Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Suppression of the renin-angiotensin system (RAS) with angiotensin-converting enzyme (ACE) inhibitors is an established method for controlling blood pressure and reducing the risk of cardiovascular disease. In addition to reducing blood pressure, suppression of the RAS is able to protect against the target-organ damage that results from hypertension. Unfortunately, despite the use of ACE inhibitors and agents from the other classes of conventional antihypertensives, effective control of blood pressure remains poor. A major contribution to this failure to control blood pressure appears to be lack of compliance with the prescribed medication, arising from the presence of unacceptable side effects. Angiotensin II type 1 (AT1) receptor blockers, such as candesartan, are the latest class of antihypertensive agent to be developed. They target the AT1-receptor - the final common pathway for all the known negative cardiovascular effects of angiotensin II - and provide pronounced antihypertensive efficacy without the side effects of cough and angioneurotic oedema that are associated with the use of ACE inhibitors.
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PMID:The renin-angiotensin system and cardiovascular disease. 1105 28

Angiotensin II type 1 (AT1) receptor blockers, such as candesartan, are attractive alternatives to ACE inhibitors in the treatment of hypertension and cardiovascular disease. Although angiotensin-converting enzyme (ACE) inhibitors are able to suppress the renin-angiotensin system (RAS), their mechanism of action may limit their clinical utility in the treatment of hypertension. For example, they act as competitive inhibitors of ACE. This means that their effects can be overcome by high levels of angiotensin I, which occur after ACE inhibition due to removal of the negative feedback effect of angiotensin II on renal renin release. ACE inhibitors are also unable to block the production of angiotensin II by non-ACE-mediated pathways. Furthermore, ACE is not a specific enzyme. Its inhibition therefore has effects on other substances, such as bradykinin, leading to the class-specific side effects associated with ACE inhibitors. Candesartan, on the other hand, binds insurmountably to the AT1-receptor, thereby providing more complete blockade of the negative cardiovascular effects of angiotensin II than is possible with ACE inhibitors. The specificity of AT1-receptor blockade also ensures that efficacy is achieved without inducing the side effect of cough that results from the non-specific consequences of ACE inhibition. Preclinical and early clinical studies demonstrate that AT1-receptor blockers produce at least the same degree of target-organ protection as has been demonstrated for ACE inhibitors. Additional benefits of AT1-receptor blockers may arise from the fact that, unlike ACE inhibitors, they do not prevent the activity of angiotensin II on AT2-receptors in the heart, which is thought to reduce cardiac remodelling. From a mechanistic perspective, therefore, AT1-receptor blockers appear to have advantages over ACE inhibitors, in terms of a more complete blockade of angiotensin II effects, while also avoiding the specific side effects associated with ACE inhibition.
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PMID:Angiotensin II type 1 receptor blockade: a novel therapeutic concept. 1105 29

The management of diabetic hypertension requires meticulous selection of agents in the antihypertension armamentorium. There may be several associated factors to be considered while treating a hypertensive diabetic. These include hyperglycemia, dyslipidemia, proteinuria, left ventricular hypertrophy and heart failure to name a few. Losartan is the first of a new class of agents in the list of antihypertensive drugs. By its selective angiotension II receptor (subtype AT1) blocking action it is postulated to bring about a more complete inhibition of the renin-angiotensin system. Thus, it might produce all the benefits of angiotensin converting enzyme (ACE) inhibitor therapy with the freedom from cough so commonly seen with the use of ACE inhibitors. This review attempts to analyze the possible benefits of losartan therapy in diabetes.
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PMID:Role of losartan therapy in the management of diabetic hypertension. 1127 47

Hypertension is a major problem throughout the developed world. Although current antihypertensive treatment regimens reduce morbidity and mortality, patients are often noncompliant, and medications may not completely normalize blood pressure. As a result, current therapy frequently does not prevent or reverse the cardiovascular remodeling that often occurs when blood pressure is chronically elevated. Blockade of the renin-angiotensin system (RAS) is effective in controlling hypertension and treating congestive heart failure. Both angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) inhibit the activity of the RAS, but these two classes of antihypertensive medications have different mechanisms of action and different pharmacologic profiles. Angiotensin-converting enzyme inhibitors block a single pathway in the production of angiotensin II (Ang II). In addition, angiotensin I is not the only substrate for ACE. The ACE inhibitors also block the degradation of bradykinin that may have potential benefits in cardiovascular disease. Bradykinin is, however, the presumed cause of cough associated with ACE inhibitor therapy. Data from clinical trials on ACE inhibitors serve to support the involvement of the RAS in the development of cardiovascular disease. Angiotensin receptor blockers act distally in the RAS to block the Ang II type 1 (AT1) receptor selectively. Thus, ARBs are more specific agents and avoid many side effects. Experimental and clinical trials have documented the efficacy of ARBs in preserving target-organ function and reversing cardiovascular remodeling. In some instances, maximal benefit may be obtained with Ang II blockade using both ARBs and ACE inhibitors. This review describes clinical trials that document the efficacy of ARBs in protecting the myocardium, blood vessels, and renal vasculature.
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PMID:Angiotensin receptor blockers: evidence for preserving target organs. 1128 62

Angiotensin II(AII) accelerates the progress of cardiovascular diseases. This was proved by the fact that the blockade of renin-angiotensin system provided clinical benefits for patients with cardiovascular diseases. This review focuses on the differences between AT1-receptor antagonist and ACE inhibitor in basic and clinical aspects. Beside decreased AII concentration, increased tissue bradykinin concentration may contribute to the beneficial effect of ACE inhibitor, on the other hand, this increases the rate of cough to decrease the compliance. Increased AII concentration by AII receptor antagonist may antagonize the binding of the drug as well as stimulate AT2 receptor subtype. ACE inhibitor can not block the effect of non-ACE AII formation, but AII receptor does. These differences should be considered for their clinical use.
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PMID:[Comparison between AngII receptor antagonist and ACE inhibitor]. 1139 5

In both diabetic and nondiabetic renal disease, reducing blood pressure with antihypertensive therapy has beneficial effects on renal function. The key role of the renin-angiotensin system in blood pressure and volume homeostasis has long been established, but its importance for the overall normal functioning of the kidney itself is also increasingly being recognized. Angiotensin-converting enzyme (ACE) inhibitors, widely and successfully used in the treatment of hypertension, may also provide renal protection independent of blood pressure reduction; however, their relatively nonspecific mode of action in blocking an early metabolic step entails major clinical disadvantages, such as accumulation of bradykinin and substance P, that may cause the characteristic ACE-inhibitor side effects of persistent dry cough and, more rarely, angioneurotic edema. Angiotensin II antagonists or receptor blockers, a new class of antihypertensive agent, selectively antagonize the AT1 receptor subtype and, because of greater specificity, do not give rise to the side effects associated with ACE inhibitors. More important, these new drugs may have mechanistic advantages over other antihypertensives, including ACE inhibitors.
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PMID:Valsartan and the kidney: review of preclinical and clinical data. 1144 69

Diabetic nephropathy has become the leading cause of terminal renal failure in all Western nations due to a steady increase of patients with the renal complication of type 2 (non-insulin-dependent) diabetes mellitus. A number of modifiable risk factors have been identified that predispose to and/or accelerate renal disease in patients with diabetes mellitus. Among these, the level of blood pressure, even in the range of normotension according to World Health Organization or Joint National Committee definition, is closely related to the rate of progression of diabetic nephropathy. This has been documented in patients with incipient (microalbuminuric) and in patients with manifest (proteinuric) diabetic renal disease. Consequently, the treatment of even normotensive diabetics has been recommended once microalbuminuria is present, and blood pressure values in the low normal range should be aimed for. The selection of antihypertensive agents is also important, however, since a 'renoprotective effect' has been documented for drugs that interfere with the renin-angiotensin-aldosterone system such as angiotensin converting enzyme inhibitors. Recently, a new class of drugs that selectively inhibits this system by specifically targeting the angiotensin II receptor has been developed. These angiotensin II subtype 1-receptor antagonists are efficacious antihypertensive agents with a side-effect profile similar to placebo. Evidence for a renoprotective effect in patients with diabetic nephropathy from a large controlled clinical trial is still awaited, but data generated in animal experiments and in smaller clinical trials are encouraging. Currently, these drugs are a valuable substitute for angiotensin converting enzyme inhibitors in patients who experience side effects such as intractable cough.
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PMID:Angiotensin II subtype 1-receptor antagonists in the treatment of diabetic nephropathy. 1145 Dec 16

Angiotensin Converting Enzyme (ACE) inhibitors represent a major advance in the treatment of: hypertension, and generally speaking, in cardiovascular prevention; myocardial infarction; cardiac failure. They have a cardio and vascular protective action by tending to correct hypertension, left ventricular hypertrophy and remodelling, endothelial dysfunction, arterial smooth muscle proliferation and thrombotic phenomena. However, besides the cough that this therapeutic class engenders, a major question remains unanswered: is there resistance to this family of drugs? In other words, does left ventricular remodelling and arterial smooth muscle proliferation continue with regular treatment at the prescribed dosages? The synthesis of angiotensin II does not only depend on the angiotensin converting enzyme but also on the quality of angiotensin I and the presence of other enzymes such as chymase. A secondary increase of angiotensin II with ACE inhibitor therapy may reflect insufficient blockade of the renin-angiotensin system or a synthesis of angiotensin II by an alternative pathway to the converting enzyme. In vivo measurement of ACE inhibition shows that blockade of the renin-angiotensin system is automatically limited due to the very accurate regulation of angiotensin II concentrations.
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PMID:[Resistance to ACE inhibitors. Myth or reality?]. 1160 63

Vasopeptidase inhibitors are a new class of cardiovascular drug that simultaneously inhibit both neutral endopeptidase and angiotensin-converting enzyme (ACE). They increase the availability of peptides that have vasodilatory and other vascular effects; they also inhibit production of angiotensin II. In animal models vasopeptidase inhibitors decrease blood pressure in low, medium, and high renin forms of hypertension, and they also appear to confer benefits in models of heart failure and ischaemic heart disease. Studies in human hypertension show that these agents are effective in decreasing blood pressure regardless of race or age. Experience with omapatrilat, the most clinically advanced of these drugs, has shown it to be more effective than currently available ACE inhibitors or other widely used antihypertensive agents. Studies with omapatrilat in congestive heart failure have shown beneficial effects on haemodynamics and symptoms. The vasopeptidase inhibitors appear to have safety profiles similar to ACE inhibitors, though the frequency of side-effects such as angio-oedema and cough remains to be established. Large trials with clinical endpoints, some already in progress, are needed to establish the place of this class of drug beside that of established therapies in conditions such as hypertension, heart failure, ischaemic heart disease, and nephropathy.
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PMID:Vasopeptidase inhibitors. 1194 97

Blockade of the renin-angiotensin system has proved an important principle in the pharmacotherapy of cardiovascular diseases. There is now overwhelming documentation on the beneficial effect of angiotensin converting enzyme inhibitors (ACE inhibitors) on mortality and morbidity in patients with cardiovascular risk factors. Such documentation is still lacking for the angiotensin II receptor antagonists which, in 1999, sold for 77% of the amount spent on ACE inhibitors in Denmark. This review assesses the therapeutic effects of angiotensin II antagonists compared with the ACE inhibitors in patients with uncomplicated essential hypertension. From 21 comparative studies with a duration of up to one year, it can be concluded that the lowering of the blood pressure with the two classes is similar. Both showed relatively few side effects, the only difference being a higher incidence of cough after ACE inhibitors. Until larger comparative long-term studies on mortality and morbidity have been conducted, angiotensin II antagonists should only be used in hypertensive patients experiencing unacceptable side effects with ACE inhibitors.
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PMID:[Angiotensin II antagonists versus ACE inhibitors in the treatment of raised blood pressure]. 1179 33


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