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Specific direct radioimmunoassay of angiotensin II (AT II) in human plasma and the effect of angiotensin converting enzyme (ACE) inhibitor

Specific direct radioimmunoassay of angiotensin II (AT II) in human plasma was developed to evaluate the dynamics of endogenous AT II in various types of hypertension. Detection limit of this method was less than 2.3 pg/ml, and normal value is less than 25 pg/ml. Cross reactivity of antibody with AT...

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Published in:Immunopharmacology 1999-10, Vol.44 (1-2), p.199-204
Main Authors: Abe, Fumiaki, Omata, Ken, Yamada, Masaaki, Tsunoda, Kazuo, Sato, Tatsuyuki, Shimizu, Tetsu, Ito, Sadayoshi, Abe, Keishi, Nakazima, Megumi, Morimoto, Taeko, Takanashi, Naoki
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container_title Immunopharmacology
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creator Abe, Fumiaki
Omata, Ken
Yamada, Masaaki
Tsunoda, Kazuo
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Ito, Sadayoshi
Abe, Keishi
Nakazima, Megumi
Morimoto, Taeko
Takanashi, Naoki
description Specific direct radioimmunoassay of angiotensin II (AT II) in human plasma was developed to evaluate the dynamics of endogenous AT II in various types of hypertension. Detection limit of this method was less than 2.3 pg/ml, and normal value is less than 25 pg/ml. Cross reactivity of antibody with AT I and III was 0.037% and 21%, respectively. There were good correlation between the value measured by direct method, and that of extraction method (r=0.96, P
doi_str_mv 10.1016/S0162-3109(99)00090-9
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Detection limit of this method was less than 2.3 pg/ml, and normal value is less than 25 pg/ml. Cross reactivity of antibody with AT I and III was 0.037% and 21%, respectively. There were good correlation between the value measured by direct method, and that of extraction method (r=0.96, P&lt;0.01) and plasma renin activity (r=0.80, P&lt;0.01). By oral administration of ACE inhibitor (captopril 50 mg), AT II levels were suppressed to 10 pg/ml or less in most patients with essential hypertension, renal parenchymal hypertension and renovascular hypertension up to 2 h. However, AT II levels in patients treated with ACE inhibitors chronically were not different from the AT II levels in patients without ACE inhibitor. In primary aldosteronism AT II was extremely low levels. AT II markedly increased by the stimulation test using furosemide (1 mg/kg i.v.). These results suggest that this method may be useful to clarify the pathophysiology of hypertension and the escape of the inhibition by ACE inhibitor.</description><identifier>ISSN: 0162-3109</identifier><identifier>DOI: 10.1016/S0162-3109(99)00090-9</identifier><identifier>PMID: 10604545</identifier><identifier>CODEN: IMMUDP</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Analysis ; Angiotensin converting enzyme (ACE) inhibitor ; Angiotensin II ; Angiotensin II - blood ; Angiotensin-Converting Enzyme Inhibitors - pharmacology ; Angiotensin-Converting Enzyme Inhibitors - therapeutic use ; Biological and medical sciences ; captopril ; dipeptidyl carboxypeptidase I inhibitors ; Female ; General pharmacology ; Humans ; Hyperaldosteronism - blood ; Hyperaldosteronism - drug therapy ; Hypertension ; Hypertension - blood ; Hypertension - drug therapy ; Hypertension, Renal - blood ; Hypertension, Renal - drug therapy ; Medical sciences ; Pharmacology. 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Detection limit of this method was less than 2.3 pg/ml, and normal value is less than 25 pg/ml. Cross reactivity of antibody with AT I and III was 0.037% and 21%, respectively. There were good correlation between the value measured by direct method, and that of extraction method (r=0.96, P&lt;0.01) and plasma renin activity (r=0.80, P&lt;0.01). By oral administration of ACE inhibitor (captopril 50 mg), AT II levels were suppressed to 10 pg/ml or less in most patients with essential hypertension, renal parenchymal hypertension and renovascular hypertension up to 2 h. However, AT II levels in patients treated with ACE inhibitors chronically were not different from the AT II levels in patients without ACE inhibitor. In primary aldosteronism AT II was extremely low levels. AT II markedly increased by the stimulation test using furosemide (1 mg/kg i.v.). These results suggest that this method may be useful to clarify the pathophysiology of hypertension and the escape of the inhibition by ACE inhibitor.</description><subject>Analysis</subject><subject>Angiotensin converting enzyme (ACE) inhibitor</subject><subject>Angiotensin II</subject><subject>Angiotensin II - blood</subject><subject>Angiotensin-Converting Enzyme Inhibitors - pharmacology</subject><subject>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>captopril</subject><subject>dipeptidyl carboxypeptidase I inhibitors</subject><subject>Female</subject><subject>General pharmacology</subject><subject>Humans</subject><subject>Hyperaldosteronism - blood</subject><subject>Hyperaldosteronism - drug therapy</subject><subject>Hypertension</subject><subject>Hypertension - blood</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension, Renal - blood</subject><subject>Hypertension, Renal - drug therapy</subject><subject>Medical sciences</subject><subject>Pharmacology. 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Detection limit of this method was less than 2.3 pg/ml, and normal value is less than 25 pg/ml. Cross reactivity of antibody with AT I and III was 0.037% and 21%, respectively. There were good correlation between the value measured by direct method, and that of extraction method (r=0.96, P&lt;0.01) and plasma renin activity (r=0.80, P&lt;0.01). By oral administration of ACE inhibitor (captopril 50 mg), AT II levels were suppressed to 10 pg/ml or less in most patients with essential hypertension, renal parenchymal hypertension and renovascular hypertension up to 2 h. However, AT II levels in patients treated with ACE inhibitors chronically were not different from the AT II levels in patients without ACE inhibitor. In primary aldosteronism AT II was extremely low levels. AT II markedly increased by the stimulation test using furosemide (1 mg/kg i.v.). These results suggest that this method may be useful to clarify the pathophysiology of hypertension and the escape of the inhibition by ACE inhibitor.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>10604545</pmid><doi>10.1016/S0162-3109(99)00090-9</doi><tpages>6</tpages></addata></record>
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ispartof Immunopharmacology, 1999-10, Vol.44 (1-2), p.199-204
issn 0162-3109
language eng
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subjects Analysis
Angiotensin converting enzyme (ACE) inhibitor
Angiotensin II
Angiotensin II - blood
Angiotensin-Converting Enzyme Inhibitors - pharmacology
Angiotensin-Converting Enzyme Inhibitors - therapeutic use
Biological and medical sciences
captopril
dipeptidyl carboxypeptidase I inhibitors
Female
General pharmacology
Humans
Hyperaldosteronism - blood
Hyperaldosteronism - drug therapy
Hypertension
Hypertension - blood
Hypertension - drug therapy
Hypertension, Renal - blood
Hypertension, Renal - drug therapy
Medical sciences
Pharmacology. Drug treatments
Pregnancy
Pregnancy Complications, Cardiovascular - blood
Pregnancy Complications, Cardiovascular - drug therapy
Radioimmunoassay - methods
Renin
title Specific direct radioimmunoassay of angiotensin II (AT II) in human plasma and the effect of angiotensin converting enzyme (ACE) inhibitor
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