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)

Since their introduction in clinical practice in 1980, ACE inhibitors have been found useful in the treatment of hypertension and CHF. In hypertension, they are effective as monotherapy in 40% to 50% of the patients, and in combination with diuretics or calcium antagonists, they are effective in up to 85% of the patients. They are well tolerated, are not associated with depression, impotence, bronchospasm or metabolic derangements such as hypokalemia, hyperuricemia or hyperglycemia, and do not have adverse effects on the quality of life. As a result, they are preferred in hypertensive patients with CHF, left ventricular dysfunction, mental depression, older age, coronary artery disease, metabolic disorders, chronic destructive pulmonary disease, and peripheral vascular disease. In CHF they cause long-lasting hemodynamic and symptomatic improvement, improve exercise tolerance, and may lower mortality in certain patient subsets. Evolving new indications for ACE inhibitors include the diagnosis of renovascular hypertension, the prediction of surgical success, the treatment of scleroderma renal crisis, the reduction of proteinuria, renal protection, cardioprotection, the improvement of arterial compliance, in Bartter's syndrome and idiopathic edema, etc. ACE inhibitors are usually well tolerated but in some instances they may cause class-specific side effects such as hypotension; usually reversible azotemia or renal failure, especially in patients with renal artery stenosis or with CHF with low blood pressure; cough; angioedema; and hyperkalemia. Differences among ACE inhibitors are emerging and include chemical class (e.g., zinc ligand), biotransformation, potency, pharmacokinetics, prodrugs, tissue effects, additional pharmacologic properties, and drug interactions.
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PMID:Angiotensin converting enzyme inhibitors. II. Clinical use. 305 46

When captopril was first introduced, it was used in high doses for severe hypertension, often in the presence of renal insufficiency, and side effects such as proteinuria, rash, neutropenia, and altered taste sensation were noted. Upon analysis, these effects were most commonly seen in patients with renal disease, autoimmune disease, or collagen vascular disease. These complications usually reversed rapidly upon discontinuation of treatment. In contrast, the growing use of the angiotensin converting enzyme inhibitors, captopril and enalapril, for treating mild to moderate hypertension and the trend toward the use of lower doses has shown these agents to be well tolerated with a low frequency of troublesome adverse effects. In fact, the original spectrum of adverse effects has virtually disappeared with the use of lower doses in patients with uncomplicated hypertension. In low doses, the converting enzyme inhibitors produce remarkably few incidences of symptomatic discomfort; the most common is skin rash, which often responds to dosage reduction. Cough and rare occurrences of angioedema have also been reported. Moreover, evidence is evolving that indicates that the converting enzyme inhibitors may sometimes decrease proteinuria and improve renal function; these effects may be especially important in diabetic hypertensive patients. Of note, these drugs can also attenuate the unwanted metabolic side effects of concurrent diuretic treatment.
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PMID:Safety issues during antihypertensive treatment with angiotensin converting enzyme inhibitors. 306 5

Cough is a well recognised though undesirable side effect during the course of treatment with angiotensin converting enzyme inhibitors (IEC). With the help of two examples we have tried to show that this cough does not have an immunological origin but rather pharmacological. Cough was suppressed by non steroidal anti-inflammatory drugs. Stemming from these observations and from two studies in the literature a patho-physiological mechanism for the cough is proposed in which treatment with IEC leads to a connection with prostaglandins, notably bronchial PGE2.
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PMID:[Cough provoked by angiotensin-converting enzyme inhibitors. Effect of non-steroidal anti-inflammatory agents]. 321 98

An examination of the principal physiological actions of angiotensin II should make it clear why in vivo attempts to inhibit the rate of angiotensin II generation have been an attractive avenue in pursuing control of high blood pressure. The major physiological effect of angiotensin II relates to its direct pressor effect, but there are supplementary blood pressure regulating actions. Therefore, if we limit the rate of angiotensin II generation by inhibiting the angiotensin converting enzyme (ACE) we should expect to control high blood pressure in a number of clinical syndromes. This paper reviews the future of ACE inhibitors in the treatment of conditions such as hypertension associated with unilateral renal artery stenosis, essential hypertension and severe and previously unresponsive hypertension, with respect not only to efficacy but also to the side-effect profile and ancillary properties. Side effects seen with this class of drug are cough, rashes (both morbilliform and urticarial) and, rarely, angio-oedema. Proteinuria, nephrotic syndrome, leukopenia and taste disturbance were previously reported with captopril but only taste disturbance, and that less frequently, is apparent at the lower doses now employed. Several studies have examined the 'quality-of-life' aspects of ACE therapy and have usually but not always reported favourably. There are features of the ACE inhibitors which make them attractive drugs, and while we should be cautious because of limited experience, we should critically and creatively examine their properties over the next years.
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PMID:Angiotensin converting enzyme inhibition in hypertension. 331 25

The efficacy, tolerability and impact on quality of life of the ACE inhibitor lisinopril were evaluated in a 12-week open, multicenter post-marketing surveillance study. 233 patients, 45 years and over with diastolic blood pressure (DBP) 95-105 mm Hg were followed after a washout period of 7 days. 22 withdrew due either to adverse reactions, mainly cough (4.3%) and dizziness (3%), or noncompliance. DBP of 90 mm Hg or less was achieved in 50.7% with once-a-day 10 mg lisinopril, in 26.1% with 20 mg and in 16.1% with 20 mg plus addition of hydrochlorothiazide, 12.5 mg; in only 7.1% was BP not controlled. Adverse reactions other than cough or dizziness were experienced by fewer than 1%. Dartmouth COOP Functional Health Assessment Charts/WONCA were used to evaluate quality of life and were found useful in the study. Compared to baseline assessments, all functional status indicators (physical fitness, feelings, daily activities, social activities, change in health and overall health) scored significantly better in all treated patients after 12 weeks. Thus, in more than 90% of patients lisinopril was well-tolerated, highly effective in lowering blood pressure and possibly (no control group) improved the quality of life of all patients.
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PMID:[A multicenter study of lisinopril in the treatment of mild to moderate hypertension]. 755 4

The successful introduction of angiotensin converting enzyme (ACE) inhibitors in the treatment of patients with essential hypertension or heart failure has increased interest in the (patho)physiological role of the renin-angiotensin system (RAS). ACE is not only involved in the formation of angiotensin II from angiotensin I, but also inactivates vasoactive substances such as bradykinin and substance P. Accumulation of these substances during treatment with ACE inhibitors may contribute to both their therapeutic action and certain adverse effects associated with their use, such as cough and angioneurotic oedema. Renin inhibitors offer an alternative approach to inhibit the RAS. The major advantage of these, still experimental, drugs is their high specificity for the RAS since angiotensinogen is the only known substrate of renin. The currently available renin inhibitors are pseudopeptides that are rapidly taken up by the liver and excreted in the bile. Consequently, these drugs are subjected to a considerable first pass effect which limits their oral bioavailability. Additionally, plasma elimination half-life times are short and the duration of action is limited. Despite these shortcomings, single oral or intravenous administration results in a 80 to 90% inhibition of plasma renin activity and a slight reduction in blood pressure in patients with hypertension. The extent of blood pressure reduction is dependent on the patient's salt balance. After 1 week of oral treatment with the renin inhibitor remikiren, the antihypertensive effect was reduced in salt-repleted hypertensive patients. Subsequent intravenous administration of the drug did not further affect blood pressure, indicating that it was not the first pass effect that was limiting the efficacy of remikiren.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical pharmacokinetics and efficacy of renin inhibitors. 758 99

Seventeen patients with migraine headaches, occurring at least twice a month, were successfully treated with an ACE inhibitor for prophylaxis. Most were given enalapril, some used lisinopril. Duration of treatment ranged from 3 months to 3 years. Side effects were generally not noted. Cough occurred in four patients. The mechanism of action is unknown. The lack of side effects and the presence of clearly sustained benefit in this small group of migraineurs should prompt further study and use of this class of drugs for prophylaxis.
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PMID:ACE inhibitors for prophylaxis of migraine headaches. 759 40

Angiotensin-converting enzyme inhibitors (ACE inhibitors) have been shown to be effective in improving symptoms and survival in patients with systolic left ventricular dysfunction. Despite their proven benefits the use of ACE inhibitors is still limited in many parts of the western world. In part, the underutilization of ACE inhibitors is due to the occurrence of side effects such as cough, renal dysfunction and first dose hypotension. These side effects are in part due to ACE inhibitor-induced bradykinin formation. Blockade of the effects of angiotensin II can however also be achieved with an angiotensin II type I receptor blocking agent such as losartan. To determine the relative safety and effectiveness of ACE inhibitors compared to an angiotensin II type I receptor blocking agent the evaluation of losartan and the elderly trial (Elite) is comparing the ACE inhibitor captopril to the angiotensin II type I receptor blocking agent losartan in elderly patients. When used ACE inhibitors are often given in doses lower than those shown to be effective in reducing mortality in the major randomized trials. Several trials are currently under way comparing low to high doses of ACE inhibitors which should provide information on the need to achieve the doses used in the major mortality studies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Importance of angiotensin-converting enzyme inhibitors in myocardial infarction and congestive heart failure: implications for clinical practice. 761 6

1. We report a controlled retrospective cohort study of respiratory adverse reactions to ACE inhibitors. Bronchospasm and cough occurred at a higher rate in patients treated with ACE inhibitors, no links with sex, past history of bronchospasm, drug type or dose were found. 2. Cohorts of 1013 patients on angiotensin converting enzyme (ACE) inhibitors and 1017 patients on lipid lowering drugs (LLDs) were compared for the occurrence of new bronchospasm, relapse of previous bronchospasm, increase of current bronchospasm, and cough. 3. The prevalence of bronchospasm was 5.5% for patients on ACE inhibitors and 2.3% for patients on LLDs, P < 0.001. The relative risk of a bronchospasm adverse reaction for a patient on an ACE inhibitor compared with a patient on a LLD was 2.39, 95% confidence interval 1.47 to 3.90. 4. No ACE inhibitor specificity, or significant sex differences were found in the prevalence of bronchospasm or cough after correcting for bias implicit in the original cohorts. The bronchospastic reactions were not dose dependent. 5. The prevalence of a past history of bronchospasm in patients reporting ACE inhibitor-induced bronchospasm (16%) was not significantly different from the prevalence in patients on ACE inhibitors without an adverse reaction (13%), P = 0.447. 6. The prevalence of ACE inhibitor cohort cough was 12.3% and 2.7% in the patients on LLDs, P < 0.0001. Cough did not occur more commonly in patients on ACE inhibitors who had experienced any bronchospasm (28%) than in patients on LLDs with bronchospasm (27%).
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PMID:Bronchospasm and cough as adverse reactions to the ACE inhibitors captopril, enalapril and lisinopril. A controlled retrospective cohort study. 761 67

Theoretical considerations and experimental data suggest that AT1-antagonists can offer the same advantages as ACE-inhibitors in the treatment of hypertensive patients without causing side effects such as angioedema and cough. The pharmacokinetic properties of these drugs suggest that AT1-antagonists can be given once-daily. Preliminary data obtained with losartan indicate that this drug, given once daily, significantly reduced blood pressure with a favourable trough to peak ratio. Moreover the hypotensive effect of this drug was similar to that exerted by other hypotensive drugs currently employed in the treatment of hypertensive patients. Losartan can be usefully combined with a thiazide diuretic inducing an additive antihypertensive effect. No negative effect on lipid and glucose profiles was recorded. Furthermore, losartan exerted an uricosuric action, thus reducing serum uric acid. Preliminary data suggest that the incidence of cough in patients treated with losartan was similar to that observed in patients receiving placebo or a thiazide diuretic. Although these data need to be confirmed by ongoing and future studies, it is tempting to hypothesize that this new class of antihypertensive drugs can offer a further useful tool in the treatment of hypertensive patients.
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PMID:[Clinical experience with angiotensin II antagonists in arterial hypertension]. 763 5


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