Effects of angiotensin I and angiotensin II in blood vessels: greater influence of converting enzyme activity in the rabbit basilar artery

1996 ◽  
Vol 354 (4) ◽  
pp. 466-473 ◽  
Author(s):  
A. Zerrouk ◽  
M. Auguet ◽  
S. Delaflotte ◽  
P. E. Chabrier
1982 ◽  
Vol 63 (s8) ◽  
pp. 199s-201s ◽  
Author(s):  
Inge E. K. Trindade ◽  
Eduardo M. Krieger

1. The extents of pulmonary degradation of bradykinin (BK) and angiotensin I (ANG I) to angiotensin II (ANG II) conversion were measured simultaneously to determine whether converting enzyme activity, in vivo, is altered in two-kidney, one-clip hypertensive rats (15, 60 and 180 days after renal artery clipping). 2. Inactivation of BK (estimated by comparing equipressor doses injected intravenously and intra-aortically) was markedly increased in these hypertensive rats: 98.5% (15 days), 98.4% (60 days) and 99.5% (180 days) vs 95.6% in control rats. All groups of hypertensive rats exhibited hyper-reactivity to intra-aortic BK, requiring doses 14–38 times smaller than the control rats to produce the same depressor response. 3. The percentage of ANG I conversion (calculated from equipressor doses of ANG I and ANG II injected intravenously) was elevated after 15 days (46.0% vs 28.1% in control rats), unchanged after 60 days (27.7%) and slightly elevated after 180 days (36.0%). Hyporeactivity to ANG II was observed 15 and 180 days after renal artery clipping (doses six times were needed to produce a standard increase in mean arterial pressure). No alterations were found in the rats at 60 days after artery clipping. 4. The increased degradation of BK cannot be explained solely by elevation of converting enzyme activity since no parallel increase in ANG I conversion was observed, indicating that other bradykininases in the lung may be involved.


1980 ◽  
Vol 48 (2) ◽  
pp. 308-312 ◽  
Author(s):  
P. J. Leuenberger ◽  
S. A. Stalcup ◽  
L. M. Greenbaum ◽  
R. B. Mellins ◽  
G. M. Turino

To determine if angiotension converting enzyme activity is altered by acute pathophysiological insults, we assessed angiotensin I conversion using a blood pressure response technique in anesthetized dogs studied during acute 100% O2 breathing and acute acid-base derangements. Also, we determined systemic vascular reactivity to angiotensin II by measuring the magnitude and duration of the arterial blood pressure response to intra-arterial injections of angiotensin II under these same conditions. Angiotensin I conversion found in normoxia [91 +/- 7 (SD)%] was unchanged by acute acidosis, alkalosis, and hyperoxia. During acute hyperoxia the mean half time of the hypertensive response increased from 68 +/- 25 (SD) s at a PaO2 of 112 +/- 18 (SD) Torr to 100 +/- 34 (SD) s at a PaO2 of 491 +/- 47 (SD) Torr (P less than 0.01). No other pathophysiological condition studied had any effect on reactivity of systemic vasculature to angiotensin II. We conclude that, except during acute hypoxia as previously shown, converting enzyme activity is resistant to other pathophysiological insults and that vascular responsiveness to angiotensin II is enhanced by hyperoxia.


1974 ◽  
Vol 47 (2) ◽  
pp. 189-192 ◽  
Author(s):  
J. G. Collier ◽  
B. F. Robinson

1. The effects of angiotensin I (AI) and angiotensin II (AII) have been compared during local infusions into peripheral arteries and veins in man. 2. Both AI and AII produced constriction of hand veins and forearm arteries; the potency of AI was somewhat less than AII. 3. When infused into the vein, the converting enzyme inhibitor SQ 20,881 abolished or markedly attenuated the effect of AI but not that of AII. 4. The results suggest the local presence of converting enzyme in human peripheral arteries and veins.


1993 ◽  
Vol 72 (2) ◽  
pp. 312-318 ◽  
Author(s):  
H Schunkert ◽  
J R Ingelfinger ◽  
A T Hirsch ◽  
Y Pinto ◽  
W J Remme ◽  
...  

2015 ◽  
Vol 5 (12) ◽  
pp. e691-e691 ◽  
Author(s):  
A Gadelha ◽  
A M Vendramini ◽  
C M Yonamine ◽  
M Nering ◽  
A Berberian ◽  
...  

1976 ◽  
Vol 51 (6) ◽  
pp. 537-543 ◽  
Author(s):  
Suzanne Oparil ◽  
J. Low ◽  
T. J. Koerner

1. A specific method is described for the measurement of angiotensin I converting enzyme activity in plasma with 125I-labelled angiotensin I used as substrate. 2. Converting enzyme activity in plasma from fifteen normal subjects, eleven patients with sarcoidosis, twelve patients with chronic obstructive pulmonary disease and three patients with shock lung was assayed by this technique. 3. Patients with sarcoidosis had increased plasma converting enzyme activity whether or not they were receiving steroid therapy. 4. Patients with chronic obstructive pulmonary disease and shock lung had decreased plasma converting enzyme activity, but extent of conversion did not correlate with the severity of the lung disease. 5. Converting enzyme activity in normal plasma could be completely inhibited by addition of exogenous angiotensin I in 0·5–2·5 × 107 times physiological concentration. Twice as much exogenous angiotensin I was needed to inhibit conversion completely in plasma from patients with sarcoidosis; one tenth as much in chronic obstructive pulmonary disease. These results indicate that plasma has a high capacity for angiotensin I conversion even in patients with pulmonary parenchymal disease. 6. Results suggest that plasma converting enzyme activity may be a reflection of pulmonary conversion and can be altered by pulmonary disease. 7. Measurement of plasma converting enzyme activity may be useful in studies designed to characterize the regulatory role of converting enzyme in the renin—angiotensin system and in cardiovascular homeostasis.


1990 ◽  
Vol 191 (3) ◽  
pp. 175-184 ◽  
Author(s):  
Ana Elena Arévalo ◽  
María Elena Ibarra-Rubio ◽  
Cristino Cruz ◽  
JoséCarlos Peńa ◽  
José Pedraza-Chaverrí

Sign in / Sign up

Export Citation Format

Share Document