Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with hypertension requiring therapy frequently present with concurrent peripheral vascular disease (PVD). This situation must be taken into account for an optimum antihypertensive treatment. In general, in patients with PVD only a cautious and gradual lowering of the blood pressure is recommended, since the decrease in poststenotic perfusion pressure may accentuate the symptoms of occlusive disease. In intermittent claudication--the most frequent manifestation of occlusive disease beta--receptor blockers today are no longer considered to be contraindicated. In the presence of critical ischemia of the legs (pain at rest and/or necroses) beta blockers should only be given with extreme caution. The agents of choice are calcium antagonists, ACE -inhibitors as well as alpha blockers and some newer vasodilating substances (e.g. Carvedilol). Conventional diuretics show disadvantages. An slightly elevated blood pressure in critical leg ischemia helps to improve the poststenotic perfusion of the affected limb. Antihypertensive treatment should not be instituted in patients whose systolic blood pressure is lower than 160 mmHg.
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PMID:[Antihypertensive therapy in arterial occlusive disease]. 168 38

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

beta-Adrenoceptor blocking drugs are widely used throughout the world, and serious adverse reactions are relatively uncommon. Many of those that do occur, including bronchospasm and peripheral ischaemia, are due primarily to blockade of beta 2-adrenoceptors. Recently developed beta-blockers with enhanced beta 1-selectivity and partial beta 2-agonist activity appear, in general, to have lesser effects upon airways function and vascular resistance, but none are regarded as being entirely 'safe' in patients with asthma. In the treatment of hypertensive patients with co-existing airways disease there are now effective alternatives to the beta-blockers, including calcium antagonists, alpha-adrenoceptor antagonists and angiotensin converting enzyme (ACE) inhibitors. However, in the presence of ischaemic heart disease, beta-blockers have specific advantages and may still be considered necessary in patients with airways disease. In this situation, agents with beta 2-agonist activity are preferable to 'conventional' beta-blockers. However, there is still some risk that bronchospasm may occur in certain individuals, and the bronchodilator response to inhaled beta 2-agonists might be impaired. In patients with peripheral vascular disease, beta-blockers with beta 2-agonist activity are less likely to worsen the symptoms and signs of peripheral ischaemia, and may reduce the prevalence of peripheral coldness, a common adverse effect of beta-blockers. There is concern that beta-blockers may have significant central effects, including impairment of memory and concentration, although these are difficult to quantify. A number of pharmacologically unpredictable adverse reactions may occur rarely, including skin reactions, alopecia and arthropathy.
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PMID:Adverse reactions with beta-adrenoceptor blocking drugs. An update. 790 48

It is well documented that in the treatment of mild or moderate hypertension selective alpha 1-inhibitors such as doxazosin and prazosin lower blood pressure to approximately the same extent as beta-blockers, diuretics, ACE inhibitors and calcium antagonists. However, treatment with selective alpha 1-inhibitors is also associated with a number of other favourable effects. For example, in contrast to most beta-blockers, selective alpha 1-inhibitors have a favourable effect on serum lipids, primarily lowering the triglycerides but also increasing the ratio of high-density lipoprotein (HDL) cholesterol:total cholesterol. In addition, selective alpha 1-inhibitors do not aggravate glucose metabolism or increase uric acid concentration, as thiazide diuretics frequently do. Some patients gain particular benefit from treatment with a selective alpha 1-inhibitor, namely those with noninsulin-dependent diabetes mellitus, peripheral vascular disease, chronic obstructive pulmonary disease, and kidney failure. While no controlled mortality trials with selective alpha 1-inhibitors have yet been completed, new vasodilator drugs such as these do lower blood pressure in a more physiological manner than traditional antihypertensive agents, and appear to cause fewer side effects. In this respect, with the exception of patients with manifest or strongly suspected coronary heart disease who are not receiving beta-blocker treatment, selective alpha 1-inhibitors should be recommended as first-line agents for the treatment of hypertension.
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PMID:Selective alpha-1 inhibitors: first- or second-line antihypertensive agents? 790 30

Patients with mild to moderate hypertension require only a simple schedule of investigations, especially if there is a history of stroke or hypertension in first degree relatives. Tests are necessary to profile other cardiovascular risk factors and to detect target organ damage with only limited screening for secondary hypertension. Careful history, physical examination, repeated blood pressure measurements over months and measurements of body mass index, random cholesterol, routine blood chemistry and urinalysis using impregnated paper strips are all that are required. More detailed investigations can be reserved for special groups such as those with peripheral vascular disease or abnormal renal function before or after treatment with angiotensin converting enzyme inhibitors or significant proteinuria or hypokalaemia. Patients with essential hypertension who are smokers with lipid abnormalities may go on to develop superimposed renovascular disease. Severe hypertension at any age and especially if there is a reliable negative family history also merits special consideration. Resistance to antihypertensive treatment is more often due to non-compliance or non-steroidal anti-inflammatory drug use or alcohol abuse than to underlying secondary causes.
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PMID:Hypertension: investigation, assessment and diagnosis. 820 68

Celiprolol is a beta 1-selective adrenoceptor antagonist (beta-blocker) which acts as a weak agonist at beta 2-adrenoceptors. The drug demonstrates vasodilator properties and does not depress heart rate to the same extent as propranolol, atenolol or metoprolol. Celiprolol has shown equivalent antihypertensive efficacy to other beta-blockers, notably propranolol, atenolol, metoprolol and pindolol, in patients aged 18 to 75 years with mild to moderate essential hypertension. The drug has also shown similar antihypertensive efficacy to the angiotensin converting enzyme inhibitor enalapril and to combination diuretic therapy with hydrochlorothiazide and amiloride. Celiprolol was equally effective in adult patients of all ages, although no data are available for patients aged over 75 years. Data from a small number of clinical trials indicate celiprolol to be as effective as both propranolol and atenolol in improving work capacity and reducing the frequency of anginal attacks in patients with stable effort angina. However, the drug has not yet been evaluated in postmyocardial infarction patients. Celiprolol offers advantages over other beta-blockers, including reduction of peripheral vascular resistance and maintenance of resting heart rate, cardiac output and renal perfusion. The drug is also associated with improvements in plasma lipid profiles and does not appear to adversely affect carbohydrate metabolism or lung function, although its use in patients with reversible obstructive pulmonary disease is not recommended. Celiprolol is therefore a highly cardioselective beta-blocker with ancillary characteristics which are potentially useful in patients with hypertension and angina complicated by other conditions commonly associated with advanced age. These include impaired glucose tolerance or diabetes mellitus, peripheral vascular disease and hyperlipidaemia. The drug may also be preferred to other beta-blockers in patients in whom a reduction in heart rate would be particularly undesirable. Further long term (> 12 months) clinical trials and pharmacoeconomic data are now required to confirm the clinical relevance of the pharmacodynamic advantages of celiprolol therapy.
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PMID:Celiprolol. An evaluation of its pharmacological properties and clinical efficacy in the management of hypertension and angina pectoris. 857 93

Hypertension is one of the most important cardiovascular risk factors. Without therapy hypertension leads to stroke, coronary heart disease with angina pectoris and myocardial infarction, kidney failure and/or peripheral vascular disease. The association between blood pressure and these cardiovascular complications can be demonstrated over the entire blood pressure range. The risk of stroke, myocardial infarction, renal failure or peripheral vascular disease increases with increasing blood pressure. Additional cardiovascular risk factors such as hyperlipidemia, smoking and diabetes involve a further increase in risk. Today hypertension can be effectively treated. To that end, diuretics, betablockers, ACE-inhibitors or calcium antagonists can be used. Alpha receptor antagonists and angiotensin AT1 receptor antagonists are also of value. The antihypertensive effectiveness of these drugs is comparable but may vary in individual patients. During antihypertensive therapy, a reduction in cerebrovascular and cardiac complications has been demonstrated for alpha methyldopa, diuretics and betablockers. In these studies, fatal and non-fatal strokes were reduced by 42%, while the reduction in cardiac events was less pronounced (14%). The reasons for this greater efficacy of antihypertensive therapy in the cerebral circulation are not clear. Other risk factors may be particularly important in the pathogenesis of coronary artery disease (e.g. genetic factors, hyperlipidemia and others) or hypertensive vascular changes in the coronary circulation may not be as reversible as they are in the cerebral circulation. The well documented correlation between stroke, myocardial infarction and hypertension, as well as the proven efficacy of antihypertensive therapy in preventing cardiovascular events, underscores the importance of effective and sustained blood pressure control in these patients.
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PMID:[Heart, brain and hypertension]. 884 9

The aim of this study was to evaluate the prevalence of renal artery stenosis in patients with clinical signs of peripheral vascular disease and hypertension. One hundred patients, mean age 69 years (range 45-88) with symptoms and clinical signs of severe peripheral ischemia, underwent aortography to determine the degree of peripheral vascular disease and possible renal artery stenosis. History of claudication, and measurement of systolic distal blood pressure (BP) and calculation of the Ankle Brachial Index was used to define the severity of peripheral vascular disease. A total of 31% had renal artery stenosis (14% greater than 50% reduction in luminal diameter). In a subgroup of patients with hypertension and peripheral vascular disease (n = 74), 34% had renal artery stenosis. In the subgroup of patients with renal artery stenosis, 81% have hypertension. Patients with renal artery stenosis and lumen reduction of more than 50%, 93% have hypertension (P < or = 0.001). In conclusion this study shows that the combination of peripheral vascular disease and hypertension is an important clinical clue for renovascular disease. Examination for reno-vascular disease in this population should be considered, since the prevalence of the condition is high. Furthermore examination for renal vascular disease in this population is mandatory, before treatment with angiotensin converting enzyme (ACE) inhibitors is initiated, since treatment might lead to serious renal function impairment.
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PMID:Prevalence of renal artery stenosis in patients with peripheral vascular disease and hypertension. 886 60

The aim of this study was to evaluate the prevalence of renal artery stenosis in patients with clinical signs of peripheral vascular disease and hypertension. One hundred patients, mean age 69 years (range 45-88) with symptoms and clinical signs of severe peripheral ischaemia, underwent aortography to determine the degree of peripheral vascular disease and possible renal artery stenosis. History of claudication and measurement of systolic distal blood pressure and calculation of the Ankle Brachial Index was used to define the severity of peripheral vascular disease. Thirty-one percent had renal artery stenosis (14% greater than 50% reduction in luminal diameter). In a subgroup of patients with hypertension and peripheral vascular disease (n = 74), 34% had renal artery stenosis. In the subgroup of patients with renal artery stenosis, 81% had hypertension. Among patients with renal artery stenosis and lumen reduction of more than 50%, 93% had hypertension (p < 0.001). In conclusion this study shows that the combination of peripheral vascular disease and hypertension is an important clinical clue for renovascular disease. Examination for renovascular disease in this population should be considered, since the prevalence of the condition is high. Furthermore, examination for renal vascular disease in this population is mandatory, before treatment with angiotensin converting enzyme inhibitors is initiated, since treatment might lead to serious renal function impairment.
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PMID:[Occurrence of renal artery stenosis in patients with peripheral arteriosclerosis and hypertension]. 941 95

Ischemic renal disease (IRD) is defined as a clinically important reduction in glomerular filtration rate or loss of renal parenchyma caused by hemodynamically significant renal artery stenosis. IRD is a common and often overlooked clinical entity that presents itself in the setting of extrarenal arteriosclerotic vascular disease in older individuals with azotemia. Eleven to 14% of end-stage renal disease (ESRD) cases are attributable to chronic IRD. A high percentage of patients entering ESRD programs are hypertensive. Many patients with a presumed diagnosis of hypertensive nephrosclerosis actually have undiagnosed ischemic nephropathy as the etiology of their ESRD. It is important for the clinician to identify IRD, because IRD is a potentially reversible cause of chronic renal failure in a hypertensive patient. Atherosclerotic renal artery disease is common among patients with coronary artery disease and aortic and peripheral vascular disease. Atherosclerotic renal artery disease is a progressive disorder, and its progression is associated with loss of renal mass and functioning. A decrease in glomerular filtration rate sufficient to cause an elevation of the serum creatinine concentration requires injury to both kidneys. Consequently, IRD can arise from one of two main clinical situations: bilateral hemodynamically significant renal artery stenosis leading to bilateral renal ischemia; and hemodynamically significant renal artery stenosis in a solitary functioning kidney, or in a kidney that is providing the majority of a patient's glomerular filtration. The primary reason for establishing the diagnosis of IRD is the hope that correction of a renal artery stenosis will lead to improvement of renal function, or a delay in progression to ESRD. There are six major clinical settings in which the clinician could suspect IRD: acute renal failure caused by the treatment of hypertension, especially with angiotensin converting enzyme inhibitors; progressive azotemia in a patient with known renovascular hypertension; acute pulmonary edema superimposed upon poorly controlled hypertension and renal failure; progressive azotemia in an elderly patient with refractory or severe hypertension; progressive azotemia in an elderly patient with evidence of atherosclerotic disease; and unexplained progressive azotemia in an elderly patient. Noninvasive testing modalities that have been used recently include the angiotensin converting enzyme inhibitor renal scan, duplex Doppler sonography, magnetic resonance angiography, and the spiral computed tomography. Treatment methods include percutaneous transluminal angioplasty, endovascular stenting, and surgical revascularization. The results of treatment for preservation of renal function have been encouraging, with stabilization or improvement in renal function observed in a significant proportion of cases.
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PMID:Ischemic renal disease: an emerging cause of chronic renal failure and end-stage renal disease. 943 40


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