bladder Activity

Effect of sustained water diuresis on prostaglandin E2 excretion in humans

1985 ◽  
Vol 248 (6) ◽  
pp. F830-F834 ◽  
Author(s):  
D. G. Roberts ◽  
R. J. Strife ◽  
J. G. Gerber ◽  
R. C. Murphy ◽  
A. S. Nies
Keyword(s):  
Prostaglandin E2 ◽  
Urine Volume ◽  
Urine Flow ◽  
Synthesis Rate ◽  
Initial Increase ◽  
Base Line ◽  
Water Diuresis ◽  
Water Load ◽  
Pge2 Synthesis ◽  
Normal Women

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.

Antidiuretic effect of acute morphine administration in the conscious rat

1982 ◽  
Vol 60 (2) ◽  
pp. 201-204 ◽  
Author(s):  
N. Wilson ◽  
J. Ngsee
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Urine Flow ◽  
Conscious Rat ◽  
Antidiuretic Effect ◽  
Morphine Administration

Morphine was administered intravenously to normal and to Brattleboro (genetically deficient in antidiuretic hormone) rats. The injection caused a significant decrease in mean arterial pressure and urine flow in all animals, including those homozygous for diabetes insipidus. It is suggested that the antidiuretic effect of morphine may occur independently of ADH release.

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