Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Drugs classified as calcium channel blockers (CHBs) are now among the most frequently prescribed drugs for the treatment of cardiovascular disease. Although the currently available CCBs have major differences in their structural and cardiovascular effects, they share the common property of blocking the transmembrane flow calcium ions through voltage gated L-type channels. These drugs have been approved for the treatment of hypertensive heart disease: they reduce left ventricular hypertrophy and improve its sequelae, such as ventricular dysrhythmias, impaired filling and contractility, and myocardial ischemia. Long-acting CCBs have been shown to reduce mortality and morbidity in elderly patients with systolic hypertension, appear to be extremely useful in patients with cyclosporin-induced hypertension, and can be used as alternatives to ACE inhibitors in patients with hypertension and concomitant diabetes mellitus, renal disease, Raynaud's phenomenon or migraine. Long-acting dihydropyridine have been shown to be effective and safe in the treatment classic angina pectoris and vasospastic angina, supraventricular arrhythmias, particularly reentrant AV-nodal tachycardia, others to be beneficial in patients with congestive heart failure, and all of them have potential for decreasing atherogenesis.
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PMID:[Calcium channel blockers in the treatment of cardiovascular disease]. 1157 40

This review focuses on the different molecular genetic findings in migraine. Familial hemiplegic migraine (FHM) is a rare subtype of migraine with aura, which is inherited as an autosomal dominant. Half the cases of FHM are caused by point mutations in the CACNA1A gene on the short arm of chromosome 19 (19p). The gene encodes a calcium ion channel. Other mutation types cause episodic ataxia 2 (EA-2). Expansions of the CAG repeat in the 3' end bring about spinocerebellar ataxia 6 (SCA 6). Some families with FHM link to loci on the long arm of chromosome 1 (1q). The genes have not yet been identified. Some families neither link to 1q nor to 19p. Population-based family and twin studies have shown that migraine both with and without aura have a multifactorial inheritance. The CACNA1A gene may be of importance for ordinary forms of migraine in a few families. Mutations in genes on the X chromosome, dopamine receptor genes, and the ACE gene appear to be involved in migraine in a few families, whereas genes for nitric oxide synthase, serotonin receptors, and mitochondrial DNA do not seem to be involved. The positive associations have not been reproduced in other studies and therefore they should be interpreted with care. It is to be hoped that in the next few years much more will be known about the molecular genetic mechanisms of migraine with and without aura. FHM is an ion channel disorder, and many factors suggest that migraine is also an ion channel disorder, which is consistent with the paroxysmal nature of the illness.
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PMID:[Molecular genetic findings in migraine]. 1172 84

Angiotensin II type 1 receptor blockers belong to a novel class of cardiovascular agents that is characterized by excellent tolerance. The overall rate of their side effects is similar to that of placebo. Specific nonproductive cough is much less common during treatment with angiotensin II blockers compared with angiotensin converting enzyme inhibitors. Nevertheless serious side effects very rarely occur with angiotensin II blockers and include cough, angioneurotic edema, anemia, liver damage, renal failure, aggravation of angina and migraine. The data of current literature concerning adverse effects of angiotensin II in different clinical situations are extensively reviewed. Angiotensin II type 1 receptor blockers are not considered to be safe in pregnancy, bilateral renal artery stenosis and severe renal or hepatic impairment.
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PMID:[Adverse effects of angiotensin II type 1 receptor blockers ]. 1249 95

Patients with chronic daily headaches (CDH) bear similarities to drug or substance abuse patients, for whom genetic liability loci have been implicated. We reviewed papers dealing with the metabolic and the genetic aspects of CDH. The relative risk for CDH in first-degree relatives is 2.1- to 3.9-fold increased compared to the general population. Genetic variation at the dopamine receptor 2 has been associated with co-morbidity of migraine with aura with major depression and anxiety, and allele D of the angiotensin converting enzyme increases the frequency of migraine without aura attacks. In CDH, analgesic abuse was significantly associated with specific functional polymorphisms at the DRD 4 and at the dopamine transporter (DAT) genes, findings implicating dopamine-related genes in CDH with drug abuse. CDH carries a substantial genetic predisposition. Molecular genetic studies are, however, still few and preliminary.
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PMID:The genetics of chronic headaches. 1281 92

Treatment with ACE inhibitors has shown to be effective in the prophylaxis of migraine attacks. The aim of this study was to explore whether among hospitalized hypertensive patients use of ACE inhibitors may reduce the risk of headache caused by nitrates. To this end, we used the GIFA database, that includes patients admitted to academic medical centres throughout Italy. We studied 1537 patients (mean age 75 +/- 10 years) receiving treatment with nitrates during a hospital stay and diagnosed with hypertension. Headaches that had a probable or definite causal relation with nitrates use based on the Naranjo algorithm were considered for this analysis. Of the total enrolled sample, 762 patients (50%) used ACE inhibitors during hospital stay. Headache caused by nitrates was recorded in 12/762 (1.6%) ACE inhibitor users and in 24/775 (3.2%) other participants (P = 0.049). After adjusting for potential confounders, ACE inhibitors use was associated with a significantly lower risk of headache (OR 0.43; 95% Confidence Intervals: 0.20-0.90). This result was confirmed if ACE inhibitors use was compared with use of other antihypertensive agents (OR 0.44; 95% CI 0.20-0.95). In conclusion, this study suggests that among hypertensive subjects use of ACE inhibitors is associated with a reduced risk of headache caused by nitrates.
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PMID:Association between ACE inhibitors use and headache caused by nitrates among hypertensive patients: results from the Italian group of pharmacoepidemiology in the elderly (GIFA). 1461 32

Recently, several angiotensin I-converting enzyme (ACE) inhibitors and an angiotensin II receptor blocker were demonstrated to have a clinically important prophylactic effect in migraine. ACE is one of the key enzymes in the rennin-angiotensin-aldosterone system, which modulates vascular tension and blood pressure. In humans, serum ACE levels are strongly genetically determined. Individuals who were homozygous for the deletion (D) allele showed increased ACE activity levels. To investigate the role of ACE polymorphism in headache, we analyzed the ACE insertion (I)/deletion (D) genotypes of 54 patients suffering from migraine with aura (MwA), 122 from migraine without aura, 78 from tension-type headache (TH), and 248 non-headache healthy controls. The ACE D allele were significantly more frequent in the MwA than controls (p<0.01). The incidence of the D/D genotype in MwA (25.9%) was significantly higher than that in controls (12.5%; p<0.01; odds ratio=5.26, 95% confidence interval: 1.69-16.34, adjusted for age and gender). No differences in the remaining groups were found. Our results support the conclusion that the D allele and the D/D genotype in the ACE gene is a genetic risk factor for Japanese MwA. There seems to be a possible relationship between ACE activity and the pathogenesis of migraine.
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PMID:Association of the insertion/deletion polymorphism of the angiotensin I-converting enzyme gene in patients of migraine with aura. 1564 78

Migraine is a common form of the chronic headache syndromes. Although the pathogenesis of migraine still remains enigmatic, there have been remarkable progress in headache research. Point mutations of P/Q-type Ca2+ channel alpha 1 subunit (CACNA1A) gene have been identified in familial hemiplegic migraine (FHM), which linked to chromosome 19 (FHM-1, OMIM 141500). Na-K ATPase alpha2 gene has been identified as the causative gene for FHM linked to 1q21-23 (FHM-2, OMIM 602481). Common forms of migraine (i.e. migraine with and without aura) seems to be caused from multifactorial genetic factors and environmental factors. An association study of allelic variation at Codon 23 (Cys or Ser) of 5HT2C-R gene in Japanese samples revealed that the Ser allele frequency in migraine with aura was significantly higher than that in the non-headache controls. However, negative association of this polymorphism have been reported in Caucasian migrainures. The C677T allelic variation of 5,10-methylenetetrahydrofolate reductase (MTHFR) are focused on in association with the coronary heart diseases and the cerebrovascular diseases. The T allelic frequency in migraine sufferers was significantly higher than that in controls. The C677T mutation of MTHFR is one of the genetic risk factors for migraine. These observations are confirmed in Turkish, Australian and Spanish samples. Positive associations of angiotensin converting enzyme (ACE) gene, endotheline receptor-A (ET-A) gene, and insulin receptor gene have been reported. Using the genomewide screen technology, significant linkage between the migraine with aura and a marker on 4q24 has been reported in Finnish families. The genome wide screen analysis will be one of the powerful strategies on exploring migraine gene. Genetic study of migraine headache is a promised and fruitful field and will provide deep understanding to migraine headache. Discovery of new responsible or susceptible genes to migraine will also open an avenue to develop new therapeutic strategy of migraine.
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PMID:[An update on the familial headache syndromes]. 1565 39

Migraine, with and without aura (MA and MO), is a prevalent and complex neurovascular disorder that is likely to be influenced by multiple genes some of which may be capable of causing vascular changes leading to disease onset. This study was conducted to determine whether the ACE I/D gene variant is involved in migraine risk and whether this variant might act in combination with the previously implicated MTHFR C677T genetic variant in 270 migraine cases and 270 matched controls. Statistical analysis of the ACE I/D variant indicated no significant difference in allele or genotype frequencies (P > 0.05). However, grouping of genotypes showed a modest, yet significant, over-representation of the DD/ID genotype in the migraine group (88%) compared to controls (81%) (OR of 1.64, 95% CI: 1.00-2.69, P = 0.048). Multivariate analysis, including genotype data for the MTHFR C677T, provided evidence that the MTHFR (TT) and ACE (ID/DD) genotypes act in combination to increase migraine susceptibility (OR = 2.18, 95% CI: 1.15-4.16, P = 0.018). This effect was greatest for the MA subtype where the genotype combination corresponded to an OR of 2.89 (95% CI:1.47-5.72, P = 0.002). In Caucasians, the ACE D allele confers a weak independent risk to migraine susceptibility and also appears to act in combination with the C677T variant in the MTHFR gene to confer a stronger influence on the disease.
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PMID:Genetic variants of angiotensin converting enzyme and methylenetetrahydrofolate reductase may act in combination to increase migraine susceptibility. 1589 94

Recent advances in genetic analysis of migraine headache are reviewed. Point mutations of P/Q -type Ca2+ channel alpha1 subunit(CACNA1A) gene and Na-K ATPase, alpha2 (ATP1A2) gene have been identified in the familial hemiplegic migraine (FHM-1 and FHM-2, respectively). Mutations in notch-3 gene cause the cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), which is an autosomal dominant inherited disorder often accompanying with migraine like headache. Serotonin (5-HT) related genes, dopamine D2 receptors (DRD2) gene, methylenetetrahydrofolate reductase (MTHFR) gene, and angiotensin converting enzyme (ACE) gene have been noticed as the susceptible genes for migraine pathogenesis. Genetic study of migraine is promising and will provide further understanding of the migraine pathophysiology. Discovery of the responsible or susceptible genes will open an avenue to develop new therapeutic strategy.
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PMID:[Genetic analysis of migraine headache: a review]. 1621 82

Studies have shown that migraine may have a major genetic component. Meanwhile, angiotensin converting enzyme (ACE) gene has been implicated as a genetic factor associated with migraine. We designed a case-control study to investigate the association between ACE and migraine in 240 migraine patients and 200 healthy controls, matched by age and sex. There was no significant difference in allelic frequency (I and D) and genotype polymorphism (DD, DI and II) of the ACE gene in migraine patients and controls. Analysis of the difference in ACE polymorphism stratified by gender revealed that male migraine patients with the homozygote DD genotype (ACE-DD) were significantly fewer than that of male controls (OR = 0.331, p = 0.045). There was no existence of a difference among the frequency and duration of headache in each subgroup of migraine patients stratified by ACE genotype. Our findings indicate that ACE-DD may have a slight protective effect against migraine in male patients.
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PMID:Homozygous deletion genotype of angiotensin converting enzyme confers protection against migraine in man. 1625 13


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