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)

The antihypertensive and metabolic responses to delapril and captopril in hypertensive patients were studied. Forty-six hypertensive patients entered the study and were divided into two groups. The delapril group included 21 essential hypertensive and five renoparenchymal hypertensive patients; while the captopril group included 11 essential hypertensive and nine renoparenchymal hypertensive patients. The patients in the delapril group took delapril 7.5 mg twice a day for 2 weeks. If the antihypertensive effect was inadequate, the dose was increased to 15mg twice a day, and then to 30mg twice a day. The period of delapril treatment was 12 weeks. The patients in the captopril group took captopril 25 mg twice a day or three times a day for 12 weeks. After delapril treatment, there were significant decreases in the systolic (from 163 +/- 17 to 141 +/- 15 mmHg) and diastolic blood pressure (from 105 +/- 13 to 91 +/- 10 mmHg). There were also significant decreases in the systolic (from 161 +/- 18 to 141 +/- 24 mmHg) and diastolic blood pressure (from 100 +/- 10 to 90 +/- 12 mmHg) after captopril treatment (p < 0.001). The pulse rates in both groups showed no significant changes after treatment. The laboratory data in both groups showed few changes after treatment. Plasma renin activity increased after delapril treatment. A cough was the side effect most commonly seen. We conclude that hypertensive patients have the same blood pressure and metabolic responses to delapril as captopril.
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PMID:[Blood pressure and metabolic response to converting enzyme inhibitor in hypertensive patients: comparison between delapril and captopril]. 136 26

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

The pharmacological activity and safety of the new angiotensin converting enzyme (ACE) inhibitor trandolapril (RU 44570) has been evaluated in ten healthy male volunteers given 2 mg once daily for seven days. Assessment criteria included evaluation of plasma ACE and renin activity and aldosterone levels in the supine and standing positions, monitoring of blood pressure, heart rate and electrocardiogram, routine blood and urine laboratory tests, and evaluation of adverse effects. Plasma ACE activity (both in the supine and standing positions) was significantly lower after the first dose and was almost completely suppressed after 7 days of treatment. Plasma renin activity with the subjects in both positions was significantly increased at the end of treatment. Plasma aldosterone did not vary significantly, except for an increase in the standing position after 7 days of wash-out. No significant changes occurred in blood pressure, heart rate, electrocardiogram, blood or urine laboratory tests. No adverse effects were reported, in particular, no orthostatic hypotension, cough or episodes of bronchospasm occurred. It is concluded that oral trandolapril 2 mg o.d. is an effective and long-lasting ACE inhibitor with a good safety profile on repeated dosing. Further studies are warranted to investigate its therapeutic application as well as its safety profile after long-term administration.
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PMID:Pharmacological activity and safety of trandolapril (RU 44570) in healthy volunteers. 164 89

Recently there has been extensive development of orally active angiotensin converting enzyme (ACE) inhibitors in addition to those already marketed, for example, captopril, enalapril, lisinopril and ramipril. It was initially thought that ACE inhibitors were likely to be most useful as antihypertensive agents in conditions in which circulating renin and angiotensin II were elevated. However, it is now clear that they can also lower arterial pressure when plasma renin is not high. In addition, they have beneficial effects in cardiac failure. Thus, captopril, enalapril, lisinopril and ramipril can be used in the treatment of mild to moderate hypertension either alone or in conjunction with diuretics or calcium antagonists. Broadly speaking, efficacy appears to be similar to that of beta-blockers or diuretics. Unfortunately, however, there are no long term studies comparing one ACE inhibitor with another or with other classes of antihypertensive agents. Furthermore, there are no prognostic studies which show that use of ACE inhibitors reduces morbidity or mortality in hypertension. Many new ACE inhibitors are undergoing clinical assessment, including alacepril, cilazapril, fosenopril, perindopril, quinapril and ramipril. The drugs vary, in that some exist in the active form whereas others are prodrugs which are converted to the active agent following absorption. In addition they each possess one of several ligands, for example, carboxyl, phosphinyl or sulfhydryl groups, and so vary in their affinity for ACE. Although many of these agents are renally excreted, a small number are metabolised via the liver (e.g. quinapril and spirapril) and this may prove advantageous in the presence of renal impairment. In common with captopril and enalapril, the new ACE inhibitors inhibit the renin-angiotensin system and initial results suggest that they are effective in lowering blood pressure in essential hypertension. Furthermore, they reduce systemic vascular resistance in the absence of a reflex tachycardia. There are a number of adverse effects which are attributable to the pharmacological mechanism of the ACE inhibitors as a group; these include hypotension, particularly in patients with high renin levels, prior diuretic use, renal impairment or in the elderly. Additional adverse effects may relate to chemical structure. The high incidence of adverse effects noted in early studies related to excess dosage and to the presence of a sulfhydryl group, which the more recently developed ACE inhibitors lack. The adverse effects most commonly reported with established and new ACE inhibitors include headache and fatigue, cough, skin rashes, hypotension and diarrhoea. As a group, ACE inhibitors have an acceptable but not negligible adverse effect burden.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin converting enzyme inhibitors and moderate hypertension. 222 19

The renin-angiotensin system has a wide range of physiological actions, and thus interference with the system has attractive therapeutic potential. The orally active angiotensin converting enzyme (ACE) inhibitors have so far been the most successful drugs in this area. They lower arterial pressure both in renovascular and essential hypertension, and their effects are enhanced by concomitant diuretic therapy or dietary salt restriction. Since, in renovascular hypertension, the affected kidney depends on enhanced local generation of angiotensin II to help preserve its function, the circulation and excretory capacity of this kidney may be compromised with ACE inhibition. ACE inhibitors can improve exercise tolerance and diminish cardiac ventricular arrhythmias in patients with heart failure. Because these drugs lower plasma aldosterone, they tend to correct potassium deficiency and hypokalemia, which may have been induced by diuretic treatment. Hypotension can occur with the first dose of ACE inhibitor, especially in sodium-depleted subjects; in patients on prior antihypertensive therapy, particularly if this includes a diuretic; and in the elderly. Not all of the actions of ACE inhibitors are necessarily due to lowering of plasma angiotensin II: accumulation of kinins may be responsible for some of the effects and side effects. Common to all ACE inhibitors are occasional rashes, cough, and, more rarely, angioedema. Apparently peculiar to captopril, and less often seen with the lower doses now employed, are taste disturbance, proteinuria, and marrow depression. ACE inhibitors, should not be used in pregnant women.
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PMID:Converting enzyme inhibitors in the treatment of hypertension. 248 62

Synthetic orally active angiotensin-converting enzyme (ACE) inhibitors have been successfully used in the treatment of congestive heart failure and hypertension, particularly in hypertensive subjects with increased renin-angiotensin-aldosterone-system activity. Adverse skin reactions, angioneurotic oedema and rapidly decreasing lung function in asthmatics have been reported following medication with ACE inhibitors. Furthermore, these drugs have been associated with a persistent dry cough in subjects without previous known bronchial hyper-reactivity. There is reason to believe that an ACE inhibitor-induced cough is due to an increased inflammatory state in the airways of susceptible individuals, and that this cough might thereby have pathophysiological features in common with the cough seen as an early symptom of asthma. All inflammatory responses, wheal and flare reactions, infiltration of neutrophils, eosinophils, basophils and monocytes were enhanced by ACE inhibitors. A dose-response relationship for the proinflammatory effect of the ACE inhibitor has been demonstrated.
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PMID:Angiotensin-converting enzyme inhibitors and their influence on inflammation, bronchial reactivity and cough. A research review. 268 32

The effect of sulindac on ACE inhibitor-induced cough was studied in eight hypertensive subjects in a randomised placebo-controlled double blind cross-over trial. There was no significant improvement in cough or sense of well-being. Blood pressure, renal function, plasma renin and ACE activity were unchanged. Sulindac however, appears to be effective in some individuals in reducing ACE inhibitor-induced cough with acceptable tolerance and few side effects. Further work is needed to elucidate the mechanism of sulindac's interaction with ACE inhibitors.
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PMID:Effect of sulindac on angiotensin converting enzyme inhibitor-induced cough: randomised placebo-controlled double-blind cross-over study. 158 37

Adverse effects of converting enzyme inhibitors are either substance-specific (neutropenia, proteinuria, skin rashes, taste disturbances) or due to the converting enzyme inhibition (hypotension, functional renal insufficiency, hyperkalemia, cough, angioedema). They are rare nowadays because of better knowledge of the pharmacokinetics and -dynamics of the converting enzyme inhibitors, resulting in lower dosage, and because of identifying patients at high risk. The dosage must be adjusted according to renal function, in order to prevent accumulation and toxicity. In addition to patients with renal insufficiency, patients at high risk are those with a stimulated renin-angiotensin-aldosterone system, i.e. patients with renovascular hypertension or heart failure. Patients with collagen vascular disease, for example, systemic lupus erythematosus or scleroderma, should not be considered for long-term therapy with converting enzyme inhibitors because of the increased risk of neutropenia. Life-threatening angioedema may develop, mainly during the first few hours after drug administration.
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PMID:[Angiotensin-converting enzyme inhibition: side effects and risks]. 285 Jun 87

Side effects of angiotensin converting enzyme (ACE) inhibitors are not common with currently recommended doses. Hypotension, hyperkalemia and renal impairment may occur under special circumstances, and relate directly to blockade of ACE, in particular when pre-treatment renin levels are high. Other adverse effects, once quite common when excessive doses of captopril were prescribed, are now rarely seen. A possible exception is cough. Though not dangerous, cough is not infrequently seen during treatment with ACE inhibitors. Experience with these drugs is insufficient to recommend their use in the hypertension of pregnancy. The "metabolic-profile" with ACE inhibitors appears favourable, since they can increase uric acid excretion and lower plasma urate levels, carbohydrate tolerance is unaltered or improved, and lipid levels are unchanged. Electrolyte and metabolic effects of thiazide diuretics are blunted by addition of an ACE inhibitor.
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PMID:Side effects and metabolic effects of converting-enzyme inhibitors. 303 29

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


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