Effect of Inhibition of Prostaglandin Synthesis on Urinary Free Dopamine Excretion in Women

1982 ◽  
Vol 62 (2) ◽  
pp. 209-213 ◽  
Author(s):  
H.-G. Güllner ◽  
D. J. Lakatua ◽  
F. C. Bartter
Keyword(s):  
Significant Contribution ◽  
Control Period ◽  
Urinary Sodium Excretion ◽  
Prostaglandin Synthesis ◽  
Sodium Retention ◽  
Natriuretic Hormone ◽  
Urinary Dopamine ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Normal Women ◽  
Indomethacin Treatment

1. The effect of inhibition of prostaglandin synthesis on urinary excretion of free dopamine, a catecholamine thought to act as a renal natriuretic hormone, was examined in six normal women. 2. The volunteer subjects were treated with indomethacin (2 mg day−1 kg−1) for 7 days. This regimen produced an immediate and significant but transient decrease in urinary sodium excretion, averaging about 80 mmol over a period of 3 days. 3. Urinary dopamine excretion during the control period was not different from that during the entire period of indomethacin treatment. 4. It is concluded that indomethacin does not affect urinary dopamine excretion. The change in intrarenal nervous release of dopamine in response to the sodium retention induced by indomethacin may have been too small to make a significant contribution to total urinary dopamine excretion.

Inhibition of Frusemide-Induced Natriuresis by Indomethacin in Patients with the Nephrotic Syndrome

1977 ◽  
Vol 52 (2) ◽  
pp. 149-151 ◽  
Author(s):  
R. G. W. L. Tiggeler ◽  
R. A. P. Koene ◽  
P. G. A. B. Wijdeveld
Keyword(s):  
Nephrotic Syndrome ◽  
Renin Angiotensin System ◽  
Prostaglandin Synthesis ◽  
Sodium Retention ◽  
Angiotensin System ◽  
Combined Use ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Natriuretic Effect ◽  
High Doses ◽  
Indomethacin Treatment

1. In four patients with nephrotic syndrome indomethacin not only reduced proteinuria but also inhibited the natriuretic effect of high doses of frusemide. 2. The inhibition of natriuresis by indomethacin could not be antagonized by albumin infusions. 3. Only the combined use of spironolactone and frusemide induced a natriuresis during indomethacin treatment. Spironolactone alone was ineffective. 4. It is suggested that inhibition of prostaglandin synthesis by indomethacin, in the presence of a stimulated renin-angiotensin system and hyperaldosteronism, may cause this strong tendency to sodium retention.

Prostaglandin blockade blunts the natriuresis of elevated renal interstitial hydrostatic pressure

1988 ◽  
Vol 254 (4) ◽  
pp. F507-F511 ◽  
Author(s):  
D. Pawlowska ◽  
J. A. Haas ◽  
J. P. Granger ◽  
J. C. Romero ◽  
F. G. Knox
Keyword(s):  
Hydrostatic Pressure ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Left Kidney ◽  
Urinary Sodium Excretion ◽  
Prostaglandin Synthesis ◽  
Urinary Sodium ◽  
Fractional Sodium Excretion ◽  
Interstitial Volume ◽  
Inhibition Of Prostaglandin Synthesis

Previous studies have shown that renal interstitial volume expansion (RIVE) increases renal interstitial hydrostatic pressure and urinary sodium excretion. In the present study we investigated whether blockade of prostaglandin synthesis inhibits the increase in fractional sodium excretion induced by RIVE. Expansion of the renal interstitial volume was achieved by injecting 50 microliters of 2.5% albumin solution into a polyethylene matrix chronically implanted in the left kidney. Fractional sodium excretion (FENa), renal interstitial hydrostatic pressure (PI), and urinary prostaglandin excretion (UPGE2) were measured before and after RIVE in eight control, seven meclofenamate-treated, and eight indomethacin-treated rats. RIVE in the control animals resulted in significant increases in PI (delta + 4.2 +/- 0.8 mmHg), in FENa (delta + 1.02 +/- 0.27%), and in UPGE2 (% delta + 150 +/- 38%) without significant changes in glomerular filtration rate. Inhibition of prostaglandin synthesis with meclofenamate or indomethacin attenuated the natriuretic response and blocked the increase in UPGE2 associated with RIVE. In summary, direct increases in renal interstitial hydrostatic pressure increase UPGE2 and urinary sodium excretion. This natriuretic response is markedly diminished by inhibition of prostaglandin synthesis. These studies suggest that prostaglandin synthesis may have an important role in mediating the natriuretic effect of increased renal interstitial hydrostatic pressure during renal interstitial volume expansion.

Effect of Indomethacin on Blood Pressure in the Normotensive Unanaesthetized Rabbit: Possible Relation to Prostaglandin Synthesis Inhibition

1979 ◽  
Vol 57 (4) ◽  
pp. 359-365 ◽  
Author(s):  
J. Colina-Chourio ◽  
J. C. McGiff ◽  
A. Nasjletti
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Control Period ◽  
Urine Volume ◽  
Urinary Sodium Excretion ◽  
Prostaglandin Synthesis ◽  
Endogenous Prostaglandins ◽  
Cumulative Difference ◽  
Aortic Blood Pressure ◽  
Regulation Of Blood Pressure

1. To test the hypothesis that endogenous prostaglandins contribute to the regulation of blood pressure, we studied the effect of an inhibitor of prostaglandin synthesis, indomethacin, on mean aortic blood pressure in the normotensive, unanaesthetized rabbit. 2. Daily administration of indomethacin at 42 μmol/kg subcutaneously, but not of vehicle only, for 14 consecutive days, elevated the average mean arterial pressure in seven rabbits from 88 ± 3 mmHg on the last day of the control period to 105 + 3 mmHg (P < 0·01) and 107 ± 2 mmHg (P < 0·01) on days 6 and 14 of indomethacin treatment respectively, and reduced the urinary excretion of prostaglandin-like substance from 1·06 ± 0·26 to 0·17 ± 0·05 nmol of prostaglandin E2 equivalents/ day (P < 0·05; n = 5). Neither indomethacin nor the vehicle affected the intake of water, the 24 h urine volume, the cumulative difference between sodium intake and urinary sodium excretion, or the plasma volume. 3. The results of the study are compatible with the hypothesis that one or more prostaglandins contribute to maintain normotension in the rabbit and that reduction in prostaglandin biosynthesis may cause blood pressure to rise.

Pathogenesis of Salt Retention in Dogs with Chronic Bile-Duct Ligation

1982 ◽  
Vol 62 (1) ◽  
pp. 65-70 ◽  
Author(s):  
C. Chaimovitz ◽  
U. Alon ◽  
O. S. Better
Keyword(s):  
Bile Duct ◽  
Sodium Excretion ◽  
Control Period ◽  
Extracellular Volume ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Sodium Retention ◽  
Plasma Aldosterone Concentration ◽  
Duct Ligation

1. The present study investigates the role of mineralocorticoids in the pathogenesis of salt retention and ascites in dogs with chronic ligation of the common bile duct (CBDL). 2. After CBDL the natriuretic response to an intravenous sodium load [0.9% sodium chloride solution (150 mmol/l): saline; 10% of body weight] was markedly depressed. Urinary sodium excretion was 285 ± 62 vs 960 ± 58 μmol/min in the control period before CBDL (P < 0.001). This antinatriuresis was associated with a significant rise in plasma aldosterone concentration, from 52.5 ± 5.5 pg/ml before CBDL to 177 ± 50 pg/ml after CBDL (P < 0.02). Ascites was present in all salt-retaining CBDL dogs. 3. Bilateral adrenalectomy resulted in disappearance of ascites and in a rise in the natriuretic response to extracellular volume expansion. Urinary sodium excretion was 770 ± 124 μmol/min, a value significantly higher than in the CBDL dogs with intact adrenals (P < 0.001). Sodium balance studies in the adrenalectomized CBDL dogs during chronic deoxycorticosterone acetate (DOCA) treatment (25 mg/day) showed that in these animals there was failure to escape from the mineralocorticoid-induced sodium retention. Glomerular filtration rate and renal plasma flow did not change during the studies. 4. The present evidence supports the thesis that sodium retention in the CBDL dog results from a dual mechanism: (a) excess of circulating aldosterone and (b) an extra-adrenal factor which prevents escape from the salt-retaining effect of mineralocorticoids, in the CBDL dogs, thereby perpetuating the antinatriuresis in these animals.

Antipyretic Activity of the Root Extracts of Xylocarpus

2019 ◽  
Vol 9 (3) ◽  
pp. 35-38
Author(s):  
Ganesh Kumar Y ◽  
Pranitha D ◽  
Phaneendra D ◽  
Madhava Reddy Ch
Keyword(s):  
Mechanisms Of Action ◽  
Prostaglandin Synthesis ◽  
The Body ◽  
Human Race ◽  
Pharmacological Activities ◽  
Standard Drug ◽  
Root Extracts ◽  
Antipyretic Activity ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Elevated Body Temperature

Various types of conditions exist in the body that causes fever and pain. Drugs that are used to treat fever are called antipyretics, and those are usually prescribed to treat elevated body temperature. But those drugs result in many other side effects like ulcers, perforations, bleedings and obstructions, which make their use questionable and limiting. Medicinal plants are used in the treatment of diseases from the starting of the human race and the process; they had been subjected to rigorous investigations and tests to establish a scientific proof and validation of the various pharmacological activities and their respective mechanisms of action in treating the herbs. Considering the anti-inflammatory properties of the plant, Xylocarpus mekongesis was investigated for its antipyretic activity in yeast method and 3doses out of which 00mg/kg body weight showed a better activity compared to the standard drug and other extracts too. The mechanism of action was similar to the paracetamol action that is inhibition of prostaglandin synthesis.

Renal sodium retention does not occur during the luteal phase of the menstrual cycle in normal women

1992 ◽  
Vol 99 (3) ◽  
pp. 247-252 ◽  
Author(s):  
D. L. BISSON ◽  
G. D. DUNSTER ◽  
J. P. O'HARE ◽  
D. HAMPTON ◽  
M. D. PENNEY
Keyword(s):  
Menstrual Cycle ◽  
Luteal Phase ◽  
Sodium Retention ◽  
Normal Women

Comparison of fast and slow pressor effects of angiotensin II in the conscious rat

1981 ◽  
Vol 241 (3) ◽  
pp. H381-H388 ◽  
Author(s):  
A. J. Brown ◽  
J. Casals-Stenzel ◽  
S. Gofford ◽  
A. F. Lever ◽  
J. J. Morton
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Control Period ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Pressor Effect ◽  
Ang Ii ◽  
Conscious Rat ◽  
Female Wistar Rats

Female Wistar rats were infused intravenously with 5% dextrose for 3 days, then with angiotensin II (ANG II) in 5% dextrose at 20 ng . kg-1 . min-1 for 7 days, and finally with dextrose for 2.5 days. ANG II raised mean arterial pressure (MAP) gradually; by the 7th day it was 49.7 mmHg higher than during the dextrose control period in the same rats. Control rats were infused with dextrose for 12.5 days; MAP did not change. Plasma ANG II concentration was measured during infusion. In hypertensive rats on the 7th day of ANG II infusion, it was six times higher than in control rats infused with dextrose. Changes of blood pressure and plasma ANG II concentration were compared in further rats infused with much larger doses of ANG II. Rats receiving 270 ng . kg-1 . min-1 for 1 h had an almost maximal direct pressor response, MAP rising 45.3 mmHg and plasma ANG II rising 32-fold compared with controls. Thus, infusion of ANG II at low dose without direct pressor effect gradually raises blood pressure to a level similar to the maximum direct pressor effect produced by larger doses of ANG II. Sodium balance and food and water intakes were also measured and did not change during prolonged infusion of ANG II at 20 ng . kg-1 . min-1. Thus, the slow pressure effect of ANG II develops at a lower and more nearly physiological plasma concentration of the peptide than do the direct pressor effect and the effects on drinking, eating, and urinary sodium excretion.

scholarly journals THE EFFECT OF INHIBITION OF PROSTAGLANDIN SYNTHESIS ON OVARIAN HYPERTROPHY IN THE RAT

Reproduction ◽  
1975 ◽  
Vol 44 (3) ◽  
pp. 473-479 ◽  
Author(s):  
V. D. CASTRACANE ◽  
L. F. TANKENOW ◽  
A. A. SHAIKH
Keyword(s):  
Prostaglandin Synthesis ◽  
Inhibition Of Prostaglandin Synthesis
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