The Conversion of [35S]PTC-Angiotensin I to PTC-Angiotensin II in Plasma of Normotensive and Hypertensive Subjects

1970 ◽  
Vol 38 (2) ◽  
pp. 217-223 ◽  
Author(s):  
E. C. Osborn ◽  
N. G. Hodges ◽  
P. T. Pickens ◽  
P. R. Willicombe ◽  
R. F. Mahler
Keyword(s):  
Angiotensin Ii ◽  
Normal Subjects ◽  
The Other ◽  
Angiotensin I ◽  
Hypertensive Patients

1. The rate of conversion of angiotensin I to angiotensin II was measured by using their [35S]PTC-analogues which can be separated and identified by radiochromatography. 2. There was no difference in the rate of conversion of one compound to the other in the plasma of normal subjects and hypertensive patients.

scholarly journals Comparison of two angiotensin II analogues in normal subjects and hypertensive patients.

1978 ◽  
Vol 25 (5) ◽  
pp. 447-452 ◽  
Author(s):  
TAKESHI HATA ◽  
TOSHIO OGIHARA ◽  
HIROSHI MIKAMI ◽  
MITSUAKI NAKAMARU ◽  
ANNA MARUYAMA ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Normal Subjects ◽  
Hypertensive Patients ◽  
Angiotensin Ii Analogues

EFFECT OF INHIBITION OF CONVERTING ENZYME ON INACTIVE RENIN IN THE CIRCULATION OF SALT-REPLETE AND SALT-DEPLETE NORMAL SUBJECTS

1980 ◽  
Vol 86 (2) ◽  
pp. 329-335 ◽  
Author(s):  
J. A. MILLAR ◽  
M. T. HAMMAT ◽  
C. I. JOHNSTON
Keyword(s):  
Angiotensin Ii ◽  
Normal Subjects ◽  
Inhibitory Influence ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Active Inhibitor ◽  
Active Renin ◽  
Angiotensin I Converting Enzyme ◽  
Inactive Renin ◽  
Orally Active

Angiotensin II exerts an inhibitory influence on active renin release from the kidney. To assess a possible role for angiotensin II in the release of inactive renin, levels in the circulation were measured before and at regular intervals after the administration of captopril, an orally active inhibitor of angiotensin I-converting enzyme, to 12 salt-replete and six salt-deplete normal subjects. Concurrent measurements of active renin, angiotensin I and angiotensin II were also performed. Basal inactive renin in the salt-deplete group was increased compared with the salt-replete subjects, but inactive renin remained constant in both groups after treatment with captopril. There were significant increases in concentrations of both active renin and angiotensin I after treatment with captopril in all subjects and corresponding decreases in angiotensin II. These results suggested that angiotensin II does not influence the release of inactive renin, in contrast with its role in the release of active renin.

Intralymphocytic Sodium in Hypertensive Patients: A Significant Correlation

1979 ◽  
Vol 57 (s5) ◽  
pp. 325s-327s ◽  
Author(s):  
E. Ambrosioni ◽  
F. Tartagni ◽  
L. Montebugnoli ◽  
B. Magnani
Keyword(s):  
Blood Pressure ◽  
Normal Subjects ◽  
Sodium Concentration ◽  
The Other ◽  
Mean Blood Pressure ◽  
Normal Blood ◽  
Normal Blood Pressure ◽  
Hypertensive Patients ◽  
Normotensive Subjects

1. Intralymphocytic sodium concentration was measured in 50 patients with essential stable hypertension, 44 patients with labile hypertension and 40 subjects with normal blood pressure. 2. Intralymphocytic sodium concentration in normotensive subjects was significantly lower than in the other two groups. 3. The concentration was significantly correlated with mean blood pressure in the group as a whole and in the groups with stable and with labile hypertension. No correlation was found in normal subjects.

scholarly journals IMMUNOLOGIC PRODUCTION OF ANTIANGIOTENSIN

1960 ◽  
Vol 111 (3) ◽  
pp. 419-427 ◽  
Author(s):  
Sharad D. Deodhar
Keyword(s):  
Biological Activity ◽  
Angiotensin Ii ◽  
Aromatic Amines ◽  
Free Amino ◽  
Parent Compound ◽  
The Other ◽  
Amino Group ◽  
Angiotensin I ◽  
Absolute Requirement ◽  
Specific Activities

Angiotensin II was coupled with bovine γ-globulin (BGG) through the following series of reactions. See PDF for Structure By determinations of the aromatic amine and tyrosine contents of p-aminobenzoylangiotensin II, the number of p-aminobenzoyl residues introduced per molecule of angiotensin II was calculated. Absorption spectra (between 250 and 500 mµ) of BGG complexes of p-aminobenzoylangiotensin II and six different para substituted aromatic amines were compared. Specific activities (dog units/millimicromole) of the different intermediate products were determined. Presence of a terminal, free amino group does not appear to be an absolute requirement for the biological activity of angiotensin II, since substitution of a p-aminobenzoyl radical in this group yields a product with 40 to 50 per cent of the activity of the parent compound. Angiotensin I, on the other hand, is completely inactivated under identical circumstances. Possible implication of this finding has been discussed.

Should blood samples for assay of plasma renin activity be chilled?

1978 ◽  
Vol 24 (11) ◽  
pp. 2042-2043 ◽  
Author(s):  
R L Emanuel ◽  
G H Williams
Keyword(s):  
Plasma Renin Activity ◽  
Room Temperature ◽  
Plasma Renin ◽  
The Other ◽  
Renin Activity ◽  
Angiotensin I ◽  
Blood Samples ◽  
Hypertensive Patients

Abstract Collecting blood on ice for renin determination reportedly may produce falsely high results. To assess the probability of this occurring under actual collection conditions, we measured renin activity in duplicate aliquots of plasma from blood samples from 25 hypertensive patients, both supine and upright, and in 10 supine normotensive controls. One aliquot of the blood was collected on ice and processed at 4 degrees C, the other at room temperature. The two aliquots showed no significant differences in renin activity. If anything, values for samples collected at room temperature were higher. Repeat determination on the same specimens stored at--20 degrees C for nine and 12 months revealed no significant changes in results for any samples, although the amount of angiotensin I found in the sample before incubation at 37 degrees C significantly increased. We conclude that it makes little difference at what temperature one collects blood for renin determination, but because of the wide fluctuations in "room" temperature we recommend that blood samples be collected on ice.

Angiotensin II Blockade in Normal Subjects and Essential Hypertensive Patients

1976 ◽  
Vol 51 (s3) ◽  
pp. 193s-196s
Author(s):  
G. A. MacGregor ◽  
P. M. Dawes
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Sodium Intake ◽  
Normal Subjects ◽  
Competitive Inhibitor ◽  
Hypertensive Patients ◽  
Sodium Diet ◽  
Incremental Rate ◽  
Standing Blood Pressure

1. Saralasin (Sar1-Ala8-angiotensin II), a competitive inhibitor of angiotensin II (AII), has been infused into normal subjects and patients with essential hypertension when deprived of sodium by 5 days of a 10 mmol/day sodium diet. 2. When saralasin was given by an incremental rate of infusion starting at 0·25 μg min—1 kg—1, sodium-deprived normal subjects showed a fall in standing blood pressure with no change in lying blood pressure, sodium-deprived normal-renin hypertensive patients showed no change in lying or standing blood pressure and sodium-deprived low-renin patients showed a significant sustained rise in lying and standing blood pressure. 3. These findings suggest that: (a) standing blood pressure in sodium-deprived normal subjects is angiotensin II dependent; (b) normal-renin hypertensive patients when sodium deprived by diet alone do not appear to be angiotensin II dependent (angiotensin II is unlikely therefore to be directly maintaining their blood pressure on their normal sodium intake); (c) the rise in blood pressure seen in low-renin hypertensive patients with saralasin may be a further way of distinguishing this group of patients.

Prorenin is present in human red blood cells

1991 ◽  
Vol 69 (9) ◽  
pp. 1394-1397 ◽  
Author(s):  
C. Troffa ◽  
G. Tonolo ◽  
P. Manunta ◽  
A. Pazzola ◽  
A. Soro ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Blood Cells ◽  
Normal Subjects ◽  
Trypsin Treatment ◽  
Angiotensin I ◽  
Hypertensive Patients ◽  
Human Red Blood Cells ◽  
Before And After ◽  
Inactive Renin ◽  
Homologous Substrate

We looked for the presence of prorenin in erythrocytes from normal subjects (n = 8), hypertensive patients (n = 8), and pregnant women (n = 8). Angiotensin I generation was measured at 37 °C, pH 5.7, in the presence of homologous substrate (1400 ng/mL) before and after trypsin activation (100 μg/mL) in (A) haemolyzed erythrocytes, (B) supernatants of haemolyzed erythrocytes, and (C) in the sixth washing of erythrocytes diluted 1:1 with a 0.1 M Tris buffer containing 0.5% bovine serum albumin and protease inhibitors. Haemolyzed erythrocytes generated angiotensin I only after trypsin treatment, and the rate of generation was the same (A) before and (B) after centrifugation at 20000g, indicating the absence of prorenin bound to the cell membranes. When aliquots of the last washing of erythrocytes (C) were tested for angiotensin I generation before and after trypsin, they did not generate angiotensin I, indicating that residual prorenin from the plasma was no longer present in our preparation. Angiotensin I generation by trypsin-treated A and B was completely abolished by preincubation with anti-renin serum. The level of prorenin was not significantly different in the erythrocytes from normal, hypertensive, and pregnant subjects (68 ± 10, 58 ± 7 and 107 ± 17 pg angiotensin I∙mL−1∙h−1, ns) in spite of their very different plasma levels (21 ± 2.5, 17 ± 2.4 and 110 ± 12 ng angiotensin I∙mL−1∙h−1, p < 0.01 for pregnant women compared with both normal and hypertensive subjects). Our data show that prorenin is present in human erythrocytes in fairly constant and clearly detectable amounts, thus suggesting a possible intracellular role for it.Key words: inactive renin, intracellular prorenin, erythrocytes, prorenin.

scholarly journals REN C-5312T, but not C-5434T, correlates to increase serum angiotensin I level in angiotensin II receptor blockers-treated hypertensive patients

2016 ◽  
Vol 11 (2) ◽  
pp. 552
Author(s):  
Mohammad Saifur Rohman ◽  
Frastiqa Fahrany ◽  
Imama Maslahah ◽  
Widodo ◽  
Mifetika Lukitasari ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Ii Receptor Blockers ◽  
Enzyme Linked Immunosorbent Assay ◽  
Angiotensin Ii Receptor ◽  
Angiotensin I ◽  
Distal Enhancer ◽  
Enhancer Activity ◽  
Hypertensive Patients ◽  
Significant Difference ◽  
Receptor Blockers

<p class="Abstract">Renin distal enhancer plays a crucial role in regulating renin gene (REN) expression. REN C-5312T enhancer<span lang="IN"> polymorphism increased enhancer activity. REN C-5434T was also identified which supposed to part of enhancer region. Therefore, this study aimed to investigate contribution of both C-5312T and C-5434T to serum angiotensin I in response to angiotensin II receptor blockers (ARB). C-5312T was identified in 46 hypertensive patients by using multiplex polymerase chain reaction (PCR), while C-5434T by using PCR-restiction fragment length of polymorphism (RFLP). Angiotensin I was measured using enzyme linked immunosorbent assay (ELISA). A significant difference of baseline angiotensin I was observed between -5312CC and -5312CT/TT (p=0.038) as well as the angiotensin I after 5 months of ARB treatment (p=0.008) in -5434CT/TT population, but not REN C-5434T. In conclusion, C-5312T resulted in increased mRNA renin level as consequence of higher enhancer activity not only at the baseline but also after 5 months ARB treatment.</span></p>

Effect of angiotensin on hypoxic pulmonary vasoconstriction in isolated dog lung

1976 ◽  
Vol 41 (1) ◽  
pp. 84-88 ◽  
Author(s):  
J. M. Alexander ◽  
M. D. Nyby ◽  
K. A. Jasberg
Keyword(s):  
Angiotensin Ii ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
The Other ◽  
Perfusion System ◽  
Angiotensin I ◽  
Pulmonary Vasoconstriction ◽  
Threefold Increase ◽  
Isolated Lung ◽  
The Right

The effects of infused angiotensin on hypoxic pulmonary vasoconstriction in blood-perfused isolated dog lungs were studied. By using a double-perfusion system we were able to perfuse the right and left lungs separately in the same animal; one lung was used as control and the other lung was experimentally modified. The vasoconstrictive response to hypoxia decreased with time in the isolated lung preparations. The infusion of either angiotensin I or angiotensin II (1.2–5.8 mug/min) caused a threefold increase in the vasoconstrictive response to hypoxia over control levels. A second hypoxic period during the infusion usually yielded a diminished response, suggesting further degeneration of the response irreversible with angiotensin. It was concluded that angiotensin I or angiotensin II temporarily enhances hypoxicpulmonary vasoconstriction in isolated dog lungs.

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