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The relevance of tissue angiotensin-converting enzyme: manifestations in mechanistic and endpoint data

Identifieur interne : 00B945 ( Main/Exploration ); précédent : 00B944; suivant : 00B946

The relevance of tissue angiotensin-converting enzyme: manifestations in mechanistic and endpoint data

Auteurs : Victor J. Dzau ; Kenneth Bernstein ; David Celermajer [États-Unis] ; Jerome Cohen ; Björn Dahlöf ; John Deanfield ; Javier Diez ; Helmut Drexler ; Roberto Ferrari ; Wiek Van Gilst ; Lennart Hansson ; Burkhard Hornig ; Ahsan Husain ; Colin Johnston ; Harold Lazar ; Eva Lonn [Canada] ; Thomas Lüscher ; John Mancini [Canada] ; Albert Mimran ; Carl Pepine ; Ton Rabelink ; Willem Remme ; Luis Ruilope ; Marcel Ruzicka [Canada] ; Heribert Schunkert ; Karl Swedberg [États-Unis] ; Thomas Unger ; Douglas Vaughan ; Michael Weber

Source :

RBID : ISTEX:F3AA4BE8EBFD160851C995AF366CE0A71B2C1DBA

Descripteurs français

English descriptors

Abstract

Abstract: Angiotensin-converting enzyme (ACE) is primarily localized (>90%) in various tissues and organs, most notably on the endothelium but also within parenchyma and inflammatory cells. Tissue ACE is now recognized as a key factor in cardiovascular and renal diseases. Endothelial dysfunction, in response to a number of risk factors or injury such as hypertension, diabetes mellitus, hypercholesteremia, and cigarette smoking, disrupts the balance of vasodilation and vasoconstriction, vascular smooth muscle cell growth, the inflammatory and oxidative state of the vessel wall, and is associated with activation of tissue ACE. Pathologic activation of local ACE can have deleterious effects on the heart, vasculature, and the kidneys. The imbalance resulting from increased local formation of angiotensin II and increased bradykinin degradation favors cardiovascular disease. Indeed, ACE inhibitors effectively reduce high blood pressure and exert cardio- and renoprotective actions. Recent evidence suggests that a principal target of ACE inhibitor action is at the tissue sites. Pharmacokinetic properties of various ACE inhibitors indicate that there are differences in their binding characteristics for tissue ACE. Clinical studies comparing the effects of antihypertensives (especially ACE inhibitors) on endothelial function suggest differences. More comparative experimental and clinical studies should address the significance of these drug differences and their impact on clinical events.

Url:
DOI: 10.1016/S0002-9149(01)01878-1


Affiliations:


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Le document en format XML

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<term>Cardiology</term>
<term>Cardiovascular</term>
<term>Cardiovascular death</term>
<term>Cardiovascular disease</term>
<term>Carotid</term>
<term>Carotid ultrasound changes</term>
<term>Cell cardiol</term>
<term>Chronic heart failure</term>
<term>Chymase</term>
<term>Circ</term>
<term>Clin</term>
<term>Clinical studies</term>
<term>Clinical trials</term>
<term>Coll cardiol</term>
<term>Congestive heart failure</term>
<term>Conventional therapy</term>
<term>Coronary</term>
<term>Coronary artery</term>
<term>Coronary artery disease</term>
<term>Coronary artery disease patients</term>
<term>Danser</term>
<term>Diabetes</term>
<term>Diabetes mellitus</term>
<term>Diabetic nephropathy</term>
<term>Diastolic</term>
<term>Dilation</term>
<term>Dysfunction</term>
<term>Ejection</term>
<term>Enalapril</term>
<term>Enalaprilat</term>
<term>Endothelial</term>
<term>Endothelial dysfunction</term>
<term>Endothelial function</term>
<term>Endothelium</term>
<term>Endpoint</term>
<term>Engl</term>
<term>Enzyme</term>
<term>Enzyme gene</term>
<term>Enzyme inhibition</term>
<term>Enzyme inhibitors</term>
<term>European trial</term>
<term>Free inhibitor</term>
<term>Gene polymorphism</term>
<term>Glomerular</term>
<term>Graft</term>
<term>Graft surgery</term>
<term>Growth factor</term>
<term>Heart failure</term>
<term>High levels</term>
<term>Hope study</term>
<term>Human heart</term>
<term>Hypertension</term>
<term>Hypertensive</term>
<term>Hypertensive rats</term>
<term>Hypertrophy</term>
<term>Important role</term>
<term>Infarct survival</term>
<term>Infarction</term>
<term>Inhibition</term>
<term>Inhibitor</term>
<term>Inhibitor action</term>
<term>Inhibitor therapy</term>
<term>Inhibitor treatment</term>
<term>Ischemic</term>
<term>Ischemic events</term>
<term>Lancet</term>
<term>Local angiotensin</term>
<term>Lorell</term>
<term>Mellitus</term>
<term>Myocardial</term>
<term>Myocardial infarction</term>
<term>Myocytes</term>
<term>Nephrol dial transplant</term>
<term>Nephropathy</term>
<term>Nitric</term>
<term>Nitric oxide</term>
<term>Nitric oxide release</term>
<term>Normotensive</term>
<term>November</term>
<term>Other antihypertensive agents</term>
<term>Overall mortality</term>
<term>Oxide</term>
<term>Perindopril</term>
<term>Pfeffer</term>
<term>Pharmacol</term>
<term>Placebo</term>
<term>Placebo enalapril</term>
<term>Polymorphism</term>
<term>Primary endpoint</term>
<term>Progression</term>
<term>Quinapril</term>
<term>Quinapril ischemic event trial</term>
<term>Quinaprilat</term>
<term>Ramipril</term>
<term>Randomized</term>
<term>Randomized trials</term>
<term>Receptor</term>
<term>Renal</term>
<term>Renal function</term>
<term>Renin</term>
<term>Risk reduction</term>
<term>Scandinavian enalapril survival study</term>
<term>Schalekamp</term>
<term>Schunkert</term>
<term>Similar results</term>
<term>Solvd</term>
<term>Systematic overview</term>
<term>Tissue enzyme</term>
<term>Tissue retention</term>
<term>Total mortality</term>
<term>Trandolapril</term>
<term>Transgenic rats</term>
<term>Ultrasound</term>
<term>Vascular</term>
<term>Vascular protection</term>
<term>Vasodilation</term>
<term>Ventricular</term>
<term>Ventricular dysfunction</term>
<term>Ventricular ejection fraction</term>
<term>Ventricular enlargement trial</term>
<term>Ventricular function</term>
<term>Ventricular hypertrophy</term>
<term>Ventricular mass</term>
<term>Yusuf</term>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr">
<term>Maladie cardio-vasculaire</term>
<term>Diabète</term>
<term>Enzyme</term>
<term>Oxyde</term>
</keywords>
</textClass>
<langUsage>
<language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">Abstract: Angiotensin-converting enzyme (ACE) is primarily localized (>90%) in various tissues and organs, most notably on the endothelium but also within parenchyma and inflammatory cells. Tissue ACE is now recognized as a key factor in cardiovascular and renal diseases. Endothelial dysfunction, in response to a number of risk factors or injury such as hypertension, diabetes mellitus, hypercholesteremia, and cigarette smoking, disrupts the balance of vasodilation and vasoconstriction, vascular smooth muscle cell growth, the inflammatory and oxidative state of the vessel wall, and is associated with activation of tissue ACE. Pathologic activation of local ACE can have deleterious effects on the heart, vasculature, and the kidneys. The imbalance resulting from increased local formation of angiotensin II and increased bradykinin degradation favors cardiovascular disease. Indeed, ACE inhibitors effectively reduce high blood pressure and exert cardio- and renoprotective actions. Recent evidence suggests that a principal target of ACE inhibitor action is at the tissue sites. Pharmacokinetic properties of various ACE inhibitors indicate that there are differences in their binding characteristics for tissue ACE. Clinical studies comparing the effects of antihypertensives (especially ACE inhibitors) on endothelial function suggest differences. More comparative experimental and clinical studies should address the significance of these drug differences and their impact on clinical events.</div>
</front>
</TEI>
<affiliations>
<list>
<country>
<li>Canada</li>
<li>États-Unis</li>
</country>
<region>
<li>District de Columbia</li>
<li>Kansas</li>
</region>
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<name sortKey="Cohen, Jerome" sort="Cohen, Jerome" uniqKey="Cohen J" first="Jerome" last="Cohen">Jerome Cohen</name>
<name sortKey="Dahlof, Bjorn" sort="Dahlof, Bjorn" uniqKey="Dahlof B" first="Björn" last="Dahlöf">Björn Dahlöf</name>
<name sortKey="Deanfield, John" sort="Deanfield, John" uniqKey="Deanfield J" first="John" last="Deanfield">John Deanfield</name>
<name sortKey="Diez, Javier" sort="Diez, Javier" uniqKey="Diez J" first="Javier" last="Diez">Javier Diez</name>
<name sortKey="Drexler, Helmut" sort="Drexler, Helmut" uniqKey="Drexler H" first="Helmut" last="Drexler">Helmut Drexler</name>
<name sortKey="Dzau, Victor J" sort="Dzau, Victor J" uniqKey="Dzau V" first="Victor J." last="Dzau">Victor J. Dzau</name>
<name sortKey="Ferrari, Roberto" sort="Ferrari, Roberto" uniqKey="Ferrari R" first="Roberto" last="Ferrari">Roberto Ferrari</name>
<name sortKey="Hansson, Lennart" sort="Hansson, Lennart" uniqKey="Hansson L" first="Lennart" last="Hansson">Lennart Hansson</name>
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<name sortKey="Husain, Ahsan" sort="Husain, Ahsan" uniqKey="Husain A" first="Ahsan" last="Husain">Ahsan Husain</name>
<name sortKey="Johnston, Colin" sort="Johnston, Colin" uniqKey="Johnston C" first="Colin" last="Johnston">Colin Johnston</name>
<name sortKey="Lazar, Harold" sort="Lazar, Harold" uniqKey="Lazar H" first="Harold" last="Lazar">Harold Lazar</name>
<name sortKey="Luscher, Thomas" sort="Luscher, Thomas" uniqKey="Luscher T" first="Thomas" last="Lüscher">Thomas Lüscher</name>
<name sortKey="Mimran, Albert" sort="Mimran, Albert" uniqKey="Mimran A" first="Albert" last="Mimran">Albert Mimran</name>
<name sortKey="Pepine, Carl" sort="Pepine, Carl" uniqKey="Pepine C" first="Carl" last="Pepine">Carl Pepine</name>
<name sortKey="Rabelink, Ton" sort="Rabelink, Ton" uniqKey="Rabelink T" first="Ton" last="Rabelink">Ton Rabelink</name>
<name sortKey="Remme, Willem" sort="Remme, Willem" uniqKey="Remme W" first="Willem" last="Remme">Willem Remme</name>
<name sortKey="Ruilope, Luis" sort="Ruilope, Luis" uniqKey="Ruilope L" first="Luis" last="Ruilope">Luis Ruilope</name>
<name sortKey="Schunkert, Heribert" sort="Schunkert, Heribert" uniqKey="Schunkert H" first="Heribert" last="Schunkert">Heribert Schunkert</name>
<name sortKey="Unger, Thomas" sort="Unger, Thomas" uniqKey="Unger T" first="Thomas" last="Unger">Thomas Unger</name>
<name sortKey="Van Gilst, Wiek" sort="Van Gilst, Wiek" uniqKey="Van Gilst W" first="Wiek" last="Van Gilst">Wiek Van Gilst</name>
<name sortKey="Vaughan, Douglas" sort="Vaughan, Douglas" uniqKey="Vaughan D" first="Douglas" last="Vaughan">Douglas Vaughan</name>
<name sortKey="Weber, Michael" sort="Weber, Michael" uniqKey="Weber M" first="Michael" last="Weber">Michael Weber</name>
</noCountry>
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<name sortKey="Celermajer, David" sort="Celermajer, David" uniqKey="Celermajer D" first="David" last="Celermajer">David Celermajer</name>
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<name sortKey="Swedberg, Karl" sort="Swedberg, Karl" uniqKey="Swedberg K" first="Karl" last="Swedberg">Karl Swedberg</name>
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<name sortKey="Lonn, Eva" sort="Lonn, Eva" uniqKey="Lonn E" first="Eva" last="Lonn">Eva Lonn</name>
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<name sortKey="Ruzicka, Marcel" sort="Ruzicka, Marcel" uniqKey="Ruzicka M" first="Marcel" last="Ruzicka">Marcel Ruzicka</name>
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</record>

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