URINARY KALLIKREIN, ALDOSTERONE, PROSTAGLANDIN E2, SODIUM, POTASSIUM, AND URINARY VOLUME IN NORMAL MAN-INTERRELATIONS AND DAY TO DAY VARIATION.

2009 ◽  
Vol 215 (S677) ◽  
pp. 30-35
Author(s):  
K. Peter Öhman ◽  
Bengt E. Karlberg
Keyword(s):  
Prostaglandin E2 ◽  
Urinary Kallikrein ◽  
Urinary Volume ◽  
Sodium Potassium ◽  
Normal Man

Effects of Prostaglandin E2 and Prostaglandin F2α Upon Urinary Kallikrein Excretion in Rats

1978 ◽  
Vol 55 (s4) ◽  
pp. 187s-189s
Author(s):  
H. R. Croxatto ◽  
R. Arriagada ◽  
M. Rojas ◽  
J. Roblero ◽  
R. Rosas
Keyword(s):  
Prostaglandin E2 ◽  
Tap Water ◽  
Extracellular Fluid ◽  
Prostaglandin F2α ◽  
Urinary Kallikrein ◽  
Kinin System ◽  
Sodium Potassium ◽  
Water Excretion ◽  
Kallikrein Kinin System ◽  
Kallikrein Activity

1. In normally hydrated rats prostaglandin F2α (PGF2α) in doses of 5 μg/100 g body weight given subcutaneously every 2 h (three times) induced a significant increase in urinary kallikrein activity, and in sodium, potassium and water excretion for 8 h after the first injection. In moderately hyperhydrated rats loaded 2·5% of body wt. with 0·5% NaCl solution, PGF2α produced similar changes in kallikrein activity and electrolyte excretion. 2. In normally hydrated rats prostaglandin E2 (PGE2) in the same conditions and doses as in 1 had no effect on kallikrein activity, showing a tendency to decrease potassium and water excretion. 3. PGE2 in doses of 5, 12·5 and 25 μg/100 g body wt. in overhydrated rats given 2·5% and 0·5% NaCl and 5% of tap water/100 g body wt. 1 h later, significantly increased kallikrein activity in the urine collected for 120 min after the injections. A significant decrease in potassium and water excretion was observed with the highest dose. 4. PGF2α, had no effect on kallikrein activity in overhydrated rats, but an increase in sodium and a decrease in potassium excretion was seen at the highest dose. 5. The different actions of PGE2 and PGF2α may be part of a regulatory mechanism associated with the kallikrein—kinin system which contributes maintainance of extracellular fluid homeostasis.

Participation of alpha-1 and alpha-2 adrenoceptors of the lateral hypothalamic area in water intake, and renal sodium, potassium and urinary volume excretion induced by central administration of angiotensin II

2000 ◽  
Vol 52 (6) ◽  
pp. 491-497 ◽  
Author(s):  
Wilson Abrão Saad ◽  
Ismael Francisco Motta Siqueira Guarda ◽  
Ana Cristini Ferreira ◽  
Luis Antonio de Arruda Camargo ◽  
Abrão Fadlala Saad Neto ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Water Intake ◽  
Lateral Hypothalamic Area ◽  
Central Administration ◽  
Urinary Volume ◽  
Hypothalamic Area ◽  
Sodium Potassium ◽  
Lateral Hypothalamic

Dependence of Urinary Prostaglandin E2 Excretion on Urinary Volume Rather than Solute Handling or Segmental Nephron Function in Man

1984 ◽  
Vol 67 (4) ◽  
pp. 413-420 ◽  
Author(s):  
Sming Kaojarern ◽  
Polavat Chennavasin ◽  
Ann Burdette ◽  
William B. Campbell ◽  
D. Craig Brater
Keyword(s):  
Prostaglandin E2 ◽  
Sodium Excretion ◽  
Fluid Intake ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Urinary Flow ◽  
Urinary Volume ◽  
Water Loading ◽  
Wide Range ◽  
Ad Libitum

1. Eight normal subjects underwent water loading alone and water loading plus 40 mg of frusemide IV, fluid intake ad libitum alone and fluid intake ad libitum plus frusemide, plus each of the preceding after pretreatment with indomethacin. 2. After frusemide administration, increases in urinary sodium excretion paralleled increases in urinary volume, and urinary prostaglandin E2 (PGE2) excretion correlated closely with sodium excretion (y = 1.03x −0.28; r = 0.940; P<.0001). 3. In the absence of the diuretic, urinary volume varied over a wide range with little change in sodium excretion. Again, urinary PGE2 excretion correlated with urinary sodium excretion (y = 0.12x + 0.05; r = 0.789; P<.002). However, the correlation differed markedly from that observed in the studies with frusemide. 4. Expressing urinary PGE2 excretion as a function of urinary volume for all of the studies resulted in a highly significant correlation (y = 10.7x −0.70; r = 0.975; P<.0001). 5. Multiple and stepwise regression analyses assessing the correlation of urinary PGE2 excretion with urinary flow rate and with indices of function of various nephron segments indicate that the correlation with urinary PGE2 could be predominantly accounted for by urinary volume. 6. We conclude that in the condition of this study in man, urinary PGE2 excretion is a correlate of urinary volume.

scholarly journals Exercise-induced proteinuria in well-trained athletes

1990 ◽  
Vol 36 (3) ◽  
pp. 562-564 ◽  
Author(s):  
A Clerico ◽  
C Giammattei ◽  
L Cecchini ◽  
A Lucchetti ◽  
L Cruschelli ◽  
...  
Keyword(s):  
Excretion Rate ◽  
Training Session ◽  
Urinary Volume ◽  
Protein Requirement ◽  
Physical Effort ◽  
Sodium Potassium ◽  
Protein Excretion ◽  
The Mean ◽  
Exercise Induced ◽  
Renal Tubular

Abstract We studied the rate of urinary excretion of albumin, alpha 1-microglobulin (as an indicator of the renal tubular involvement), sodium, potassium, and creatinine in the basal state (overnight urine collection) and after physical exercise (training session) in 10 professional cyclists, to verify whether protein excretion is increased even in well-trained athletes after physical effort. In addition, we wanted to understand whether the origin of exercise-induced proteinuria was glomerular, tubular, or both. Compared with the basal state (overnight collection), exercise significantly (P less than 0.01) increased the excretion rate of albumin (4.2 +/- 2.6 micrograms/min vs 18.1 +/- 10.6 micrograms/min, mean +/- SD), Na, and K, and also the urinary volume. Creatinine output was not affected by exercise. The mean (+/- SD) overnight excretion rate of albumin by athletes was quite similar to that found for 91 healthy nonathletes at rest (4.6 +/- 2.7 micrograms/min). The mean exercise-related excretion of alpha 1-microglobulin by the athletes significantly exceeded the overnight value (6.6 vs 0.3 mg/L, P = 0.037). Our study indicates that (a) albuminuria furnishes the greater contribution to the increase in exercise-induced proteinuria; (b) the exercise proteinuria is both glomerular and tubular in origin, and is reversible; (c) the enhanced protein requirement of athletes may in part be due to the recurrent excretion of proteins in the urine after physical effort.

Lithium-induced diuretic effect of antidiuretic hormone in rats

1976 ◽  
Vol 231 (6) ◽  
pp. 1754-1759 ◽  
Author(s):  
TP Dousa ◽  
LD Barnes
Keyword(s):  
Antidiuretic Hormone ◽  
Low Dose ◽  
Free Water ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Urinary Volume ◽  
Free Water Clearance ◽  
Sodium Potassium ◽  
Collecting Ducts

The effect of a low dose of lithium (1 meq/kg per day) on renal function and its response to antidiuretic hormone (ADH) was studied in unanesthetized rats. This dose of lithium itself had no influence on renal water and electrolyte excretion, but lithium-treated rats responded paradoxically to exogenous ADH by increases in urinary volume, excretion of total solutes, sodium, potassium, and phosphate. Administration of ADH in the presence of lithium led to a lowering of urine osmolality, but free water clearance was not significantly reduced. Adenylate cyclase from the renal medulla of animals treated with ADH and lithium had a lower response to synthetic vasopressin in vitro than in animals treated with lithium alone. The results suggest that exogenous ADHis diuretic in the presence of a low concentration of lithilm. The predominant mechanism for this diuresis is probably inhibition of electrolyte and isomotic water reabbsorption in various nephron segments, including those proximal to the collecting ducts. ADH also markedly increased urinary excretion of lithium and appears to promote accumulation of lithium in the renal medulla.

scholarly journals Effect of propranolol on the airway response to prostaglandin E2 in normal man.

1981 ◽  
Vol 12 (5) ◽  
pp. 731-735 ◽  
Author(s):  
RV Seth ◽  
VS Clarke ◽  
RA Lewis ◽  
AE Tattersfield
Keyword(s):  
Prostaglandin E2 ◽  
Airway Response ◽  
Normal Man

Urinary Kallikrein and Plasma Renin during the Reversal of Renovascular Hypertension in Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 263s-266s
Author(s):  
O. P. Gulati ◽  
O. A. Carretero ◽  
T. Morino ◽  
N. B. Oza
Keyword(s):  
Plasma Renin Activity ◽  
Renal Artery ◽  
Renovascular Hypertension ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Renin Activity ◽  
Experimental Hypertension ◽  
Urinary Kallikrein ◽  
Sodium Potassium ◽  
Water Excretion

1. Urinary kallikrein, sodium, potassium and water excretion, and plasma renin activity were measured before and during the reversal of experimental hypertension produced by unclamping the renal artery in rats. 2. Kallikrein excretion decreased significantly after unclamping, suggesting that it does not play a significant role in the reversal of hypertension. 3. A decrease in plasma renin activity coupled with a slight increase of sodium excretion was observed, indicating that these might participate in the reversal of hypertension.

THE EFFECT OF VASOPRESSIN (PITRESSIN) ADMINISTRATION ON SODIUM, POTASSIUM AND UREA EXCRETION IN RATS WITH AND WITHOUT DIABETES INSIPIDUS (DI), WITH A NOTE ON THE EXCRETION OF VASOPRESSIN IN THE DI RAT

1973 ◽  
Vol 56 (1) ◽  
pp. 111-120 ◽  
Author(s):  
J. F. LAYCOCK ◽  
P. G. WILLIAMS
Keyword(s):  
Urinary Excretion ◽  
Diabetes Insipidus ◽  
Potassium Excretion ◽  
Urinary Volume ◽  
Brattleboro Rat ◽  
Sodium Potassium ◽  
Urea Excretion ◽  
Antidiuretic Activity ◽  
Minimum Dose ◽  
Hereditary Hypothalamic Diabetes Insipidus

SUMMARY The effect of the administration of vasopressin as subcutaneous Pitressin Tannate in oil (PTO) was studied in the Brattleboro rat. Rats with hereditary hypothalamic diabetes insipidus (DI), and rats heterozygous for this abnormality, were used. A minimum dose of 1000 mu. of PTO/24 h was necessary to restore the urinary volume and osmolality of DI rats to values comparable with those of heterozygous rats. The urinary excretion of antidiuretic activity in DI rats was shown to be related to the dose of PTO. Sodium and urea excretion, but not potassium excretion, were reduced by up to 50% in the DI rat. No comparable changes were produced in the heterozygous rat. The possible mechanisms of these actions of vasopressin are discussed.

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