β-2 Adrenergic Receptor Variants Affect Resting Blood Pressure and Agonist-Induced Vasodilation in Young Adult Caucasians

Gratze, Gerfried; Fortin, Jürgen; Labugger, Ralf; Binder, A.; Kotanko, Peter; Timmermann, Bernd; Luft, Friedrich C.; Hoehe, Margret R.; Skrabal, F.

doi:10.1161/01.hyp.33.6.1425

Cited by 148 publications

(105 citation statements)

References 29 publications

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“…The findings demonstrate that the subjects carrying the Gly16 allele could have leptin resistance as well as blunted leptin-mediated plasma NE responses (sympathetic nerve activation). Further, the Gly16 allele has been described as a down-regulator of β2-adrenoceptor function (15,(38)(39)(40)(41). Thus, we could propose that a blunted β2-adrenoceptor function (15) and leptin resistance might be possible mechanisms in weight gain and BP elevation in obese subjects carrying the Gly16 allele of Arg16Gly, β2-adrenoceptor polymorphisms.…”

Section: Trp64argmentioning

confidence: 96%

.BETA.2- and .BETA.3-Adrenoceptor Polymorphisms Relate to Subsequent Weight Gain and Blood Pressure Elevation in Obese Normotensive Individuals

et al. 2006

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Section: Trp64argmentioning

confidence: 96%

.BETA.2- and .BETA.3-Adrenoceptor Polymorphisms Relate to Subsequent Weight Gain and Blood Pressure Elevation in Obese Normotensive Individuals

et al. 2006

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“…The β2AR polymorphisms accounted for ∼2% of the observed variation in blood pressure (Bray et al 2000). While results of some groups confirmed the association between the 16Gly allele and blood pressure (Kotanko et al 1997;Rosmond et al 2000;Gratze et al 1999), others found opposite effects, i.e., an association between the 16Arg allele and hypertension (Busjahn et al 2000;Bengtsson et al 2001a,b;Timmermann et al 1998) or no effects at all (Herrmann et al 2002;Kato et al 2001;Xie et al 2000; for a recent meta-analysis see Hahntow et al 2006). Again, differing inclusion of haplotypes, variations in ethnicities and different study designs may contribute to these sobering results.…”

Section: Genetic Variants In β-Adrenoceptor Genesmentioning

confidence: 98%

Genetics of arterial hypertension and hypotension

Rosskopf

Schürks

Rimmbach

et al. 2007

Naunyn-Schmied Arch Pharmacol

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Human hypertension affects affects more than 20% of the adult population in industrialized countries, and it is implicated in millions of deaths worldwide each year from stroke, heart failure and ischemic heart disease. Available evidence suggests a major genetic impact on blood pressure regulation. Studies in monogenic hypertension revealed that renal salt and volume regulation systems are predominantly involved in the genesis of these disorders. Mutations here affect the synthesis of mineralocorticoids, the function of the mineralocorticoid receptor, epithelial sodium channels and their regulation by a new class of kinases, termed WNK kinases. It has been learned from monogenic hypotension that almost all ion transporters involved in the renal uptake of Na + have a major impact on blood pressure regulation. For essential hypertension as a complex disease, many candidate genes have been analysed. These include components of the reninangiotensin-aldosterone system, adducin, β-adrenoceptors, G protein subunits, regulators of G protein signalling (RGS) proteins, Rho kinases and G protein receptor kinases. At present, the individual impact of common polymorphisms in these genes on the observed blood pressure variation, on risk for stroke and as predictors of antihypertensive responses remains small and clinically irrelevant. Nevertheless, these studies have greatly augmented our knowledge on the regulation of renal functions, cellular signal transduction and the integration of both. Together, this provides the basis for the identification of novel drug targets and, hopefully, innovative antihypertensive drugs.

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“…Specifically, studies have shown that b 1 -AR genotype is a significant predictor of blood pressure and ejection fraction responses to b-blockers, [4][5][6][7][8] and responses to b 2 agonists have been associated with b 2 -AR polymorphisms. 9,10 Dobutamine is a potent synthetic intravenous inotrope that is principally an agonist at b 1 -AR with mild stimulatory effects at b 2 -AR and a 1 -AR. A recent study in healthy volunteers pretreated with atropine showed that b 1 -AR codon 389 genotype was associated with greater contractile and systolic blood pressure (SBP) response to dobutamine.…”

Section: Introductionmentioning

confidence: 99%

β-Adrenergic receptor gene polymorphisms and hemodynamic response to dobutamine during dobutamine stress echocardiography

et al. 2008

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Our objective was to determine if b 1 -adrenergic receptor (b 1 -AR) and b 2 -AR gene polymorphisms influence heart rate (HR), systolic blood pressure (SBP) and diastolic blood pressure (DBP) response to dobutamine during dobutamine stress echocardiography (DSE). Patients (n ¼ 163) undergoing clinically indicated DSE were enrolled. Dobutamine doses were titrated from 5 to 40 mg kg À1 min À1 at 3 min intervals and HR, SBP and DBP were measured. Genotypes were determined for b 1 -AR Ser49Gly, b 1 -AR Arg389-Gly, b 2 -AR Arg16Gly and b 2 -AR Gln27Glu polymorphisms by polymerase chain reaction-restriction fragment length polymorphism analysis, pyrosequencing and single primer extension methods. b 2 -AR Glu27 homozygotes had a greater HR response at the highest dobutamine dose than Gln27 carriers (P ¼ 0.002). b 2 -AR Gly16 homozygotes had a lower HR response during 5-30 mg kg À1 min À1 of the dobutamine infusion protocol compared to Arg16 carriers (P ¼ 0.03). Differences in SBP by b 2 -AR codon 16 genotype and DBP by b 1 -AR codon 389 genotype were found at baseline and were maintained throughout DSE (P ¼ 0.06 and 0.02, respectively). However, the magnitude of SBP and DBP response to dobutamine did not differ significantly by b 2 -AR codon 16 or b 1 -AR codon 389 genotypes, respectively. These data suggest that the four selected b 1 -and b 2 -AR polymorphisms do not substantially influence the magnitude of hemodynamic response to dobutamine during DSE.

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β-2 Adrenergic Receptor Variants Affect Resting Blood Pressure and Agonist-Induced Vasodilation in Young Adult Caucasians

Cited by 148 publications

References 29 publications

.BETA.2- and .BETA.3-Adrenoceptor Polymorphisms Relate to Subsequent Weight Gain and Blood Pressure Elevation in Obese Normotensive Individuals

.BETA.2- and .BETA.3-Adrenoceptor Polymorphisms Relate to Subsequent Weight Gain and Blood Pressure Elevation in Obese Normotensive Individuals

Genetics of arterial hypertension and hypotension

β-Adrenergic receptor gene polymorphisms and hemodynamic response to dobutamine during dobutamine stress echocardiography

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