تراجع فيتامين B- 12 لدى الحامل قد يعرض الجنين لتشوهات

أكدت دراسة طبية جديدة نشرت في الولايات المتحدة أن تراجع مستوى فيتامين B- 12 لدى الحامل قد يعرض الجنين لمخاطر الإصابة بتشوهات خلقية خطيرة أكثر بخمس مرات من اللواتي يكون مستوى هذا الفيتامين خلال فترات حملهن بالنسب الصحية المطلوبة.
وأظهرت الدراسة التي نشرت في مجلة Pediatrics لشهر مارس/ آذار أن المرأة التي يكون مستوى هذا الفيتامين متدنيا لديها، قد يكون جنينها معرضا للإصابة بعاهة في الجهاز العصبي أكثر من تلك التي تكون كمية هذه الفيتامينات عالية لديها.
وحذر الطبيب جيمس ميلز من المعاهد الوطنية الأميركية للصحة المسؤول الرئيسي عن هذه الدراسة، من ضرورة عدم انتظار المرأة لتكون حاملا للبدء بتناول هذا الفيتامين لأن الأوان يكون قد فات. وقام واضعو الدراسة بتحليل عينات دم عند بدء الحمل لدى مجموعة من ثلاث نساء في ايرلندا بين عامي 1983 و1990.
وخلال هذه الفترة كانت المرأة الحامل في هذا البلد قلما تتناول فيتامينات. وسجل في ايرلندا نسبة عالية من الأطفال الذين يعانون من تشوهات خلقية في الجهاز العصبي لدى الجنين وغالبا ما تعاونت المعاهد الوطنية الأميركية للصحة مع الباحثين الايرلنديين لكشف سبب ذلك.
وخلصت الدراسة إلى أن النساء الحوامل اللواتي يتبعن حمية نباتية وبالتالي تكون مستويات فيتامين B- 12 منخفضة لديهن، قد يعرضن الجنين لعاهات في الجهاز العصبي.
يذكر أن المرأة التي تتناول القليل من اللحوم أو المنتجات الحيوانية معرضة لمخاطر أكبر بأن تكون مستويات فيتامين B- 12 لديها منخفضة، وكذلك المرأة التي تعاني من مشاكل معوية التي تمنعها من امتصاص كمية كافية من هذه الفيتامينات.
والفيتامين B- 12 متوفر بكميات عالية أساسا في الحليب واللحوم والبيض والدواجن والحبوب.
ويمكن أن يصاب الجهاز العصبي بتشوهات خلقية للدماغ أو النخاع الشوكي لدى الجنين في المراحل الأولى من تكوينه. وفي مراحل لاحقة قد تتحول إلى عاهات في العمود الفقري أو الجمجمة.

التفاؤل يطيل عمر المرأة والتشاؤم يقصره

أوضحت دراسة أجراها باحثون أميركيون في جامعة بيتسبرغ بولاية بنسيلفانيا أن النساء المتفائلات يتمتعن بحياة أفضل مقارنة بالمتشائمات منهن.

وجاء في الدراسة، التي تتبعت سلوك أكثر من 100 ألف امرأة تراوحت أعمارهن بين 50 عاما و70 عاما أن معدلات الوفاة انخفضت لدى النساء اللواتي اتسمن بالتفاؤل بنسبة 14 بالمئة مقارنة بالمتشائمات منهن.

وتابعت الدراسة أن المتشائمات من النساء يتعرضن لاحتمال إصابتهن بأمراض القلب بنسبة 30 بالمئة مقارنة بالمتفائلات اللواتي تقل لديهن احتمالات الإصابة بارتفاع ضغط الدم والسكري.

وقالت الدكتورة هيلاري تيندل، التي أشرفت على الدراسة في الاجتماع السنوي للمنظمة الأميركية للأمراض النفسية إن النساء اللواتي يتسمن بالنزعة التشاؤمية تبلغ نسبة الوفاة لديهن 16 بالمئة مقارنة بالنساء الأقل تشاؤما.

وختمت الدكتورة تيندل أن مشكلة المتشائم تكمن في إحساسه بأنه يشعر دائما بالإخفاق.

مسبار لحل مشكلة الشخير المزمنة

عند حلول الليل تبدأ في بعض غرف النوم في شتى بقاع العالم موسيقى نشاز يشكو من سماعها أحيانًا الجيران والمقصود هنا الشخير. إذ بينت احصاءات المانية ان اكثر من اربعة ملايين شخص في المانيا يصدر عنهم شخير خلال النوم بشكل مزعج وسبعة اضعاف هذا العدد يشخر بشكل عادي وغير منتظم. ولا تؤدي هذا المشكلة فقط الى ازعاج الشريك في السرير بل تتعداه في بعض الاحيان الى تأثيث غرفة نوم مستقلة للزوج او الزوجة بعد أن يصبح لا نفع من الهزة لإيقاظ من يشخر. واهتم معهد DGSM مركز البحوث البرليني لحالات الشخير وعلاج النوم بهذه المشكلة، فاتضح له بعد دراسة حالات كثيرة ان مطلق الشخير هو في اغلب الاحيان الرجل ( 4 من 5 حالات) لكن اذا ما ايقظته زوجته ينكر التهمة ويتحدث بكلمات غير واضحة ثم يعود للنوم والشخير، مما يدفع بالزوجة الى حمل غطاءها والبحث عن مكان هادئ يكون احيانًا في سرير اولادها.

وبحسب دارسة المانية حديثة فإن ظاهرة الشخير تعني ان النائم يعاني من توقف منتظم للتنفس ويسمى باليونانية Apnoia او السكون الهادئ ، وبحسب التفسير العلمي يعني انقطاع التنفس الذي يحدث على دفعات ويدوم بضع ثوان.
وقد تكون الطريقة التي بدأت في المانيا هي احد اهم الحلول للشخير، حيث يتم كي الجزء اللحمي الطري الذي يتدلى من سقف الحلق لانه المسبب الرئيس في سد مجرى الهواء لفترات متفاوتة عند النوم على الظهر، وبدلا من استخدام المباضع الجراحية يلجأ الجراح الان الى هذه العملية البسيطة التي لا تحتاج ايضا إلى الاقامة في المستشفى وذلك عن طريق مسبار.

وبحسب شرح الدكتور برند شتاين مدير الشركة التي صنعت المسبار في ميونيخ لايلاف فان العملية يجريها طبيب الانف والاذن والحنجرة بعد تخدير موضعي بسيط لا يختلف عن تخدير طبيب الانسان لسن الجزء الاخير من الفم. ثم يدخل المسبار المشكل من سلكين لقطبي السالب والموجب والمتصل بموجات راديو عالية في آخر الفم، الى ان يصل الى القطعة اللحمية الرخوة ( طرطوفة) التي تنزل من سقف الحلق ، فيغرزه فيها على عمق 8 ملم. ومع درجة حرارة تصل الى الستين يتم كي هذا الجزء بدون اسالة دم. بعدها يظهر محيط باهت اللون ينكمش من نفسه بعد اقل من اسبوعين ويبقى من( الطرطوفة) جزء بسيط .
وتستغرق العملية اقل من 15 دقيقة ولا داعي لتناول مضاد حيوي بعد ذلك لكن قد يحتاج المرء الى مسكن بسيط مع مراجعة الطبيب مرة واحدة فقط بعد اسبوعين او ثلاثة اسابيع.
وتسمى هذا التقنية الطبية الجديدة Bioplare Sonde اي موجات راديو مؤثرة يبقى التيار الكهربائي فيها نشيطا فقط بين القطبين السالب والموجب اللذين يشكلان رأس المسبار، مما لا يحلق الضرر حتى بالذين اجريت لهم عملية قسطرة.

وتعود اسباب الشخير بالدرجة الاولى الى استرخاء كامل عضلات الجسم اثناء النوم بخاصة على الظهر، حيث يبقى الفم مفتوحًا وتدخل اليه كميات من الهواء ترتطم ( بالطرطوفة) في سقف الحلق وهي طويلة لدى البعض، وهذه العملية تحدث ارتجاجًا يؤدي الى سد مجرى الهواء قليلاً فيصدر صوت خشن وهو الشخير او شهقة اثناء وكان ا لنائم اصيب باختناق. اما اشتداده فيكون نتيجة تراخي عضلات البلعوم والحلق وبالتالي سد هذه القطعة اللحمية الرخوة واللسان مجرى الهواء العلوي، فيسبب ذلك اعطاء الدماغ اوامر مشوشة للعضلات من اجل الاسترخاء.
وفي محاولة عضلات التنفس في البطن التغلب على هذا العائق، ولكن من دون نجاح، يصبح النائم المتعب في هذه الاثناء اقل هدوءًا، فيتقلب يمينًا ويسارًا محاولاً الاستيقاظ من دون فائدة، لكن اذا ما تمكنت هذا العضلات من التخلص من الضغط وحررت مجرى الهواء العلوي افسحت الفرصة للتنفس لمدة ثوان فيتحول ذلك الى شخير.

وبحسب قول الدكتور شتاين تتكرر هذا الحالة حتى 400 مرة في الليلة الواحدة وتدوم ما بين بضع ثوان ودقيقة مما يؤدي الى نقصان الاوكسيجين في الدم وتكون نتيجة ذلك عدم وصول ما يكفي من هذا المادة المهمة للحياة الى الدماغ وعضلات القلب، وقذف الجسم المرتجف المزيد من هورمونات الارهاق. لذا فلا عجب من اصابة الشخص الذي يشخر بالتعب الشديد اثناء العمل فمن ساعات النوم الست العادية لم يتنفس مدة ساعة على الاقل اذا ما جمعت الدقائق والثواني فينعكس ذلك على نشاطه في اليوم التالي.

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ACE inhibitor
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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[hide]
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 See also
11 References
//

[edit] 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 exist, on the market, combination products combining an ACE inhibitor with a thiazide (usually hydrochlorothiazide) in a single tablet to allow easy administration by patients.

[edit] 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 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.

[edit] 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 effect[citation 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).

[edit] Adverse effects
Common adverse drug reactions (less than 1% of patients) include: hypotension, cough, hyperkalemia, headache, dizziness, fatigue, nausea and 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. 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. Suppression of angiotensin II leads to a decrease in aldosterone levels. Since aldosterone is responsible for increasing the excretion of potassium, ACE inhibitors ultimately cause retention of potassium.
A severe allergic reaction can occur that rarely can affect the bowel wall and secondarily cause abdominal pain. This "anaphylactic" reaction is very rare as well.
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]

[edit] Examples
ACE inhibitors can be divided into three groups based on their molecular structure:

[edit] Sulfhydryl-containing agents
Captopril (trade name Capoten), the first ACE inhibitor
Zofenopril

[edit] 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)

[edit] Phosphonate-containing agents
Fosinopril (Monopril) is the only member of this group

[edit] 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 shown to have ACE-inhibiting and antihypertensive functions.[7]

[edit] 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.
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.[citation needed]

[edit] 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
Hemodialysis 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.

[edit] 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.

[edit] 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.[9][10] 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.[12][13]
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]

[edit] 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.

[edit] See also
Angiotensin II receptor antagonist
Angiotensin Receptor Blockers: Drug discovery and development

[edit] References
^ Human Physiology, Silverthorn (Pearson Benjamin Cummings 2004)
^ a b Rossi S, editor. 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) 阻害薬誘発性の咳嗽発現とACE遺伝子型,血漿中ブラジキニン,サブスタンスP及びACE阻害薬濃度との関連性 [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;121(3):253-7. Japanese. PMID 11265121
^ Thomas MC. Diuretics, ACE inhibitors and NSAIDs - the triple whammy. Med J Aust 2000;172(4):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-arginine(9)-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;24(4):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;354(23):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;11(10):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;26(22):2361-7. PMID 16105846
^ Finnegan PM, Gleason BL. Combination ACE inhibitors and angiotensin II receptor blockers for hypertension. Ann Pharmacother 2003;37(6):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;6(7):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;111(25):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;64(1):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.
[show]
v • d • eAntihypertensives: agents acting on the renin-angiotensin system (C09)
ACE inhibitors("-pril")
Alacepril • Benazepril • Captopril • Cilazapril • Delapril • Enalapril # • Fosinopril • Imidapril • Lisinopril • Moexipril • Perindopril • Quinapril • Ramipril • Rentiapril • Spirapril • Temocapril • Trandolapril • Zofenopril
AIIRAs/("-sartan")
Azilsartan • Candesartan • Eprosartan • Irbesartan • Losartan • Olmesartan • Tasosartan • Telmisartan • Valsartan
Renin inhibitors/("-kiren")
Aliskiren • Remikiren
# = WHO-EM
[show]
v • d • eMajor 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 (Antiplatelets, Anticoagulants, Thrombolytics/fibrinolytics) • Antihemorrhagics (Platelets, Coagulants, Antifibrinolytics)
Cardiovascular system (C)
cardiac therapy/antianginals (Cardiac glycosides, Antiarrhythmics, Cardiac stimulants)
Antihypertensives • Diuretics • Vasodilators • Beta blockers • Calcium channel blockers • renin-angiotensin system (ACE inhibitors, Angiotensin II receptor antagonists, Renin inhibitors)Antihyperlipidemics (Statins, Fibrates, Bile acid sequestrants)
Skin (D)
Emollients • Cicatrizants • Antipruritics • Antipsoriatics • Medicated dressings
Reproductive system (G)
Hormonal contraception • Fertility agents • SERMs • Sex hormones
Endocrine system (H)
Hypothalamic-pituitary hormones • Corticosteroids (Glucocorticoids, Mineralocorticoids) • Sex hormones • Thyroid hormones/Antithyroid agents
Infections and infestations (J, P)
Antibiotics • Antifungals • Antimycobacterials (Tuberculosis treatment, Leprostatic agents) • Antivirals • Vaccines • Antiparasitics (Antiprotozoals, Anthelmintics) • Ectoparasiticide
Malignant disease (L01-L02)
Anticancer agents (Antimetabolites, Alkylating, Spindle poisons, Antineoplastic, Topoisomerase inhibitors)
Immune disease (L03-L04)
Immunomodulators (Immunostimulants, Immunosuppressants)
Muscles, bones, and joints (M)
Anabolic steroids • Anti-inflammatories (NSAIDs) • Antirheumatics • Corticosteroids • Muscle relaxants • Bisphosphonates
Brain and nervous system (N)
Anesthetics (General, Local) • Analgesics • Antimigraines • Anticonvulsants • Mood stabilizers • Antiparkinson drugsPsycholeptics (Anxiolytics, Antipsychotics, Hypnotics/Sedatives) • Psychoanaleptics (Antidepressants, Stimulants/Psychostimulants)
Respiratory system (R)
Decongestants • Bronchodilators • Cough medicines • H1 antagonists
Sensory organs (S)
Ophthalmologicals • Otologicals
Other ATC (V)
Antidotes • Contrast media • Radiopharmaceuticals • Dressings
[show]
v • d • ePharmacology: enzyme inhibition
Class
Competitive inhibition · Uncompetitive inhibition · Non-competitive inhibition · Suicide inhibition · Mixed inhibition
Substrate
Oxidoreductase (EC 1)
Aromatase · Lipoxygenase · Monoamine oxidase · COX-2 · Xanthine oxidase · Dihydrofolate reductase · Ribonucleotide reductase · 5-alpha-reductase
Transferase (EC 2)
Integrase · Protein kinase · Reverse transcriptase · COMT · Thymidylate synthase · Dihydropteroate synthetase · Farnesyltransferase
Hydrolase (EC 3)
Acetylcholinesterase · Phosphodiesterase · Protease (ACE, Trypsin) · Histone deacetylase · Dipeptidyl peptidase-4
Lyase (EC 4)
Carbonic anhydrase · Dopa decarboxylase
Retrieved from "http://en.wikipedia.org/wiki/ACE_inhibitor"
Categories: ACE inhibitors Antihypertensive agents
Hidden categories: All articles with unsourced statements Articles with unsourced statements since May 2008 Articles with unsourced statements since December 2008
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