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14-September-2008 18:38:50 - ACE inhibitor Redirected from ACE-inhibitor Captopril, the first ACE inhibitor Captopril, the first ACE inhibitor ACE inhibitors, or inhibitors of Angiotensin-Converting Enzyme, are a group of pharmaceuticals that are used primarily in treatment of hypertension and congestive heart failure, in some cases as the drugs of first choice. Contents 1 Clinical use 2 The renin-angiotensin-aldosterone system RAAS 3 Effects 4 Adverse effects 5 Examples 5.1 Sulfhydryl-containing agents 5.2 Dicarboxylate-containing agents 5.3 Phosphonate-containing agents 5.4 Naturally occurring 6 Comparative information 7 Contraindications and precautions 8 Angiotensin II receptor antagonists 8.1 Use in combination 9 History 10 References Clinical use Indications for ACE inhibitors include: Prevention of cardiovascular disorders Congestive heart failure CHF Hypertension Left ventricular dysfunction Prevention of nephropathy in diabetes mellitus In several of these indications, ACE inhibitors are used first-line as several agents in the class have been clinically shown to be superior to other classes of drugs in the reduction of morbidity and mortality. ACE inhibitors are often combined with diuretics in the control of hypertension usually a thiazide, when an ACE inhibitor alone proves insufficient; and in chronic heart failure usually furosemide for improved symptomatic control. Thus there exists, on the market, combination products combining an ACE inhibitor with a thiazide usually hydrochlorothiazide in a single tablet to allow easy administration by patients. The renin-angiotensin-aldosterone system RAAS Main article: Renin-angiotensin system This system is activated in response to hypotension, decreased sodium concentration in the distal tubule, decreased blood volume and renal sympathetic nerve stimulation. In such a situation, the kidneys release renin which cleaves the liver-derived angiotensinogen into Angiotensin I. Angiotensin I is then converted to angiotensin II via the angiotensin-converting-enzyme ACE in the pulmonary circulation as well as in the endothelium of blood vessels in many parts of the body.1 The system in general aims to increase blood pressure. Recently 2008, scientists have found that blocking this system increases the rate of metabolism. Current studies involve modifying the ACE inhibitor drugs and targeting the RAAS system, strictly for weight loss. Effects ACE inhibitors lower arteriolar resistance and increase venous capacity; increase cardiac output and cardiac index, stroke work and volume, lower renovascular resistance, and lead to increased natriuresis excretion of sodium in the urine. Normally, angiotensin II will have the following effects: vasoconstriction narrowing of blood vessels, which may lead to increased blood pressure and hypertension Specifically, angiotensin II constricts the efferent arterioles of the kidney, leading to increased perfusion pressure in the glomeruli. Ventricular remodeling of the heart, which may lead to ventricular hypertrophy and CHF stimulate the adrenal cortex to release aldosterone, a hormone that acts on kidney tubules to retain sodium and chloride ions and excrete potassium. Sodium is a water-holding molecule, so water is also retained, which leads to increased blood volume, hence an increase in blood pressure. stimulate the posterior pituitary into releasing vasopressin also known as anti-diuretic hormone ADH which also acts on the kidneys to increase water retention. decrease renal protein kinase C With ACE inhibitor use, the effects of angiotensin II are prevented, leading to decreased blood pressure. Epidemiological and clinical studies have shown that ACE inhibitors reduce the progress of diabetic nephropathy independently from their blood pressure-lowering effectcitation needed . This action of ACE inhibitors is utilised in the prevention of diabetic renal failure. ACE inhibitors have been shown to be effective for indications other than hypertension even in patients with normal blood pressure. The use of a maximum dose of ACE inhibitors in such patients including for prevention of diabetic nephropathy, congestive heart failure, prophylaxis of cardiovascular events is justified because it improves clinical outcomes, independent of the blood pressure lowering effect of ACE inhibitors. Such therapy, of course, requires careful and gradual titration of the dose to prevent the effects of rapidly decreasing blood pressure dizziness, fainting, etc. Adverse effects Common adverse drug reactions ≥1% of patients include: hypotension, cough, hyperkalemia, headache, dizziness, fatigue, nausea, renal impairment.2 A persistent dry cough is a relatively common adverse effect believed to be associated with the increases in bradykinin levels produced by ACE inhibitors, although the role of bradykinin in producing these symptoms remains disputed by some authors.3 Patients who experience this cough are often switched to angiotensin II receptor antagonists. Rash and taste disturbances, infrequent with most ACE inhibitors, are more prevalent in captopril and is attributed to its sulfhydryl moiety. This has led to decreased use of captopril in clinical setting, although it is still used in scintigraphy of the kidney. Renal impairment is a significant adverse effect of all ACE inhibitors. The reason for this is still unknown. Some suggest that it is associated with their effect on angiotensin II-mediated homeostatic functions such as renal blood flow. Renal blood flow may be affected by Angiotensin II because it vasoconstricts the efferent arterioles of the glomeruli of the kidney, thereby increasing glomerular filtration rate GFR. Hence, by reducing angiotensin II levels, ACE inhibitors may reduce GFR, a marker of renal function. However this is actually untrue as whilst the efferent arteriole is more relaxed, so too is the afferent arteriole which acts to increase GFR in a compensatory manner. Specifically, ACE inhibitors can induce or exacerbate renal impairment in patients with renal artery stenosis. This is especially a problem if the patient is also concomitantly taking an NSAID and a diuretic - the so-called triple whammy effect - such patients are at very high risk of developing renal failure.4 ACE inhibitors may cause hyperkalemia, because angiotensin II increases aldosterone release. Since aldosterone is responsible for increasing the excretion of potassium, ACE inhibitors ultimately cause retention of potassium. Some patients develop angioedema due to increased bradykinin levels. There appears to be a genetic predisposition towards this adverse effect in patients who degrade bradykinin slower than average.5 Examples ACE inhibitors can be divided into three groups based on their molecular structure: Sulfhydryl-containing agents Captopril trade name Capoten, the first ACE inhibitor Zofenopril Dicarboxylate-containing agents This is the largest group, including: Enalapril Vasotec/Renitec Ramipril Altace/Tritace/Ramace/Ramiwin Quinapril Accupril Perindopril Coversyl/Aceon Lisinopril Lisodur/Lopril/Novatec/Prinivil/Zestril Benazepril Lotensin Phosphonate-containing agents Fosinopril Monopril, the only member Naturally occurring Casokinins and lactokinins are breakdown products of casein and whey that occur naturally after ingestion of milk products, especially cultured milk. Their role in blood pressure control is uncertain.6 The tripeptides Val-Pro-Pro and Ile-Pro-Pro produced by the probiotic Lactobacillus helveticus have been show to have ACE-inhibiting and antihypertensive functions.7 Comparative information Comparatively, all ACE inhibitors have similar antihypertensive efficacy when equivalent doses are administered. The main point-of-difference lies with captopril, the first ACE inhibitor, which has a shorter duration of action and increased incidence of certain adverse effects cf. captopril. Certain agents in the ACE inhibitor class have been proven, in large clinical studies, to reduce mortality post-myocardial infarction, prevent development of heart failure, etc. The ACE inhibitor most prominently recognized for these qualities is ramipril Altace. Because ramipril has been shown to reduce mortality rates even among patient groups not suffering from hypertension, there is widespread belief that ramipril's benefits may extend beyond those of the general abilities it holds in common with other members of the ACE inhibitor class. Contraindications and precautions The ACE inhibitors are contraindicated in patients with: Previous angioedema associated with ACE inhibitor therapy Renal artery stenosis bilateral, or unilateral with a solitary functioning kidney ACE inhibitors should be used with caution in patients with: Impaired renal function Aortic valve stenosis or cardiac outflow obstruction Hypovolaemia or dehydration Haemodialysis with high flux polyacrylonitrile membranes ACE inhibitors are ADEC Pregnancy category D, and should be avoided in women who are likely to become pregnant.2 In the U.S., ACE inhibitors are required to be labelled with a black box warning concerning the risk of birth defects when taking during the second and third trimester. It has also been found that use of ACE inhibitors in the first trimester is also associated with a risk of major congenital malformations, particularly affecting the cardiovascular and central nervous systems.8 Potassium supplementation should be used with caution and under medical supervision owing to the hyperkalaemic effect of ACE inhibitors. Angiotensin II receptor antagonists ACE inhibitors share many common characteristics with another class of cardiovascular drugs called angiotensin II receptor antagonists, which are often used when patients are intolerant of the adverse effects produced by ACE inhibitors. ACE inhibitors do not completely prevent the formation of angiotensin II, as there are other conversion pathways, and so angiotensin II receptor antagonists may be useful because they act to prevent the action of angiotensin II at the AT1 receptor. Use in combination While counterintuitive at first glance, the combination therapy of angiotensin II receptor antagonists with ACE inhibitors may be superior to either agent alone. This combination may increase levels of bradykinin while blocking the generation of angiotensin II and its activity at the AT1 receptor. This 'dual blockade' may be more effective than using an ACE inhibitor alone, because angiotensin II can be generated via non-ACE-dependent pathways. Preliminary studies suggest that this combination of pharmacologic agents may be advantageous in the treatment of essential hypertension, chronic heart failure, and nephropathy.910 However, more studies are needed to confirm these highly preliminary results. While statistically significant results have been obtained for its role in treating hypertension, clinical significance may be lacking.11 Patients with heart failure may benefit from the combination in terms of reducing morbidity and ventricular remodeling.1213 The most compelling evidence has been found for the treatment of nephropathy: this combination therapy partially reversed the proteinuria and also exhibited a renoprotective effect in patients afflicted with diabetic nephropathy,9 and pediatric IgA nephropathy.14 History Main article: ACE inhibitors drug design The first step in the development of ACE inhibitors was the discovery of angiotensin converting enzyme ACE in plasma by Leonard T. Skeggs and his colleagues in 1956. The conversion of the inactive angiotensin I to the potent angiotensin II was thought to take place in the plasma. However, in 1967, Kevin K. F. Ng and John R. Vane showed that the plasma ACE was too slow to account for the conversion of angiotensin I to angiotensin II in vivo. Subsequent investigation showed that rapid conversion occurs during its passage through the pulmonary circulation.15 Bradykinin is rapidly inactivated in the circulating blood and it disappears completely in a single passage through the pulmonary circulation. Angiotensin I also disappears in the pulmonary circulation due to its conversion to angiotensin II. Furthermore, angiotensin II passes through the lungs without any loss. The inactivation of bradykinin and the conversion of angiotensin I to angiotensin II in the lungs was thought to be caused by the same enzyme.16 In 1970, Ng and Vane using bradykinin potentiating factor BPF provided by Sérgio Henrique Ferreira showed that the conversion of angiotensin I to angiotensin II was inhibited during its passage through the pulmonary circulation.17 Bradykinin potentiating factor BPF is derived from the venom of the pit viper Bothrops jararaca. It is a family of peptides and its potentiating action is linked to inhibition of bradykinin by ACE. Molecular analysis of BPF yielded a nonapeptide BPF teprotide SQ 20,881 which showed the greatest ACE inhibition potency and hypotensive effect in vivo. Teprotide had limited clinical value, due to its peptide nature and lack of activity when given orally. In the early 1970s, knowledge of the structure-activity relationship required for inhibition of ACE was growing. David Cushman, Miguel Ondetti and colleagues used peptide analogues to study the structure of ACE, using carboxypeptidase A as a model. Their discoveries led to the development of captopril, the first orally-active ACE inhibitor in 1975. Captopril was approved by the United States Food and Drug Administration in 1981. The first non-sulfhydryl-containing ACE inhibitor enalapril was marketed two years later. Since then, at least twelve other ACE inhibitors have been marketed. References ^ Human Physiology, Silverthorn Pearson Benjamin Cummings 2004 ^ a b Rossi S, or. Australian Medicines Handbook 2006. Adelaide: Australian Medicines Handbook; 2006. ISBN 0-9757919-2-3. ^ Okumura H, Nishimura E, Kariya S, et al. Angiotensin-converting enzyme ACE 阻害薬誘発性ã?®å’³å—½ç™ºç?¾ã?¨ACEé?ºä¼?å?åž‹,血漿ä¸ãƒ–ラジã‚ニン,サブスタンスPå?Šã?³ACE阻害薬濃度ã?¨ã?®é–¢é€£æ€§ No relation between angiotensin-converting enzyme ACE inhibitor-induced cough and ACE gene polymorphism, plasma bradykinin, substance P and ACE inhibitor concentration in Japanese patients. Yakugaku Zasshi 2001;1213:253-7. Japanese. PMID 11265121 ^ Thomas MC. Diuretics, ACE inhibitors and NSAIDs - the triple whammy. Med J Aust 2000;1724:184-185. PMID 10772593 ^ Molinaro G, Cugno M, Perez M, et al. Angiotensin-converting enzyme inhibitor-associated angioedema is characterized by a slower degradation of des-arginine9-bradykinin. J Pharmacol Exp Ther 2002;303:232-7. PMID 12235256. ^ FitzGerald RJ, Murray BA, Walsh DJ. Hypotensive peptides from milk proteins. J Nutr 2004;134:980S-8S. PMID 15051858. ^ Aihara K, Kajimoto O, Hirata H, Takahashi R, Nakamura Y. Effect of powdered fermented milk with Lactobacillus helveticus on subjects with high-normal blood pressure or mild hypertension. J Am Coll Nutr. 2005 Aug;244:257-65 PMID 16093403. ^ Cooper WO, Hernandez-Diaz S, Arbogast PG, Dudley JA, Dyer S, Gideon PS, et al. Major congenital malformations after first-trimester exposure to ACE inhibitors. N Engl J Med 2006;35423:2443-51. PMID 16760444 ^ a b Luno J, Praga M, de Vinuesa SG. The reno-protective effect of the dual blockade of the renin angiotensin system RAS. Curr Pharm Des 2005;1110:1291-300. PMID 15853685 ^ van de Wal RM, van Veldhuisen DJ, van Gilst WH, Voors AA. Addition of an angiotensin receptor blocker to full-dose ACE-inhibition: controversial or common sense? Eur Heart J 2005;2622:2361-7. PMID 16105846 ^ Finnegan PM, Gleason BL. Combination ACE inhibitors and angiotensin II receptor blockers for hypertension. Ann Pharmacother 2003;376:886-9. PMID 12773079 ^ Krum H, Carson P, Farsang C, et al. Effect of valsartan added to background ACE inhibitor therapy in patients with heart failure: results from Val-HeFT. Eur J Heart Fail 2004;67:937-45. PMID 15556056 ^ Solomon SD, Skali H, Anavekar NS, et al. Changes in ventricular size and function in patients treated with valsartan, captopril, or both after myocardial infarction. Circulation 2005;11125:3411-9. PMID 15967846 ^ Yang Y, Ohta K, Shimizu M, et al. Treatment with low-dose angiotensin-converting enzyme inhibitor ACEI plus angiotensin II receptor blocker ARB in pediatric patients with IgA nephropathy. Clin Nephrol 2005;641:35-40. PMID 16047643 ^ K.K.F.Ng and J.R.Vane: Conversion of angiotensin I to angiotensin II. Nature 1967, 216, 762-766 ^ K.K.F.Ng and J.R.Vane: Fate of angiotensin I in the circulation. Nature 1968, 218, 144-150. ^ K.K.F.Ng and J.R.Vane: Some properties of angiotensin converting enzyme in the lung in vivo. Nature 1970, 225, 1142-1144. v d e Agents acting on the renin-angiotensin system C09 ACE inhibitors Alacepril Benazepril Captopril Cilazapril Delapril Enalapril Fosinopril Imidapril Lisinopril Moexipril Perindopril Quinapril Ramipril Rentiapril Spirapril Temocapril Trandolapril Zofenopril Angiotensin II receptor antagonists AIIRA Azilsartan Candesartan Eprosartan Irbesartan Losartan Olmesartan Tasosartan Telmisartan Valsartan Renin inhibitors Aliskiren Remikiren v d e Major drug groups Gastrointestinal tract/metabolism A stomach acid Antacids, H2 antagonists, Proton pump inhibitors Antiemetics Laxatives Antidiarrhoeals/Antipropulsives Anti-obesity drugs Anti-diabetics Vitamins Dietary minerals Blood and blood forming organs B Antithrombotics Anticoagulants, Antiplatelets, Thrombolytics Antihemorrhagics Cardiovascular system C cardiac therapy/antianginals Cardiac glycosides, Antiarrhythmics, Cardiac stimulant Antihypertensives Diuretics Vasodilators Beta blockers renin-angiotensin system ACE inhibitors, Angiotensin II receptor antagonists, Renin inhibitors Antihyperlipidemics Skin D Emollients Cicatrizant Antipruritics Reproductive system G Hormonal contraception Fertility agents SERMs Sex hormones Endocrine system H Corticosteroids Sex hormones Thyroid hormones Antithyroid agent Infections and infestations J, P Antibiotics Antivirals Vaccines Antifungals Antiparasitic Antiprotozoals, Anthelmintics Malignant and immune disease L Anticancer agents Immunostimulators Immunosuppressants Muscles, bones, and joints M Anabolic steroids Anti-inflammatories NSAID Antirheumatics Corticosteroids Muscle relaxants Brain and nervous system N Anesthetics General, Local Analgesics Anticonvulsants Mood stabilizers Psycholeptic Anxiolytics, Antipsychotics, Hypnotics/Sedatives Psychoanaleptic Antidepressants, Stimulants/Psychostimulants Respiratory system R Bronchodilators Decongestants H1 antagonists Other ATC V Antidotes Contrast media Radiopharmaceuticals Dressing v d e Pharmacology: enzyme inhibition Class Competitive inhibition - Uncompetitive inhibition - Non-competitive inhibition - Suicide inhibition - Mixed inhibition Substrate Oxidoreductase EC 1: Aromatase inhibitors - Lipoxygenase inhibitor - Monoamine oxidase inhibitors - COX-2 inhibitor Transferase EC 2: Integrase inhibitor - Protein kinase inhibitors - Reverse transcriptase inhibitors - COMT inhibitors Hydrolase EC 3: Acetylcholinesterase inhibitors - Phosphodiesterase inhibitors - Protease inhibitors ACE inhibitor, Trypsin inhibitor - Histone deacetylase inhibitor Lyase EC 4: Carbonic anhydrase inhibitors Retrieved from http://en..org/wiki/ACE_inhibitor Categories: ACE inhibitors | Antihypertensive agentsHidden categories: All articles with statements | Articles with statements since May 2008 Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Türkçe العربية Deutsch Español Français Hrvatski Italiano Nederlands 日本語 ‪Norsk nynorsk‬ Polski Português Svenska ไทย ä¸æ–‡ This page was last modified on 28 August 2008, at 12:01
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