Inhibition of angiotensin conversion and prevention of renal hypertension

1975 ◽  
Vol 228 (2) ◽  
pp. 448-453 ◽  
Author(s):  
Miller ED ◽  
AI Samuels ◽  
E Haber ◽  
AC Barger
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Renovascular Hypertension ◽  
Renal Hypertension ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin System ◽  
The One ◽  
Renal Artery Constriction

Renal artery constriction in the unilaterally nephrectomized, trained dog, with maintained renal arterial hypotension, produces a prompt increase in systemic renin activity and blood pressure. The hypertension normally induced by renal artery stenosis is prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro (SQ 20, 881), which blocks conversion of angiotensin I to angiotensin II. Constant intravenous infusion of the inhibitor over several days of renal artery constriction prevents the development of chronic renovascular hypertension. Furthermore, a single injection of the nonapeptide restores blood pressure to normal in the early phase of renovascular hypertension, but becomes progressively less effective as salt and water retention occurs in the chronic stage when plasma renin activity returns to control levels. These data provide strong evidence that the renin-angiotensin system is responsible for the initiation of renovascular hypertension in the one-kidney Goldblatt dog, but that other factors become increasingly important in chronic renovascular hypertension.

What Stimulates the Renin—Angiotensin System in Rats with two-Kidney Renal Hypertension?

1983 ◽  
Vol 64 (5) ◽  
pp. 463-470
Author(s):  
Y. Takata ◽  
A. E. Doyle ◽  
M. Veroni ◽  
S. G. Duffy
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Contralateral Kidney ◽  
The One ◽  
Renin Content

1. Blood pressure, the hypotensive effect of captopril, plasma renin activity, renal renin content and kidney weight were measured in the two-kidney—one-clip model, the one-kidney—one-clip model and the two-kidney—one-clip model with the ureter of the contralateral kidney ligated in rats. The ureteric ligation was performed to abolish urinary excretion from the contralateral kidney in the two-kidney—one-clip model. 2. The development of hypertension after renal artery constriction was earlier and greater in the one-kidney—one-clip model and the two-kidney—one-clip model with ureter of the contralateral kidney ligated than in the two-kidney—one-clip model. A single oral dose of captopril produced a greater fall in blood pressure in both the two-kidney models than in the one-kidney—one-clip group. 3. Plasma renin activity and renal renin content of the clipped kidney were higher in the two-kidney model rats, whether or not the ureter had been ligated, than in the one-kidney—one-clip model animals, although more than half the rats from the two-kidney model had normal values. There was a significant correlation between plasma renin activity and the response to captopril in all groups, whereas in none of the three groups was the correlation between plasma renin activity and blood pressure significant. 4. The clipped kidney had a higher renin content than did the contralateral kidney, and the weight of the ischaemic kidney was decreased compared with the contralateral kidney whether it was untouched or had its ureter ligated. The weight of the clipped kidney was in the order one-kidney—one-clip model > two-kidney—one-clip model with ureter of the contralateral kidney ligated > two-kidney—one-clip model. 5. It was concluded that the renin-angiotensin system was stimulated to the similar degree in some animals for the two-kidney—one-clip models, whether or not the ureter of the contralateral kidney had been ligated, compared with the one-kidney—one-clip animals. This finding suggests that the contralateral kidney can stimulate renin secretion and synthesis in the clipped kidney independently of Na+ excretion.

Snakes and Hypertension

2017 ◽  
Vol 126 (2) ◽  
pp. 321-324
Author(s):  
Edward D. Miller
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Renovascular Hypertension ◽  
Perfusion Pressure ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Renal Perfusion Pressure ◽  
Renal Artery Constriction

Abstract Inhibition of Angiotensin Conversion in Experimental Renovascular Hypertension. By Miller ED Jr, Samuels A, Haber E, and Barger AC. Science 1972; 177:1108–9. Reprinted with permission from AAAS. Constriction of the renal artery and controlled reduction of renal perfusion pressure is followed by a prompt increase in systemic renin activity and a concomitant rise in blood pressure in trained, unanesthetized dogs. The elevated blood pressure induced by the renal artery stenosis can be prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro, which blocks conversion of angiotensin I to angiotensin II. Further, the nonapeptide can restore systemic pressure to normal in the early phase of renovascular hypertension. These results offer strong evidence that the renin– angiotensin system is responsible for the initiation of hypertension in the unilaterally nephrectomized dog with renal artery constriction.

Urinary Prostaglandin E2 and Kallikrein Excretion in Glucocrticoid Hypertension in Rats

1983 ◽  
Vol 65 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Michiko Handa ◽  
Kazuoki Kondo ◽  
Hiromichi Suzuki ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Prostaglandin E2 ◽  
Urine Volume ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Concurrent Administration ◽  
Angiotensin System

1. Oral administration of dexamethasone (about 2.5 × 10-7 mol/day) caused hypertension in rats. The blood pressure rose from 108 ± 6 (mean ± sd) to 156 ± 17 mmHg on the seventh day. The urine volume and urinary excretion of sodium were increased. The plasma renin activity and plasma aldosterone were unchanged. However, the urinary excretions of prostaglandin E2 (UPGE2V) and kallikrein (Ukall.V) were markedly decreased throughout the experiment. 2. With concurrent administration of captopril, the elevation of blood pressure was partially prevented. in this group of rats, the plasma renin activity was elevated and the reductions in UPGE2V and Ukall.V were partially prevented. 3. Based on these results, it is suggested that suppression of the kallikrein—kinin and prostaglandin systems, in addition to involvement of the renin-angiotensin system, is one of the factors contributing to the hypertensive action of dexamethasone.

DOSE-DEPENDENT BIFURCATION ANALYSIS OF PLASMA RENIN ACTIVITY AFTER NICARDIPINE TREATMENT

2019 ◽  
pp. 84-88
Author(s):  
Kaloyan Yankov
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Bifurcation Analysis ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Stability ◽  
The Impact

Renin-angiotensin system is one of the general regulatory mechanisms of blood pressure. The activity of the system depends on the rate of renin secretion, therefore, plasma renin activity (PRA) is one of the main variables that mediates the effect of a number of factors on blood pressure. Consequently, the impact of a particular drug on blood pressure disorders can be evaluated by the PRA changes. In clinical practice, the administered therapeutic dose is of critical nature, and a number of methods are known for its calculation. In the present study, applying bifurcation analysis the range of the administered doses of the nicardipine (antihypertensive drug) are determined. The bifurcation diagrams show how the stability of the renin-angiotensin system depends on the administered dose.

Role of the Brain Iso-Renin-Angiotensin System in Experimental Hypertension in Rats

1981 ◽  
Vol 61 (2) ◽  
pp. 175-180 ◽  
Author(s):  
Hiromichi Suzuki ◽  
Kazuoki Kondo ◽  
Michiko Handa ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Cerebral Ventricles ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Brain

1. To examine the possible participation of the brain iso-renin-angiotensin system in the control of blood pressure, as well as in the regulation of plasma renin activity, saralasin and captopril were injected into the cerebral ventricles of three types of experimental hypertensive rats with different plasma renin profiles. 2. Injection of saralasin and captopril into the cerebral ventricles resulted in a significant decrease in blood pressure of two-kidney, one-clip Goldblatt hypertensive rats (11 ± 2 and 9 ± 3 mmHg respectively) and that of spontaneously hypertensive rats (13 ± 2 and 12 ± 2 mmHg respectively), but in deoxycorticosterone (DOC)-salt hypertensive rats injection of these two agents showed a significant increase in blood pressure (13 ± 2 and 12 ± 3 mmHg respectively). 3. The plasma renin activity was markedly decreased after injection of saralasin and captopril into the cerebral ventricles of two-kidney, one-clip Goldblatt hypertensive rats. Conversely, in DOC-salt hypertensive rats, the plasma renin activity was markedly increased after injection of these two agents. In spontaneously hypertensive rats these agents caused no significant change in plasma renin activity. 4. These findings suggest that the brain iso-renin-angiotensin system participates in the central regulation of blood pressure and may be responsible for modulation of the peripheral renin-angiotensin system.

Changes in Plasma Renin Activity and Blood Pressure after Acute and Chronic Administration of β-Adrenergic Receptor-Blocking Drugs

1974 ◽  
Vol 48 (s2) ◽  
pp. 81s-83s
Author(s):  
T. Morgan ◽  
S. Carney ◽  
R. Roberts
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Renin Angiotensin System ◽  
Chronic Administration ◽  
Plasma Renin ◽  
Renin Activity ◽  
Hypotensive Action ◽  
Angiotensin System ◽  
Basal Plasma ◽  
Adrenergic Blocking

1. Prindolol and propranolol chronically cause a fall in mean blood pressure and mean plasma renin activity, but no correlation was observed between the two variables. 2. The response of blood pressure to prindolol and propranolol was not predicted by the basal plasma renin activity. 3. Propranolol administered acutely caused the plasma renin activity to fall with no acute change in blood pressure, whereas prindolol caused the blood pressure to fall with no change in plasma renin activity. 4. The effects of β-adrenergic-blocking drugs on plasma renin activity and blood pressure can be dissociated and it is unlikely that their hypotensive action is mediated through the renin-angiotensin system. 5. Basal plasma renin activity does not identify the patients who will respond to β-adrenergic-blocking drugs.

Surgical Reversal of Renovascular Hypertension in Rats: Changes in Blood Pressure, Plasma and Aortic Renin

1983 ◽  
Vol 65 (1) ◽  
pp. 33-36 ◽  
Author(s):  
Joan M. Brice ◽  
G. I. Russell ◽  
R. F. Bing ◽  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Vascular Tissue ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Hypertensive Rats ◽  
Normal Range ◽  
Angiotensin System ◽  
Pressure Plasma ◽  
Before And After

1. Blood pressure, plasma and aortic renin concentrations were measured in Goldblatt two-kidney one-clip hypertensive rats before and after surgical correction by removing the renal artery clip. 2. Blood pressure fell rapidly in the first hour and then more slowly over 24 h. 3. Plasma renin concentration fell into the normal range by 3 h after unclipping. 4. Aortic renin concentration was markedly raised in hypertensive rats and declined slowly after unclipping, being virtually unchanged at 3 h and reaching normal levels at 24 h. 5. The fall in blood pressure produced by removal of the renal artery clip in Goldblatt two-kidney one-clip hypertensive rats does not depend upon the renin-angiotensin system in plasma and vascular tissue and indicates that a renal vasodepressor system may be involved.

scholarly journals DOSE-DEPENDENT BIFURCATION ANALYSIS OF PLASMA RENIN ACTIVITY AFTER NICARDIPINE TREATMENT

2019 ◽  
Vol 7 (3) ◽  
pp. 179-183
Author(s):  
Kaloyan Yankov
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Bifurcation Analysis ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Stability ◽  
The Impact

Renin-angiotensin system is one of the general regulatory mechanisms of blood pressure. The activity of the system depends on the rate of renin secretion, therefore, plasma renin activity (PRA) is one of the main variables that mediates the effect of a number of factors on blood pressure. Consequently, the impact of a particular drug on blood pressure disorders can be evaluated by the PRA changes. In clinical practice, the administered therapeutic dose is of critical nature, and a number of methods are known for its calculation. In the present study, applying bifurcation analysis the range of the administered doses of the nicardipine (antihypertensive drug) are determined. The bifurcation diagrams show how the stability of the renin-angiotensin system depends on the administered dose.

Plasma Renin Activity as a Function of Age in Two New Strains of Spontaneously Hypertensive and Normotensive Rats

1976 ◽  
Vol 50 (2) ◽  
pp. 103-107 ◽  
Author(s):  
Madeleine Vincent ◽  
Jeanne Dupont ◽  
J. Sassard
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Inverse Relationship ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Fold Increase ◽  
Renin Activity ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Ether Anaesthesia

1. Strains of spontaneously hypertensive and normotensive rats were selected by repeated inbreeding. 2. Brief ether anaesthesia was shown to produce a two- to three-fold increase in plasma renin activity in both strains. 3. Plasma renin activity was significantly higher in young spontaneously hypertensive than in normotensive rats of the same age (5–7 weeks). After the ninth week plasma renin activity decreased and, at week 45, became significantly lower in hypertensive than in normotensive rats. 4. When hypertension was established a significant inverse relationship was found between plasma renin activity and systolic blood pressure in spontaneously hypertensive and in normotensive rats. 5. It seems unlikely that the renin—angiotensin system plays a major role in the maintenance of the established spontaneous hypertension in this strain. However, renin hypersecretion may be important in the early pre-hypertensive stage of genetic hypertension in rats.

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