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Peptides present in the non-digestible fraction of common beans (Phaseolus vulgaris L.) inhibit the angiotensin-I converting enzyme by interacting with its catalytic cavity independent of their antioxidant capacity.

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The aim was to evaluate the angiotensin-I converting enzyme (ACE) inhibitory potential and the antioxidant capacity of pure synthesized peptides (GLTSK, LSGNK, GEGSGA, MPACGSS and MTEEY) originally identified in the non-digestible fraction (NDF) of common beans (P. vulgaris L.) that had previously

Association of left ventricular systolic performance and cavity size with angiotensin-converting enzyme genotype in idiopathic dilated cardiomyopathy.

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The insertion-deletion (ID) polymorphism of the angiotensin-converting enzyme (ACE) gene is a marker linked to differences in plasma and cardiac ACE activity as well as to an increased mortality in patients with idiopathic heart failure. We examined the possibility that ACE gene ID variants are

Evaluation of direct transport pathways of glycine receptor antagonists and an angiotensin antagonist from the nasal cavity to the central nervous system in the rat model.

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OBJECTIVE The aim of this study was to investigate and quantify drug movement to the brain via the neuro-olfactory system after intranasal dosing of four model drugs; three glycine receptor antagonists and one angiotensin antagonist. METHODS The drugs were dosed to rats via intranasal or intravenous

[Changes in the indices of hemodynamics and of the metabolism of bradykinin, angiotensin I and prostaglandin E1 in the lungs of rats with spontaneous hypertension exposed to a galvanic current on the chest cavity].

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Perinatal 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure sensitizes offspring to angiotensin II-induced hypertension.

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In utero and lactational exposure of mice to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads to cardiac hypertrophy and hydronephrosis in adulthood. We tested the hypothesis that perinatal TCDD exposure increases the susceptibility to cardiovascular disease when offspring are exposed to a common

Angiotensin-(1-7) Promotes Resolution of Neutrophilic Inflammation in a Model of Antigen-Induced Arthritis in Mice.

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Defective resolution of inflammation may be crucial for the initiation and development of chronic inflammatory diseases, such as arthritis. Therefore, it has been suggested that therapeutic strategies based on molecules that facilitate inflammation resolution present great potential for the

Inhibition of Angiotensin II Receptor I Prevents Inflammation and Bone Loss in Periodontitis.

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BACKGROUND Periodontal disease is characterized by alveolar bone destruction and degenerative lesions of the periodontal ligament (PDL); it is initiated by bacterial infection of the oral cavity, but the clinical effects are secondary to an aberrant host immune response. Primary hypertension (PH),

Calpain inhibition attenuates angiotensin II-induced abdominal aortic aneurysms and atherosclerosis in low-density lipoprotein receptor-deficient mice.

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Chronic infusion of angiotensin II (AngII) augments atherosclerosis and abdominal aortic aneurysm (AAA) formation in hypercholesterolemic mice. AngII-induced AAAs are associated with medial macrophage accumulation and matrix metalloproteinase (MMP) activation. Inhibition of calpain, a

Clinical experience with angiotensin-converting enzyme inhibitor-induced angioedema.

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OBJECTIVE To understand the presentation and clinical course of angiotensin-converting enzyme (ACE) inhibitor-induced angioedema and to determine management factors associated with progression to airway compromise. METHODS Retrospective chart review of patients taking ACE inhibitors who presented to

Metabolism of angiotensin I by different tissues in the intact animal.

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To quantify regional conversion of angiotensin (ANG) I to ANG II and its degradation to peptides other than ANG II, monoiodinated 125I-labeled ANG I was given to anesthetized pigs by constant infusion into the left cardiac ventricle. At steady state, blood samples were taken from the aorta and

Increased angiotensin-converting enzyme activity in the left ventricle after infarction.

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An increase in angiotensin-converting enzyme (ACE) activity has been observed in the heart after myocardial infarction (MI). Since most studies have been conducted in chronically infarcted individuals exhibiting variable degrees of heart failure, the present study was designed to determine ACE

Angiotensin blockade inhibits increased JNKs, AP-1 and NF- kappa B DNA-binding activities in myocardial infarcted rats.

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Inhibition of the renin-angiotensin system has been shown to prevent left ventricular remodeling after myocardial infarction. However, the effect of angiotensin on the signal transduction pathway of left ventricular remodeling after myocardial infarction is as yet unknown. The purpose of this study

Angiotensin-converting enzyme (ACE) inhibitor-associated angioedema of the stomach and small intestine: a case report.

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This is a case report on a 45-year old African-American female with newly diagnosed hypertension, who was started on a combination pill of amlodipine/benazapril 10/5 mg. The very next day, she presented at the emergency room (ER) with abdominal pain, nausea and vomiting. Physical exam, complete

[Structural and ultrastructural changes induced by angiotensin II in the cerebral cortex of animals].

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Structure of capillaries, pericapillary glia and neurons of the sensomotor cerebral cortex was studied in rats after intraperitoneal injections of angiotensin-II (0.05 mg/kg of the body weight) administered once for 1, 3, 7, 14 and 21 days. The animals were decapitated 5 and 15 min after a single

Angiotensin converting enzyme inhibition therapy following myocardial infarction. Rationale for clinical trials.

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Progressive enlargement following myocardial infarction can be anticipated to adversely effect outcome since prognosis is intimately related to the degree of left ventricular dysfunction and resultant ventricular cavity size. Recent experimental and clinical data have indicated that chronic

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