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)

Captopril is an orally active angiotensin-converting enzyme inhibitor that has been widely used in treating hypertension. We present a case of cough associated with captopril treatment in a patient with essential hypertension.
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PMID:Cough associated with the use of captopril. 389 84

The effects of inhibition of angiotensin converting enzyme (ACE) and glycopyrrolate on cough caused by inhaled capsaicin were investigated in a double-blind, randomised cross-over study in twelve normal volunteers. The capsaicin challenge was performed before and 2 h after dosing with 75 mg captopril or matched placebo given orally, and 20, 40 and 60 min after giving 1 mg glycopyrrolate i.v. to each subject. Captopril and placebo did not alter the cough response when compared to baseline. Glycopyrrolate, however, caused a significant increase in the threshold sensitivity (D2) from baseline, and a significant decrease in the total cough response at 40 and 60 min both after captopril and placebo. The D2-baseline and D2-40 min after glycopyrrolate (mean SD), respectively, were 3.2 (1.0); 17.9 (4.2) after placebo and 2.5 (8.5); 23.6 (6.9) after captopril. Elimination of vagal influences implies attenuation of the effects of tachykinins but not those prostaglandins. We postulate that tachykinins, such as substance P, play a more important role than prostaglandins in capsaicin-induced cough. We conclude that the vagus is important in the capsaicin-induced cough reflex, but, as suppression of this reflex by glycopyrrolate was delayed, the relevant receptors are either poorly accessible peripheral receptors or they are located in the central nervous system.
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PMID:Effects of glycopyrrolate on capsaicin-induced cough in normal volunteers treated with captopril. 795 39

Posttransplant erythrocytosis (PTE) represents a common complication in allograft recipients with normal renal function. Although the pathogenesis is not completely known, an alteration in the regulation of erythropoietin production by native kidneys or by renal allograft have been implicated as the main causes. Traditional therapies include repeated phlebotomies, bilateral native nephrectomies, and anticoagulant therapy. Recently, theophylline has been proposed as an effective therapy, although without general acceptance. Also, angiotensin-converting enzyme inhibitors have been involved in the development of anemia in chronic renal failure and dialysis patients. The aim of the present study was to demonstrate the efficacy of captopril on long-term treatment of PTE. Nineteen renal allograft recipients affected with severe PTE were included in the study. All patients had their native kidneys and none had a renal tumor or hydronephrosis. Restrictive criteria for PTE were applied to all patients and other causes of erythrocytosis were rationally excluded. Captopril was administered at a dose of 25 mg/24 hr (12.5 mg b.i.d.) during 12 months and no change on the initial dose was made during follow-up. After 3 months of captopril therapy and during the study period, significant reductions in hematocrit (P < 0.001), hemoglobin (P < 0.001), and RBC count (P < 0.001) were obtained in all patients. Erythropoietin levels decreased significantly during the study period, although the values were within the normal range of our laboratory. Captopril was well tolerated and only 1 patient had to be withdrawn from the drug because of dry cough. The present study has shown that captopril, at a low dose, represents a safe and effective therapy for PTE, without remarkable side effects or graft dysfunction. Long-term treatment with captopril in PTE did not induce anemia.
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PMID:Efficacy of captopril on posttransplant erythrocytosis. Long-term follow-up. 805 53

The pharmacology of angiotensin-converting-enzyme (ACE) inhibitors and their role in the renin-angiotensin system (RAS) are described, and pharmacokinetic properties and common adverse events are presented. ACE inhibitors play a vital role in the RAS by regulating the potent vasoconstrictor angiotensin II. All ACE inhibitors share the same basic structure; however, they can be separated on the basis of their functional (binding) group: carboxyl, sulfhydryl, or phosphinyl. These functional groups are, in part, responsible for differences in the pharmacokinetic and safety profiles of these agents. Captopril and lisinopril are the only ACE inhibitors that are not prodrugs requiring activation through hepatic biotransformation. Differences among the ACE inhibitors in lipophilicity are described; fosinopril has the greatest lipophilicity and lisinopril the least. ACE is found in numerous tissues, and there is increasing evidence of differences among ACE inhibitors in their ability to inhibit tissue ACE. Most ACE inhibitors are eliminated mainly by the kidneys and to a lesser extent through the liver. Lisinopril is the only ACE inhibitor that does not require hepatic metabolism. In the selection of an ACE inhibitor for once-daily use to treat hypertension, differences in trough-peak ratios are clinically relevant. Fosinopril, ramipril, and trandolapril have minimum trough-peak ratios of 50% or greater. ACE inhibitors are generally well tolerated, with hypotension, cough, and hyperkalemia being the most frequently reported adverse effects for the entire class. Drug interactions across the ACE inhibitor class as well as agent-specific interactions are described. Factors to be considered in the selection of an ACE inhibitor include differences in potency, affinity for ACE, pharmacokinetics, and toxicity that are related to structural properties of the drug; whether the trough-peak ratio enables use of a once-daily dose; and potential adverse effects related to a drug's functional (binding) group.
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PMID:Overview of the angiotensin-converting-enzyme inhibitors. 1103 16

Cough is an important side effect of Angiotensin Converting Enzyme Inhibitor (ACEI) therapy. The incidence of cough was investigated in a prospective 8 week study in 250 hypertensive patients receiving ACEI alone or in combination with other agents. Enalapril (5-20 mg/day), Lisinopril (5-20 mg/day), Captopril (25-75 mg/day) or Ramipril (5-15 mg/day) was prescribed to patients, who were followed up at weekly visits. Cough developed in 73 of the 250 patients i.e. an incidence of 29.2%. Females had a higher incidence of cough as compared to males--37.9% versus 15.5% (p < 0.001) and there was no significant difference in the cough incidence in the various age groups. A dry, non-productive cough developed in all patients within 4 weeks of ACEI initiation. Increased nocturnal intensity of cough was reported by 79.4% patients. Cough incidence was 34.4%, 24.3% and 18.1% in patients on Enalapril, Ramipril and Lisinopril, respectively. Cough was not dose related and was not related to smoking. There was no statistically significant difference among patients on ACEI alone or in combination with beta blockers, calcium channel blockers or diuretics. Of the 18 patients with ACEI induced cough who received Indomethacin, 50 mg bid, 8 reported complete cure and cough was reduced in intensity in the remaining ten.
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PMID:Angiotensin converting enzyme inhibitors and cough--a north Indian study. 1127 88

The aim of this study was to explore and compare initial treatment effects of captopril (Tensiomin) and sodium dimercaptosulphonate (DMPS) on a relatively large series of Wilson's disease inpatients. Two important markers of anticopper efficacy: serum sulphydryl and 24 h urinary copper levels in the patients were evaluated before and after treatment. The patients were randomly subdivided into 4 groups to allow statistical analysis (ANOVA) of the values recorded. The protocol was an open-label study of all the patients treated for 8 weeks (i.e., all the patients except those in the no-drug group), and a further six-month follow-up (post hospitalization) of the 14 patients administered captopril. Several copper-related variables were studied to evaluate the effect of the drugs on copper, and several biochemical and clinical variables were studied to evaluate potential toxic effects. Captopril was found to have a significant anticopper effect and did not markedly raise serum sulphydryl levels within this limited patient sample; the anticopper efficacy of captopril was, however, found to be markedly lower than that of DMPS; DMPS was found to raise the patients' serum sulphydryl and urinary copper levels. Evaluation of data from individual patients revealed evidence of a toxic side effect in only 1 patient, treated with DMPS, who exhibited transiently raised serum alanine aminotransferases, while no serious adverse events, upstanding syncope, irritating cough and leukopenia induced by captopril were noted. The results obtained in this four-group sample suggest that captopril might be a mild anticopper agent for Wilson's disease, possibly relieving the hepatic portal hypertension, but that DMPS has a greater field of anticopper efficiency than captopril. The authors also discuss recent experience of the overall treatment in China.
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PMID:Anticopper efficacy of captopril and sodium dimercaptosulphonate in patients with Wilson's disease. 1470 96

The aim of this trial was to examine the efficacy and safety of antihypertensive fixed combination lisinopril plus hydrochlorothiazide (Lopril H, Bosnalijek dd) in the treatment of essential arterial hypertension. In our trial we included 297 patients, aged 54.65+/-9.6 years, with treated or untreated hypertension and with high risk of cardiac events, in an opened trial of therapy based on lisinopril plus hydrochlorothiazide. Upon the examination by physicians, patients were divided into three groups in accordance with European Society of Cardiology guidelines for the management of arterial hypertension. Patients from five European countries were followed up for a period of 12 weeks. Duration of treatment was 12 weeks. We adjusted daily doses of lisinopril plus hydrochlorothiazide after every clinical examination and recorded adverse effects of drugs. After 12 weeks of treatment, 288 patients (96%) were evaluated for efficacy, tolerability and safety. In almost 81.5% patients with mild, moderate and severe hypertension, we recorded a reduction in blood pressure to approximately normal values SBP and DBP (140/90 mmHg). Drug-related side-effects occurred in 11 patients (3.66%). The most commonly reported adverse effects associated with lisinopril plus hydrochlorothiazide were cough (5) and dry mouth (5). This research has proved good efficacy of fixed combination lisinopril plus hydrochlorothiazide with more than 97% patients. Based on subjective estimation by patients: this drug improved quality of life in all cases.
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PMID:Fixed combination lisinopril plus hydro-chlorothiazide in the treatment of essential arterial hypertension: an opened, multi-centre, prospective clinical trial. 1803

Cardiovascular disease is the leading cause of death in American adults. Furthermore, the incidence of congestive heart failure is on the rise as a major cause of hospitalization and mortality in this population. Angiotensin Converting Enzyme (ACE) inhibitors prevent the production of angiotensin II, which has been shown to reduce mortality in patients with congestive heart failure. Angiotensin II receptor blockers (ARB) were developed as a direct inhibitor of angiotensin II. ARBs have been shown to be effective in the treatment of patients with systolic heart failure but do not cause chronic coughing which is a common side effect of ACE inhibitors. In theory, a compound that has the combined effect of an ACE inhibitor and an ARB should be more effective in treating heart failure patients than either agents alone. Therefore, the purpose of this manuscript is to design and discuss the benefits of a new molecule, which combines captopril, an ACE inhibitor, with losartan, an ARB. In this experiment Captopril and Losartan were modified and synthesized separately and combined by homo or mono coupling. This was achieved by taking advantage of PEG (Polyethylene glycol) as a linker. It is expected that this molecule will have the combined modes of action of both ACEs and ARBs. Benefits from combination therapy include; increased efficacy, reduced adverse effects, convenience, compliance, and prolonged duration. Consequently, this combined molecule is expected to block the production of angiotensin II more efficiently and effectively. Although captopril and losartan work in the same system by blocking the effect of angiotensin II they have different action sites and mechanisms some patents are also discussed. Losartan blocks the AT1 receptor which is expressed on the cell surface, while captopril inhibits ACE, preventing production of angiotensin II, which is present in both the plasma and on the cell surface, especially on endothelial and smooth muscle cells.
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PMID:A novel design of combining the angiotensin converting enzyme (ACE) inhibitor captopril with the angiotensin receptor blocker (ARB) losartan using homo coupling via PEG diacid linker. 2455 91


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