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The gain-of-function G389R variant of the β1-adrenoceptor does not influence blood pressure or heart rate response to β-blockade in hypertensive subjects. / O'Shaughnessy, K.M.; Fu, B.; Dickerson, Claire; Thurston, D.; Brown, M.J.

In: Clinical Science, Vol. 99, No. 3, 2000, p. 233-238.

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@article{f8049703f1db4420831edc840d725e33,
title = "The gain-of-function G389R variant of the β1-adrenoceptor does not influence blood pressure or heart rate response to β-blockade in hypertensive subjects",
abstract = "Mutation scanning of the b1-adrenoceptor gene has identified a polymorphism, G389R, that markedly affects G-protein coupling of the receptor and resulting cAMP production. We have investigated the effect of this functionally active polymorphism on clinical response to b-adrenoceptor blockade. Two cohorts of untreated hypertensive patients randomly assigned to a b1-selective b-blocker at the start of antihypertensive therapy were studied retrospectively to see if the G389R polymorphism influenced the response in terms of blood pressure and heart rate. The blood pressure and heart rate responses to treatment were assessed 4 weeks later and compared with the G389R genotype, ascertained by PCR/restriction fragment length polymorphism. The falls in blood pressure and heart rate for the first group (n = 92) by genotype were: GG, 20.1±3.5/13.9±2.7 mmHg (systolic/diastolic blood pressure), 18.4±2.2 beats/min; GR, 20.0±2.2/15.0±1.3 mmHg, 16.5±1.5 beats/min; RR, 20.8±2.3/13.4±1.1 mmHg, 16.0±1.4 beats/min. For the second group (n = 55) the corresponding falls were: GG, 17.0±4.3/11.2±3.4 mmHg, 12.0±3.5 beats/min; GR, 16.6±1.8/14.4±1.1 mmHg, 13.1±2.1 beats/min; RR, 18.0±1.6/13.0±1.4 mmHg, 14.4±1.4 beats/min. The G389R genotype also failed to have a significant effect on pretreatment blood pressure or heart rate in either group. These data suggest that, despite clear functional differences between the G389R receptor variants expressed in vitro, the polymorphism does not affect the haemodynamic response of hypertensive subjects to chronic b1-adrenoceptor blockade.",
author = "K.M. O'Shaughnessy and B. Fu and Claire Dickerson and D. Thurston and M.J. Brown",
note = "Original article can be found at: http://www.clinsci.org/cs/099/cs0990233.htm Copyright The Biochemical Society and the Medical Research Society [Full text of this article is not available in the UHRA]",
year = "2000",
language = "English",
volume = "99",
pages = "233--238",
journal = "Clinical Science",
issn = "0143-5221",
publisher = "Portland Press Ltd.",
number = "3",

}

RIS

TY - JOUR

T1 - The gain-of-function G389R variant of the β1-adrenoceptor does not influence blood pressure or heart rate response to β-blockade in hypertensive subjects

AU - O'Shaughnessy, K.M.

AU - Fu, B.

AU - Dickerson, Claire

AU - Thurston, D.

AU - Brown, M.J.

N1 - Original article can be found at: http://www.clinsci.org/cs/099/cs0990233.htm Copyright The Biochemical Society and the Medical Research Society [Full text of this article is not available in the UHRA]

PY - 2000

Y1 - 2000

N2 - Mutation scanning of the b1-adrenoceptor gene has identified a polymorphism, G389R, that markedly affects G-protein coupling of the receptor and resulting cAMP production. We have investigated the effect of this functionally active polymorphism on clinical response to b-adrenoceptor blockade. Two cohorts of untreated hypertensive patients randomly assigned to a b1-selective b-blocker at the start of antihypertensive therapy were studied retrospectively to see if the G389R polymorphism influenced the response in terms of blood pressure and heart rate. The blood pressure and heart rate responses to treatment were assessed 4 weeks later and compared with the G389R genotype, ascertained by PCR/restriction fragment length polymorphism. The falls in blood pressure and heart rate for the first group (n = 92) by genotype were: GG, 20.1±3.5/13.9±2.7 mmHg (systolic/diastolic blood pressure), 18.4±2.2 beats/min; GR, 20.0±2.2/15.0±1.3 mmHg, 16.5±1.5 beats/min; RR, 20.8±2.3/13.4±1.1 mmHg, 16.0±1.4 beats/min. For the second group (n = 55) the corresponding falls were: GG, 17.0±4.3/11.2±3.4 mmHg, 12.0±3.5 beats/min; GR, 16.6±1.8/14.4±1.1 mmHg, 13.1±2.1 beats/min; RR, 18.0±1.6/13.0±1.4 mmHg, 14.4±1.4 beats/min. The G389R genotype also failed to have a significant effect on pretreatment blood pressure or heart rate in either group. These data suggest that, despite clear functional differences between the G389R receptor variants expressed in vitro, the polymorphism does not affect the haemodynamic response of hypertensive subjects to chronic b1-adrenoceptor blockade.

AB - Mutation scanning of the b1-adrenoceptor gene has identified a polymorphism, G389R, that markedly affects G-protein coupling of the receptor and resulting cAMP production. We have investigated the effect of this functionally active polymorphism on clinical response to b-adrenoceptor blockade. Two cohorts of untreated hypertensive patients randomly assigned to a b1-selective b-blocker at the start of antihypertensive therapy were studied retrospectively to see if the G389R polymorphism influenced the response in terms of blood pressure and heart rate. The blood pressure and heart rate responses to treatment were assessed 4 weeks later and compared with the G389R genotype, ascertained by PCR/restriction fragment length polymorphism. The falls in blood pressure and heart rate for the first group (n = 92) by genotype were: GG, 20.1±3.5/13.9±2.7 mmHg (systolic/diastolic blood pressure), 18.4±2.2 beats/min; GR, 20.0±2.2/15.0±1.3 mmHg, 16.5±1.5 beats/min; RR, 20.8±2.3/13.4±1.1 mmHg, 16.0±1.4 beats/min. For the second group (n = 55) the corresponding falls were: GG, 17.0±4.3/11.2±3.4 mmHg, 12.0±3.5 beats/min; GR, 16.6±1.8/14.4±1.1 mmHg, 13.1±2.1 beats/min; RR, 18.0±1.6/13.0±1.4 mmHg, 14.4±1.4 beats/min. The G389R genotype also failed to have a significant effect on pretreatment blood pressure or heart rate in either group. These data suggest that, despite clear functional differences between the G389R receptor variants expressed in vitro, the polymorphism does not affect the haemodynamic response of hypertensive subjects to chronic b1-adrenoceptor blockade.

M3 - Article

VL - 99

SP - 233

EP - 238

JO - Clinical Science

JF - Clinical Science

SN - 0143-5221

IS - 3

ER -