β2-Adrenergic receptor polymorphisms at amino acid 16 differentially influence agonist-stimulated blood pressure and peripheral blood flow in normal individuals

Hoit, Brian D.; Suresh, Damodhar P.; Craft, Laura P.; Walsh, Richard A.; Liggett, Stephen B.

doi:10.1016/s0002-8703(00)90099-1

Cited by 79 publications

(65 citation statements)

References 19 publications

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“…The Gly 16 Arg polymorphism is of particular interest as the Gly16 variant is associated with an attenuated vasodilatory response to catecholamines. 43 The frequency of this variant is markedly lower in blacks 44,45 but whether the presence of this variant is associated with differences in PRA remains to be seen.…”

Section: Renin-angiotensinogen Reactionmentioning

confidence: 96%

Why is plasma renin activity lower in populations of African origin?

Sagnella

2000

J Hum Hypertens

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Plasma renin activity is significantly lower in black people compared with whites independent of age and blood pressure status. The lower PRA appears to be due to a reduction in the rate of secretion of renin but the exact mechanistic events underlying such differences in renin release between blacks and whites are still not fully understood. Nevertheless, given the paramount importance of the renin-angiotensin system in the control of sodium balance, a most likely explanation is that the lower renin is a consequence of differences in renal sodium handling between blacks and whites. The lower PRA does not reflect differences in dietary sodium intake but the evidence available suggests that the low PRA could be part of the corrective mechanisms designed to maintain sodium balance in the presence of an increased tendency for sodium retention in black people. While it is possible that several factors may contribute to the reduced PRA, more recent investigation at

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Section: Renin-angiotensinogen Reactionmentioning

confidence: 96%

Why is plasma renin activity lower in populations of African origin?

Sagnella

2000

J Hum Hypertens

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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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“…As the functional implications of the Arg16Gly and Gln27Glu polymorphisms were revealed in vitro, their effects on the agonist-induced vasodilator response have also been investigated in vivo, and the results were controversial. 19,[20][21][22][23] Moreover, there was also no significant association detected between the blood pressure response to hydrochlorothiazide or atenolol and the Arg16Gly polymorphism in several studies. 24,25 An attenuation of b-adrenergic function and a potentiation of a-adrenergic function in cardiovascular tissues have been shown in hypertensive patients, suggesting the development of a postsynaptic a1 function dominance during the development and evolution of hypertension.…”

Section: Discussionmentioning

confidence: 94%

Arg347Cys polymorphism of α1A-adrenoceptor gene is associated with blood pressure response to nifedipine GITS in Chinese hypertensive patients

et al. 2009

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Our objectives were to evaluate whether polymorphisms in the a1A-and b2-adrenoceptor genes influence blood pressure response to nifedipine gastrointestinal therapeutic system (GITS). Hypertensive patients received daily treatment with an oral dosage of 30 mg nifedipine GITS for 16 days. Genotypes of the Arg347Cys polymorphism in the a1A-adrenoceptor gene and the Arg16Gly and Gln27Glu polymorphisms in the b2-adrenoceptor gene were determined by TaqMan single-nucleotide polymorphism genotyping assay. The sixteenth-day steady-state plasma concentration of nifedipine was measured using HPLC with UV detection. Multivariate linear regression was performed in a total of 447 patients to evaluate the effects of these polymorphisms on blood pressure response to nifedipine GITS. Patients carrying the Cys347 allele of the a1A-adrenoceptor gene had a greater systolic blood pressure reduction than did those carrying two Arg347 alleles of the a1A-adrenoceptor gene (32.5±14.0 versus 27.3±15.5 mm Hg, respectively, P¼0.006). However, diastolic blood pressure reduction was not associated with the Arg347Cys polymorphism in the a1A-adrenoceptor gene. In addition, no significant associations were observed between blood pressure reduction and two polymorphisms in the b2-adrenoceptor gene. Our data suggest that the Arg347Cys polymorphism in the a1A-adrenoceptor gene may be used to predict blood pressure response to nifedipine GITS in

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β2-Adrenergic receptor polymorphisms at amino acid 16 differentially influence agonist-stimulated blood pressure and peripheral blood flow in normal individuals

Cited by 79 publications

References 19 publications

Why is plasma renin activity lower in populations of African origin?

Why is plasma renin activity lower in populations of African origin?

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

Arg347Cys polymorphism of α1A-adrenoceptor gene is associated with blood pressure response to nifedipine GITS in Chinese hypertensive patients

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