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)

Angiotensin-converting enzyme (ACE) inhibitors are increasingly used to control hypertension although cough, sometimes severe enough to require discontinuance, is a well-described side effect of these drugs. Manufacturers' labeling indicates that this side effect occurs with a much lower frequency than is reported in the literature. This article describes the incidence of cough as a side effect of ACE inhibitors in a small inner-city practice and presents two reports of patients who required discontinuance of ACE inhibitors for this symptom. It is suggested that, consistent with the recent literature, the incidence of this symptom is more frequent than suggested by manufacturers' labeling, at least in this population.
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PMID:Cough requiring discontinuance of angiotensin-converting enzyme inhibitors in an urban inner-city population. 129 95

Angiotensin-converting enzyme (ACE) inhibitors are useful first-line drugs in the therapy of mild and moderate hypertension. Adverse reactions to this drug class are rarely serious. Hypotension, cough, rash, and taste disturbance are uncommon; reduced glomerular filtration and hyperkalemia occur infrequently; angioedema is rare and neutropenia is extremely rare. Quinapril is a new ACE inhibitor that is converted to biologically active quinaprilat in the liver. This ACE inhibitor has a rapid onset of action and inhibits local tissue converting enzyme systems in kidney, heart, and brain, as well as in the circulating renin-angiotensin system. Clinically significant adverse effects of quinapril occur at low rates. In 1,771 patients receiving quinapril, the reported incidence of the first occurrence of orthostatic hypotension was comparable to that seen in patients receiving placebo. In other studies, headache was reported by up to 4.7% of patients receiving quinapril, which is comparable to reported incidences of headache in patients receiving other ACE inhibitors. Other adverse events reported at rates greater than 1% include cough with associated rhinitis and bronchitis, dizziness, and somnolence. Such adverse events have only rarely led to the withdrawal of patients from clinical studies of quinapril.
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PMID:Adverse effects of angiotensin-converting enzyme inhibitors in antihypertensive therapy with focus on quinapril. 154 39

Sodium nitroprusside causes cyanide poisoning at currently recommended infusion rates. Serum thiocyanate concentrations are of no value in detecting cyanide poisoning caused by nitroprusside. Methemoglobinemia in those patients receiving intravenous nitroglycerin may seriously impair oxygen delivery and is not always accompanied by cyanosis in anemic patients. Angiotensin-converting enzyme inhibitors are responsible for a plethora of adverse effects, including renal insufficiency, hypotension, angioedema, cough, and increased insulin sensitivity.
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PMID:Toxic effects of drugs used in the ICU. Nitroprusside, nitroglycerin, and angiotensin-converting enzyme inhibitors. 190 24

In recent years, studies of the regulation of the airways have focused to an increasing degree on the roles of neuropeptides. Several peptides have been shown to be present in airways and mediate such diverse responses as ion transport, mucus secretion, bronchospasm or relaxation, edema, cough, changes in vascular permeability, and neutrophil chemotaxis. More recently, studies have described the roles of peptidases, most notably neutral endopeptidase (NEP, also known as enkephalinase, or E.C. 3.4.24.11) and kininase II (also known as angiotensin-converting enzyme, or E.C. 3.4.15.1) in modulating peptide-induced responses. The enzymes cleave a wide variety of peptides, generating metabolites that are inactive in the systems studied to date. Thus inhibitors of NEP potentiate responses to peptides that are cleaved by it. Therefore, NEP plays roles in modulating peptide-induced effects analogous to the role of acetylcholinesterase in modulating cholinergic neurotransmission. In several experimental respiratory diseases, the activity of neutral endopeptidase is decreased, resulting in increased responses to peptides. The therapeutic application of recombinant NEP protects the airways from the adverse actions of stimuli that release inflammatory peptides, and induction of the NEP gene expression by glucocorticoids suggest a possible mechanism for the action of these steroids in treating airway diseases such as asthma, chronic bronchitis, or cystic fibrosis.
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PMID:Roles of neutral endopeptidase in airways. 201 45

Angiotensin-converting enzyme inhibitors (ACEI) constitute an effective and well tolerated class of drugs for the treatment of arterial hypertension. Yet they have been blamed for the occurrence of side-effects the most frequently reported of which are renal function impairment, hypotension and cough. For this reason, the renal function of hypertensive patients has been evaluated after short - and long - term treatment with perindopril. In patients with normal renal function on short-term treatment (1 and 5 days) perindopril produced an increase of renal plasma flow without change in glomerular filtration. In long-term treatment (up to 18 months), no significant change in plasma creatinine level was observed. In old age hypertensive patients or in patients with chronic renal failure glomerular filtration was also preserved, apart from rare cases of creatinine clearance reduction, notably after addition of hydrochlorothiazide. A very slight and clinically not significant rise of kaliemia was noted when perindopril was used as single-drug treatment. Cases of symptomatic hypotension were rare (0.2 p. 100), even in situations of water and salt depletion. Among the other side-effects of ACEI, cough, which has more recently been described, has carefully been looked for. Its incidence has been determined in a double-blind trial comparing perindopril (1.2 p. 100) with captopril (2.4 p. 100). It has also been evaluated in a long-term study involving 632 hypertensive patients, 391 of whom were treated for 1 year; its incidence then was 2.9 p. 100, and drug withdrawal was required in 8 cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Tolerance and safety of the use of perindopril]. 250 18

The respective prevalence of hypertension and asthma is sufficient for their combined existence to be far from rare. The effects of certain antihypertensive drugs, e.g., alpha 2-adrenoceptor agonists, on the bronchi may be either harmful or beneficial. When inhaled, alpha 2-agonists reduce the immediate bronchial response to allergens, whereas when ingested they aggravate the bronchial response to histamine and all the more so when their effect on the central nervous system is greater. Therefore, there has been much interest in agents such as the new oxazoline derivative, rilmenidine, which has less central effects than clonidine, an imidazoline compound of reference. Calcium antagonists inhibit smooth muscle contraction and release of mast cell inflammatory mediators. In asthmatic subjects, their short-term administration leads to a modest improvement in spontaneous bronchial obstruction, has only a partial protective action against various nonspecific or allergenic stimuli, and slightly reinforces the beneficial effect of beta 2-agonists. Beta-adrenoceptor antagonists aggravate bronchial obstruction and nonspecific bronchial hyperreactivity in asthmatic subjects. These harmful effects are dose-dependent, have even been reported after the administration of eyedrops, and are common to all beta-blockers. Angiotensin-converting enzyme inhibitors increase bronchial hyperreactivity in patients who develop cough during treatment and may, in certain cases, worsen or even induce asthma, probably by opposing inactivation by hydrolysis of tachykinins and of bradykinins.
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PMID:Bronchial effects of alpha 2-adrenoceptor agonists and of other antihypertensive agents in asthma. 257 Dec 93

Angiotensin-converting enzyme inhibitors sometimes cause cough; the mechanism is unknown. We therefore studied the effects of ambulatory treatment with captopril on pulmonary function and on nonspecific bronchial responsiveness to methacholine in 15 hypertensive subjects. Lung volumes, expiratory flows and nonspecific bronchial responsiveness to methacholine using doses up to 64 g/L were measured before and four and eight weeks after captopril treatment was started. Throughout the study the subjects recorded respiratory symptoms and peak expiratory flow rates. In four subjects a persistent cough developed related to the use of captopril, but this was not associated with the development of airflow obstruction or bronchial hyperresponsiveness. The mean provocative concentration of methacholine that resulted in a 20% fall in the forced expiratory volume in 1 s was 43.6 +/- 1.8 g/L after eight weeks of captopril treatment compared with 61.6 +/- 1.2 g/L at the baseline evaluation. We concluded that there was no significant change in lung function during treatment with captopril. The development of a cough related to this medication is not associated with the development of airflow obstruction or airway hyperresponsiveness.
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PMID:Pulmonary function and airway responsiveness during long-term therapy with captopril. 265 33

Angiotensin-converting enzyme (ACE) inhibitors are a group of drugs recently introduced to treat hypertension and congestive heart failure. There are many reports of a dry cough in patients treated with (ACE) inhibitors, but this is often considered a rare side effect. Eleven of 30 patients treated with the investigational ACE inhibitor cilazapril complained about a chronic cough.
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PMID:Cough caused by cilazapril. 296 78

Angiotensin-converting enzyme (ACE) inhibitors are one of the first drugs of choice for the treatment of hypertension. However, there have been many reports of persistent chronic dry cough and inflammatory skin reactions (rash and/or angioedema, etc.) induced by ACE inhibitors. In this study, in order to evaluate the cough and inflammatory reaction, we measured the number of citric acid-induced coughs and the intradermal inflammation with ovalbumin in guinea pigs consecutively treated with ACE inhibitors (lisinopril, enalaprilat and imidapril) for 3 days. The number of citric acid-induced coughs and the inflammatory responses were significantly enhanced by treatment with lisinopril and enalaprilat, whereas imidapril produced no change in either response. These results correspond to the frequency of adverse effects in clinical practice, which suggests that imidapril has the least ability to induce the inflammatory skin response and cough. Furthermore, the enhancement produced by the ACE inhibitors in the number of coughs and the inflammatory responses were significantly reduced by pretreatment with indomethacin (prostaglandin synthesis inhibitor). This finding suggests that PGs at least participate in the mechanism for ACE inhibitor-induced cough and inflammatory skin response.
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PMID:Toxicodynamic analysis of cough and inflammatory reactions by angiotensin-converting enzyme inhibitors in guinea pig. 747 83

Angiotensin-converting enzyme (ACE) inhibitor therapy has recently been shown to be effective in the treatment of post-renal transplant erythrocytosis (PTE). In an attempt to assess the effect of drug treatment on serum erythropoietin level, glomerular filtration rate, and urinary protein excretion, we prospectively evaluated 8 consecutive cadaveric renal transplant recipients with PTE treated with ACE inhibitor therapy for 3 months. In response to ACE inhibition, the mean hematocrit (HCT) value decreased from 53.7 +/- 0.6% before treatment to 42.7 +/- 2.2% at the conclusion of the study (p = 0.03). However, 1 patient failed to respond to ACE inhibition (HCT > 50%), and 2 patients with PTE developed anemia (HCT < 35%) while maintained on drug treatment. Although the mean serum erythropoietin level decreased during ACE inhibition (from 22.8 +/- 8.4 to 9.4 +/- 5.3 mU/ml; p = 0.06), a consistent change in individual erythropoietin levels was not identified. At the conclusion of the study, the serum erythropoietin levels were undetectable in 4 patients, decreased in 1, unchanged in 2, and increased in the only patient with PTE who failed to respond to drug treatment. All patients tolerated the ACE inhibitor therapy without developing cough or hyperkalemia. In addition, serum creatinine levels, 125I-iothalamate clearances, and mean arterial blood pressures were unchanged throughout the study. Microalbuminuria (spot urinary albumin/creatinine ratio between 30 and 200 mg/g) developed in 5 patients with PTE and coincided with the onset of erythrocytosis (25.2 +/- 7 mg/g before PTE and 76.3 +/- 36.7 mg/g at the time of PTE detection).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association of post-renal transplant erythrocytosis and microalbuminuria: response to angiotensin-converting enzyme inhibition. 757 90


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