Analysis of an exon 1 polymorphism of the B2 bradykinin receptor gene and its transcript in normal subjects and patients with C1 inhibitor deficiency

Lung, Chien C.; Chan, Edward K. L.; Zuraw, Bruce L.

doi:10.1016/s0091-6749(97)70310-5

Cited by 60 publications

(64 citation statements)

References 29 publications

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“…Because the distribution of the B2 receptor polymorphisms depends on ethnicity (Lung et al, 1997), we have only recruited Caucasians in the study and have separately compared the respective German groups to rule out ethnical confounding. We have observed a loss of significance for atopic dermatitis and for the association of late onset asthma with the allele 2G in the German groups.…”

Section: B2 Receptor Polymorphisms and Childhood Asthma 887mentioning

confidence: 99%

Polymorphisms in the Bradykinin B2 Receptor Gene and Childhood Asthma

Kusser¹,

Braun²,

Praun³

et al. 2001

Biological Chemistry

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Section: B2 Receptor Polymorphisms and Childhood Asthma 887mentioning

confidence: 99%

Polymorphisms in the Bradykinin B2 Receptor Gene and Childhood Asthma

Kusser¹,

Braun²,

Praun³

et al. 2001

Biological Chemistry

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“…3 These studies have focused in a functional polymorphism described in exon 1 of the bradykinin type 2 receptor gene (BDKRB2), 4 in which the presence ( þ 9 bp) rather than the absence (À9 bp) of a 9-base pair sequence was associated with lower gene transcriptional activity. 5,6 If raised kinin activity is indeed vascular protective, we would anticipate that low bradykinin receptor activity, as marked by the þ 9 bp allele, would be associated with increased cardiovascular risk. According with these facts, the present study aimed to evaluate whether þ 9 bp/À9 bp polymorphism was associated with blood pressure (BP) variation on an admixture urban population.…”

mentioning

confidence: 99%

Insertion/deletion polymorphism of the bradykinin type 2 receptor gene influence diastolic blood pressure

et al. 2009

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“…Genotyping for the presence/absence of a 9-bp sequence, a 21 to 29 nonanucleotide variant (5Ј-GGTGGTGAC-3Ј) in a region of the 5Ј-untranslated sequence, 10 involved a radioactive-labeling/PCR technique. The assay was carried out in whole blood with the use of GeneReleaser (Bioventures) according to the manufacturer's recommendations.…”

Section: B2bkr ؉/؊ Genotype Determinationmentioning

confidence: 99%

“…The assay was carried out in whole blood with the use of GeneReleaser (Bioventures) according to the manufacturer's recommendations. Reagent concentrations in the 15-mL PCR reaction were 330 nmol/L each for sense (5Ј-CTG TTC CCG CCG CCA CTC CA-3Ј) and reverse (5Ј-CAG AGG TGA GGC GGC TGG AG-3Ј) primers, 10 166 mmol/L deoxynucleotide triphosphates, 3.0 mmol/L MgCl 2 , and 0.15 U of Taq polymerase. The sense primer was labeled at the 5Ј end with […”

Section: B2bkr ؉/؊ Genotype Determinationmentioning

confidence: 99%

“…A recent report implicating an association of an exon 1 polymorphism on B2BKR and bradykinin-induced angioedema in patients with C1-inhibitor deficiency, 10 as well as with the fact that angioedema is yet another side effect of ACEIs, strongly raises the possible involvement of B2BKR genotype in the underlying ACEI-induced cough mechanism and the clinical manifestations associated with ACEI treatment.…”

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confidence: 99%

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Three Candidate Genes and Angiotensin-Converting Enzyme Inhibitor–Related Cough

et al. 1998

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Abstract-Unexplained, persistent cough limits the use of angiotensin-converting enzyme (ACE) inhibitors in a significant number of patients. It has been speculated that occurrence of this adverse effect is genetically predetermined; in particular, variants of the genes encoding ACE, chymase, and B2-bradykinin receptor have been implicated. To investigate this question, we determined genotypes for common polymorphisms for these three genes in subjects with a history of ACE inhibitor-related cough. Specificity of the adverse effect was confirmed by a blinded, double-crossover design protocol in which subjects were rechallenged with either lisinopril or placebo. Key Words: angiotensin-converting enzyme inhibitors Ⅲ cough Ⅲ angiotensin-converting enzyme Ⅲ chymase Ⅲ receptors, bradykinin Ⅲ polymorphism Ⅲ genetics A ngiotensin-converting enzyme inhibitors are widely used for the treatment of hypertension and are presently the uncontested drugs of choice for the treatment of congestive heart failure.1 The major adverse effect encountered with ACEI treatment, and the most frequent reason for withdrawal of the drug, is a persistent, dry (nonproductive) cough.2,3 So far, no specific risk factors or patient characteristics that would predict the occurrence of this cough have been identified, and the underlying mechanism remains unclear; however, it has been speculated that the kininogen-kinin (bradykinin) system may be involved: inhibition of ACE may result in a local accumulation of bradykinin, which in turn may lead to the activation of proinflammatory peptides (eg, substance P, phospholipase C and/or A 2 , prostaglandins, neuropeptide Y) and to local release of histamine in the airways.2,3 Because cough is a class effect of ACEIs, and because its occurrence is not predicted by any external factors, it seems reasonable to suspect that a primary, genetically determined characteristic resulting in alteration of drug action or drug metabolism may be responsible. 4A prime candidate for a protein that might interact differentially with ACEIs on the basis of genetic variation is, of course, ACE itself. Thus, the I/D polymorphism of ACE has recently been proposed as possibly being involved in ACEIinduced cough, 4-6 a speculation fueled by the observation that the incidence of cough among patients under ACEI treatment is roughly similar to the proportion of the population that is homozygous for the ACE insertional allele (about 15% to 20%).More recently, a possible link between ACEI treatmentassociated adverse effects and chymase has also been suggested: as chymase represents an alternative pathway for the activation of angiotensin II, it is possible that ACE inhibition may lead to an increased biological significance of this enzyme. Release of chymase from mast cells results in a range of profound proinflammatory changes; in the dermis, this is associated with skin rashes, whereas in the lungs bronchial and pulmonary infiltration with inflammatory cells and altered regulation of vasoactive peptides 7,8 are observed. A recent re...

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Analysis of an exon 1 polymorphism of the B2 bradykinin receptor gene and its transcript in normal subjects and patients with C1 inhibitor deficiency

Cited by 60 publications

References 29 publications

Polymorphisms in the Bradykinin B2 Receptor Gene and Childhood Asthma

Polymorphisms in the Bradykinin B2 Receptor Gene and Childhood Asthma

Insertion/deletion polymorphism of the bradykinin type 2 receptor gene influence diastolic blood pressure

Three Candidate Genes and Angiotensin-Converting Enzyme Inhibitor–Related Cough

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