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.

Determination of Renin-Dependency and Sodium-Dependency in the Three Renin Sub-Groups of Essential Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 197s-200s
Author(s):  
H. Gavras ◽  
A. Ribeiro ◽  
H. R. Brunner ◽  
I. Gavras
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Renin Angiotensin System ◽  
Sodium Balance ◽  
Sodium Depletion ◽  
Angiotensin System ◽  
Variable Capacity ◽  
Sodium Dependency ◽  
Degree Of Participation

1. In all three renin sub-groups of essential hypertension, the state of sodium balance determines the degree of participation of the renin-angiotensin system in sustaining high blood pressure. 2. Even the low-renin type can become renin-dependent when sufficient sodium depletion has been achieved. 3. The main difference between patients of these sub-groups appears to be their variable capacity to become depleted of sodium under standard dietary regimens.

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.

Blood pressure effects of renin inhibition by human renin antiserum in normotensive marmosets

1984 ◽  
Vol 246 (3) ◽  
pp. F309-F316 ◽  
Author(s):  
J. B. Michel ◽  
J. Wood ◽  
K. Hofbauer ◽  
P. Corvol ◽  
J. Menard
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Pressure Effects ◽  
Sodium Balance ◽  
New World Monkeys ◽  
Common Marmosets ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Human Renin

The effects on blood pressure of an antiserum against pure human kidney renin were studied in conscious and anesthetized (pentobarbital, 24 mg X kg-1 i.p.) small new world monkeys (common marmosets). The antiserum inhibited the enzymatic activity of renin by 50% in a dilution of 1:45,000 in marmoset and 1:50,000 in human plasma. The antiserum (0.2 ml i.v.) decreased blood pressure in conscious marmosets on normal sodium intake by 15 +/- 5 (SD) mmHg and after salt depletion by 31 +/- 13 mmHg. A converting enzyme inhibitor (teprotide, 2 mg X kg-1 i.v.) induced a comparable fall in blood pressure: -16 +/- 10 and -30 +/- 10 mmHg, respectively. Similar effects were observed on blood pressure of anesthetized marmosets. The correlation between pretreatment plasma renin concentration and the maximum fall in blood pressure was significant and identical for the experiments with antiserum and teprotide. These results demonstrate that antisera against human renin can be used for the specific blockade of the renin-angiotensin system in primates. In normotensive marmosets the renin-angiotensin system participates in the maintenance of blood pressure, to a degree depending on the state of sodium balance.

Sodium Retention Versus Renin–Angiotensin System In Experimental Renal Hypertension

1973 ◽  
Vol 51 (3) ◽  
pp. 238-241 ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Blood Pressure ◽  
Renal Hypertension ◽  
Renin Angiotensin System ◽  
Sodium Balance ◽  
Sodium Retention ◽  
Sodium Depletion ◽  
Dual Nature ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Experimental Renal Hypertension

The relative importance of sodium retention versus the renin–angiotensin pressor response in hypertension caused by constriction of one renal artery and contralateral nephrectomy in the rat was assessed. Attempts were made to lower the blood pressure by changing sodium balance while plasma renin activity was measured. Acute sodium depletion (furosemide) had no measurable effect on the pressure seemingly because activation of the renin–angiotensin system prevented a fall in pressure. However, the pressure decreased rapidly and markedly in response to sodium depletion when the renin-angiotensin system was suppressed by (a) removing the sole remaining kidney after the sodium depletion or (b) pretreating the animals with deoxycorticosterone and salt. These results emphasize the dual nature of the control of blood pressure by the kidney in experimental renal hypertension.

Rate of activation of renin-angiotensin-aldosterone axis and sodium intake in rats

1989 ◽  
Vol 256 (5) ◽  
pp. H1311-H1315 ◽  
Author(s):  
E. Holtzman ◽  
L. M. Braley ◽  
A. Menachery ◽  
G. H. Williams ◽  
N. K. Hollenberg
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Sodium Intake ◽  
Pressor Response ◽  
Renin Angiotensin System ◽  
Sodium Balance ◽  
Plasma Aldosterone Concentration ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Rate Of Activation

When sodium intake in the rat is reduced abruptly from the typical high level to a very low level (0.02%), sodium excretion falls exponentially, with a half time of 2-3 h. The result is that the rat achieves external sodium balance, in which intake equals excretion, on the new low intake within a few hours. In this study, we assessed the rate of activation of the renin-angiotensin-aldosterone axis and its contribution to blood pressure during that interval. Plasma renin activity and angiotensin II concentration had risen sharply within 8 h and did not change over the next 40 h. Plasma aldosterone concentration, on the other hand, continued to rise over 48 h. Within 8 h, blood pressure dependency on angiotensin II had increased sharply, as assessed by depressor responses to an angiotensin antagonist (Sar1-Ala8-angiotensin II) and to converting-enzyme inhibition (captopril). The depressor response to neither agent changed over the next 40 h. The pressor response to angiotensin II was blunted significantly by 8 h and also did not change over the next 40 h. The findings indicate that the rapid tempo of sodium homeostasis in the rat is matched by an equally rapid tempo of activation of the renin-angiotensin system, although the factors responsible for aldosterone release are probably more complex. Experiments to assess the renin-angiotensin system in the rat must be designed with this rapid tempo in mind.

Terlipressin Versus  Norepinephrine to Correct Refractory Arterial Hypotension after General Anesthesia in Patients Chronically Treated with Renin-Angiotensin System Inhibitors

2003 ◽  
Vol 98 (6) ◽  
pp. 1338-1344 ◽  
Author(s):  
Gilles Boccara ◽  
Alexandre Ouattara ◽  
Gilles Godet ◽  
Eric Dufresne ◽  
Michèle Bertrand ◽  
...  
Keyword(s):  
Blood Pressure ◽  
General Anesthesia ◽  
Arterial Blood Pressure ◽  
Renin Angiotensin System ◽  
Arterial Hypotension ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Long Term Treatment ◽  
Systolic Arterial Blood Pressure

Background Terlipressin, a precursor that is metabolized to lysine-vasopressin, has been proposed as a drug for treatment of intraoperative arterial hypotension refractory to ephedrine in patients who have received long-term treatment with renin-angiotensin system inhibitors. The authors compared the effectiveness of terlipressin and norepinephrine to correct hypotension in these patients. Methods Among 42 patients scheduled for elective carotid endarterectomy, 20 had arterial hypotension following general anesthesia that was refractory to ephedrine. These patients were the basis of the study. After randomization, they received either 1 mg intravenous terlipressin (n = 10) or norepinephrine infusion (n = 10). Beat-by-beat recordings of systolic arterial blood pressure and heart rate were stored on a computer. The intraoperative maximum and minimum values of blood pressure and heart rate, and the time spent with systolic arterial blood pressure below 90 mmHg and above 160 mmHg, were used as indices of hemodynamic stability. Data are expressed as median (95% confidence interval). Results Terlipressin and norepinephrine corrected arterial hypotension in all cases. However, time spent with systolic arterial blood pressure below 90 mmHg was less in the terlipressin group (0 s [0-120 s] vs. 510 s [120-1011 s]; P < 0.001). Nonresponse to treatment (defined as three boluses of terlipressin or three changes in norepinephrine infusion) occurred in zero and eight cases (P < 0.05), respectively. Conclusions In patients who received long-term treatment with renin-angiotensin system inhibitors, intraoperative refractory arterial hypotension was corrected with both terlipressin and norepinephrine. However, terlipressin was more rapidly effective for maintaining normal systolic arterial blood pressure during general anesthesia.

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