ABSTRACT
Myocardial ischemia, cerebral ischemia and myocardial infarction are the most important complications of hypertension and atherosclerotic disease in developing countries. Angiotensin converting enzyme [ACE] inhibitors are among the drugs used to treat hypertension and heart failure. Captopril is an ACE-inhibitor which also has antioxidant properties. This study was conducted to assess the antioxidant effects of captopril on malondialdehyde [MDA], conjugated dienes [CD] and serum antioxidant capacity before and after treatment. This interventional prospective single-blind study was conducted on 34 mildly hypertensive individuals and 34 patients with stage I and II heart failure. MDA, CD and serum antioxidant capacity were measured in all samples. The patients were then given 50 mg captopril tablets 2-3 times daily. The measurements were repeated 1.5 months later. Comparison of mean MDA, CD and serum antioxidant capacity in hypertensive patients and patients with heart failure before and after drug administration revealed no significant difference in any of the parameters studied. Existing evidence is suggestive of the strong antioxidative properties of captopril in vitro, although these effects have not been borne out by some studies. In the present study, comparison of the results of MDA, CD and serum antioxidant measurements before and after the period of treatment with captopril did not reveal any statistically significant difference
Subject(s)
Humans , Male , Female , Captopril , Hypertension/drug therapy , Heart Failure/drug therapy , Antioxidants , Captopril/metabolism , Clinical Trials as Topic , Prospective Studies , Single-Blind MethodABSTRACT
Inhibition of angiotensin converting enzyme(EC 3.4,15.1, ACE) in presence of captopril, lisinopril and enalapril were investigated in kidney, lung and serum of sheep using Hip-His-Leu(HHL) as substrate. The activity in kidney, lung and serum was inhibited at HHL concentration above 5 mM. The inhibitory constants (IC50) ranged between 5.6 nM for serum ACE with lisinopril and 70000 nM for renal ACE with enalapril while Ki ranged from 1.0 nM for serum ACE with lisinopril to 12000 nM for kidney ACE with enalapril. Differences in inhibition observed in different tissues suggest that the inhibitors may block function(s) of ACE to varying degrees in each tissue.
Subject(s)
Angiotensin-Converting Enzyme Inhibitors/metabolism , Animals , Captopril/metabolism , Enalapril/metabolism , Kidney/enzymology , Kinetics , Lisinopril/metabolism , Lung/enzymology , Oligopeptides , Peptidyl-Dipeptidase A/blood , SheepSubject(s)
Cattle , Dogs , Rabbits , Humans , Animals , Angiotensin II/physiology , Angiotensin II/metabolism , Captopril/metabolism , Catecholamines/metabolism , Catecholamines/physiology , In Vitro Techniques , Norepinephrine/metabolism , Norepinephrine/physiology , Peptidyl-Dipeptidase A/drug effects , Peptidyl-Dipeptidase A/physiology , Renin-Angiotensin System/drug effects , Renin-Angiotensin System/physiology , Sympathetic Nervous System/enzymology , Sympathetic Nervous System/physiologyABSTRACT
El captopril (CAP) es un inhibidor de la enzima convertasa, que tiene como el efecto farmacológico mayor la interrupción del sistema renina-angiotensina, aunque su acciòn sobre el metabolismo de las quininas y las prostaglandinas explican otros de los efectos de esta droga. Los vasos sanguíneos y el riñón son los principales órganos donde se produce la respuesta farmacológica del CAP, con sus efectos fundamentales: vasodilatación, y aumentos de la diuresis y natriuresis. Estas acciones han determinado el amplio uso del CAP en la hipertensiòn arterial y la insuficiencia cardiaca congestiva, y últimamente en enfermedades renales
Subject(s)
Captopril/metabolism , Captopril/pharmacology , Captopril/therapeutic use , Hypertension/therapy , Heart Failure/therapy , Kidney Diseases/therapyABSTRACT
Os autores estudaram as variaçöes induzidas na pressäo arterial sistêmica e as modificaçöes promovidas na hemodinâmica e funçäo renais de 9 pacientes cirróticos com ascite, em tratamento convencional após uso oral de 25mg de captopril. Concluem que o sistema renina-angiotensina (SRA) näo é o principal determinante dos níveis pressóricos sistêmicos do grupo examinado e que a inibiçäo do SRA intra-renal reduz a filtraçäo glomerular e a quantidade excretada de sódio destes pacientes
Subject(s)
Captopril/therapeutic use , Liver Cirrhosis, Alcoholic/drug therapy , Captopril/metabolism , HemodynamicsABSTRACT
Se evaluó el efecto antihipertensivo agudo y crónico del captopril, inhibidor de la enzima convertidora de la angiotensina, en siete pacientes, tres varones y cuatro mujeres, de 31 a 60 años de edad. Cuatro pacientes tuvieron hipertensión arterial esencial de grado grave, con valores de presión arterial diastólica mayores de 115 mm Hg, y tres de grado moderado con cifras de 110 a 115 mm Hg. Los pacientes no habían reaccionado adecuadamente al tratamiento triple ordinario. Se observó el efecto agudo de 25 mg de captopril oral en todos los pacientes durante 180 minutos. La tensión arterial disminuyó un promedio de 30 mm Hg para la sistólica y 18 mm Hg para la diastólica. Se observó también el efecto crónico de seis meses de captopril oral a dosis promedio de 346 mg/día acompañado de un diurético (clorotiazida, 1 g, o clortalidona, 200 mg) en todos los pacientes, lográndose disminución de las cifras de la presión sistólica de 170.0 + ou - 8.2 a 148.5 + ou - 16.8 mm Hg, y de la diastólica de 121.4 + ou - 9.4 a 97.9 + ou - 12.9 mm Hg. Tres pacientes tuvieron disminución de los valores de presión diastólica a 90 mm Hg. La actividad de renina plasmática aumentó de 1.4 + ou - 0.9 a 4.6 + ou - 4.2 ng/ml/h. No se observaron efectos colaterales de importancia. Se concluye que el captopril es un fármaco antiphipertensivo potente y eficaz para el tratamiento de la hipertensión arterial esencial moderada a grave resistence a otros agentes antihipertensivos, que produce escasas reacciones adversas