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.

Effect of a Competitive Angiotensin Antagonist on the Renal Haemodynamic Changes Induced by Inhibition of Prostaglandin Synthesis in Rats

1974 ◽  
Vol 48 (s2) ◽  
pp. 299s-302s ◽  
Author(s):  
A. Mimran ◽  
D. Casellas ◽  
M. Dupont ◽  
P. Barjon
Keyword(s):  
Blood Pressure ◽  
Pressure Effect ◽  
Renin Angiotensin System ◽  
Prostaglandin Synthesis ◽  
Sodium Balance ◽  
Angiotensin System ◽  
Blood Pressure Effect ◽  
Haemodynamic Changes ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Angiotensin Receptor Blockade

1. Inhibition of prostaglandin synthesis by indomethacin induced an increase in blood pressure which did not occur when rats were bilaterally nephrectomized. 2. The blood pressure effect was related to the state of sodium balance and thus to the activity of the renin-angiotensin system. 3. Indomethacin induced a decrease in renal blood flow. 4. Angiotensin receptor blockade with Sar1-Ala8-angiotensin II blunted the blood pressure effect and prevented the renal haemodynamic changes induced by indomethacin.

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.

scholarly journals A Study of the Renin-Angiotensin System and the Blood Volume in the Nephrotic Syndrome

1986 ◽  
Vol 1 (1) ◽  
pp. 72-78
Author(s):  
Ho Dae Yoo ◽  
Kwang Su Choi ◽  
Man Hong Jung ◽  
Won Sik Lee ◽  
Jae Woo Lee ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Blood Volume ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

HYPERALDOSTERONISM IN THE SODIUM-DEPLETED RAT: MODE OF ALDOSTERONE-STIMULATING ACTION OF FRUSEMIDE

1979 ◽  
Vol 82 (1) ◽  
pp. 7-15 ◽  
Author(s):  
A. SPÄT ◽  
ÉVA TARJÁN ◽  
G. TÓTH
Keyword(s):  
Adrenal Glands ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Prostaglandin Synthesis ◽  
Angiotensin System ◽  
Adrenal Response ◽  
The Mean ◽  
Glomerulosa Cells ◽  
Mean Concentration ◽  
Vehicle Treated Control

SUMMARY The mechanism of diuretic-induced hyperaldosteronism was examined in dexamethasone-pretreated rats. The diuretic drug frusemide brought about a rapid increase in plasma renin activity and aldosterone concentration in serum. Half an hour after the administration of frusemide the mean concentration of aldosterone was 25 times higher than in vehicle-treated control animals. Administration of SQ 20,881, an inhibitor of angiotensin converting enzyme, prevented the adrenal response to frusemide. The response of aldosterone was completely blocked by indomethacin. This drug reduced renin release and probably also inhibited the effect on the adrenal glands of angiotensin, released in response to frusemide. Our results indicate that the effects of diuretics on the adrenal glomerulosa cells are mediated by the renin–angiotensin system also in the rat. Hyperaldosteronism is dependent on the maintenance of prostaglandin synthesis. ACTH has no essential role in this response.

Dietary protein increases plasma renin and reduces pressor reactivity to angiotensin II

1986 ◽  
Vol 251 (1) ◽  
pp. F34-F39 ◽  
Author(s):  
M. S. Paller ◽  
T. H. Hostetter
Keyword(s):  
Angiotensin Ii ◽  
Dietary Protein ◽  
Pressor Response ◽  
Renin Angiotensin System ◽  
Chronic Administration ◽  
Plasma Renin ◽  
Prostaglandin Synthesis ◽  
Plasma Aldosterone ◽  
Ang Ii ◽  
Inhibition Of Prostaglandin Synthesis

The effect of dietary protein on the renin-angiotensin system was studied in rats. Rats were fed isocaloric, 50% (high protein, HP), or 6% (low protein, LP) protein diets with identical electrolyte content for 10 days. Food intake and electrolyte excretion were equivalent on the two diets. Plasma renin activity (PRA) was higher in HP (10.0 +/- 2.5 vs. 3.5 +/- 0.5 ng ANG I . ml-1 . h-1, P less than 0.02) as was plasma aldosterone. However, in conscious rats mean arterial pressure (MAP) was not different between groups. The pressor response to graded doses of angiotensin II (ANG II) was diminished by 30-60% with HP (all doses, P less than 0.05). ANG II binding by mesenteric artery smooth muscle particles did not differ between HP and LP. Chronic administration of captopril did not normalize the pressor response in HP. Urinary prostaglandin (PG) E and 6-keto-PGF1 alpha excretion was markedly increased by the HP diet. Acute inhibition of prostaglandin synthesis with meclofenamate restored the pressor response to ANG II in HP to that in LP. In summary, a HP diet increased PRA, plasma aldosterone, urinary PGE, and 6-keto-PGF1 alpha and decreased pressor responsiveness to ANG II. Resistance to ANG II was not reversed by chronic converting enzyme inhibition but was abolished by inhibition of prostaglandin synthesis.

Renovascular resistance and noradrenaline

1975 ◽  
Vol 229 (6) ◽  
pp. 1649-1653 ◽  
Author(s):  
L Bomzon ◽  
C Rosendorff
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Blocking Agent ◽  
Competitive Inhibitor ◽  
Renal Nerves ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Alpha Adrenergic Receptors ◽  
High Doses ◽  
Adrenergic Blocking

Stimulation of the renal nerves can cause cortical vasoconstriction either by direct activation of vascular smooth muscle or by the generation of angiotensin II following renin release from the juxtaglomerular cells. High doses ( greater than 5 mug/min) of the renal neurotransmitter noradrenaline (NA) infused into the renal artery of the baboon causes cortical vasoconstriction. This NA-induced vasoconstriction is significantly reduced (P less than 0.001) by SQ20881, an inhibitor of converting enzyme, and by saralasin, a competitive inhibitor of angiotensin II. These results suggest that NA stimulates the renin-angiotensin mechanism. The further addition of the alpha-adrenergic blocking agent, phenoxybenzamine, to the NA-SQ20881 or NA-saralasin infusate completely abolishes NA-induced cortical vasoconstriction. These results suggest that NA-induced cortical vasoconstriction in the kidney is mediated by activation of both the renin-angiotensin system and alpha-adrenergic receptors.

Sign in / Sign up

Export Citation Format

Share Document