The effect of the converting enzyme inhibitor HOE 498 on the renin angiotensin system of normal volunteers

1985 ◽  
Vol 329 (1) ◽  
pp. 63-69 ◽  
Author(s):  
J. P. Bussien ◽  
J. Nussberger ◽  
M. Porchet ◽  
B. Waeber ◽  
H. R. Brunner ◽  
...  
Keyword(s):  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Normal Volunteers ◽  
Converting Enzyme Inhibitor ◽  
Hoe 498

Response of Chronic Renovascular Hypertension to Surgical Correction or Prolonged Blockade of the Renin–Angiotensin System by Two Inhibitors in the Rat

1980 ◽  
Vol 58 (1) ◽  
pp. 15-20 ◽  
Author(s):  
H. Thurston ◽  
R. F. Bing ◽  
E. S. Marks ◽  
J. D. Swales
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Blood Pressure Response ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Chronic Hypertension ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Converting Enzyme Inhibitor

1. Removal of the renal artery constriction but not of the clipped kidney restored the blood pressure to normal levels in Goldblatt two-kidney rats with hypertension of more than 4 months' duration. 2. Despite the differences in blood pressure response, both surgical procedures lowered plasma renin concentration to normal or below normal values. 3. Administration of the oral converting enzyme inhibitor SQ 14 225 produced a marked fall in blood pressure in Goldblatt kidney rats with chronic hypertension. However, a prolonged infusion of the angiotensin II antagonist saralasin was quite ineffective. The difference in response to the two inhibitors may have been due to bradykinin potentiation by the converting enzyme inhibitor. 4. Although plasma renin is often elevated in Goldblatt two-kidney rats with hypertension of more than 4 months' duration, the renin-angiotensin system plays no role in the maintenance of blood pressure at this stage.

Vasodepressor Property of the Converting Enzyme Inhibitor Captopril (SQ 14 225): The Role of Factors other than Renin-Angiotensin Blockade in the Rat

1980 ◽  
Vol 58 (1) ◽  
pp. 1-6 ◽  
Author(s):  
E. S. Marks ◽  
R. F. Bing ◽  
H. Thurston ◽  
J. D. Swales
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Converting Enzyme Inhibitor ◽  
Blood Pressure Fall ◽  
Angiotensin Blockade ◽  
Pressure Fall

1. The peptide converting enzyme inhibitor captopril was given (1·25 mg/kg intravenously) to normal and nephrectomized rats and rats with renovascular and deoxycorticosterone hypertension. 2. Captopril lowered blood pressure to a small extent in normal and nephrectomized rats. Bradykinin infusion in nephrectomized animals, however, potentiated the vasodepressor action of captopril. 3. Captopril produced a major blood pressure fall in the early stages of Goldblatt two-kidney one-clip hypertension: even when hypertension had been present for more than 4 months, a substantial vasodepressor action was seen. Rats with deoxycorticosterone-induced hypertension also showed a significant blood pressure fall. 4. Captopril was given to salt-loaded and salt-depleted rats in which the renin-angiotensin system had been blocked by infusion of the competitive angiotensin II antagonist saralasin. Captopril still lowered blood pressure in the salt-depleted group. 5. Captopril lowers blood pressure in situations where the renin-angiotensin system is not responsible for blood pressure maintenance. Further, the fall in blood pressure produced in Goldblatt two-kidney one-clip hypertension is greater than would be predicted on the basis of renin-angiotensin blockade. It is likely therefore that captopril lowers blood pressure by an action additional to angiotensin blockade. Bradykinin potentiation is one possible mechanism by which this may take place.

An Experimental Model of Encapsulating Peritoneal Sclerosis

2009 ◽  
Vol 29 (2_suppl) ◽  
pp. 49-50 ◽  
Author(s):  
Tokihiko Sawada ◽  
Yasuo Ishii ◽  
Ichiro Nakajima ◽  
Shohei Fuchinoue ◽  
Keiichi Kubota ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Angiotensin Converting Enzyme Inhibitor ◽  
Transforming Growth Factor ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Dependent Manner ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Converting Enzyme Inhibitor

In Japan, only about 3% of all patients with end-stage renal disease are maintained by continuous ambulatory peritoneal dialysis (CAPD). Although the reasons for the low proportion of patients receiving CAPD are multifactorial, encapsulating peritoneal sclerosis (EPS), a fatal complication of CAPD, is a major factor. In 1995 we developed a rat model of EPS, and in 2001 also developed an EPS model in mice. These rodent EPS models are reliable, reproducible, and inexpensive and have been used by other investigators. The renin–angiotensin system negatively regulates the transforming growth factor-beta signaling pathway, which plays a major role in tissue fibrosis. To investigate the anti-EPS effect of renin–angiotensin system inhibition, an angiotensin-converting enzyme inhibitor, quinapril, was administered to an EPS model in mice. Quinapril was found to inhibit EPS, both macro- and microscopically, in a dose-dependent manner. We report our experience of developing the experimental in vivo EPS model, and the inhibitory effect of this angiotensin-converting enzyme inhibitor on EPS.

scholarly journals The angiotensin-converting enzyme inhibitor captopril rescues mice from endotoxin-induced lethal hepatitis

2016 ◽  
Vol 23 (2) ◽  
pp. 128-135 ◽  
Author(s):  
Pu Ge ◽  
Rong Jiang ◽  
Xin Yao ◽  
Jing Li ◽  
Jie Dai ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Angiotensin Converting Enzyme Inhibitor ◽  
Fulminant Hepatitis ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Converting Enzyme Inhibitor ◽  
Tnf Α

The renin–angiotensin system is classically regarded as a crucial regulator of circulatory homeostasis, but recent studies also revealed its pro-inflammatory roles. The beneficial effects of the angiotensin-converting enzyme inhibitor (ACEI) in severe inflammatory injury in the lung and heart have been previously reported, but its potential effects on lethal hepatitis were unknown. In this study, a mouse model with LPS/d-galactosamine (GalN)-induced fulminant hepatitis were used to test the protective potential of captopril, a representative ACEI. The results indicated that treatment with captopril significantly decreased the plasma level of alanine aminotransferase and aspartate aminotransferase, alleviated the histopathological damage of the liver tissue and improve the survival rate of LPS/GalN-challenged mice. These effects were accompanied by reduced mRNA levels of TNF-α and IL-6 in the liver, and decreased protein level of TNF-α and IL-6 in the plasma. In addition, the activation of caspases 3, 8 and 9, and the presence of TUNEL-positive apoptotic cells, were also suppressed by captopril treatment. The above evidence suggested that the renin–angiotensin system might be involved in the development of LPS/GalN-induced fulminant hepatitis and ACEI might have potential value in lethal hepatitis.

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