Beta-adrenergic receptor gene polymorphisms and cardiovascular reactivity to stress in Black adolescents and young adults

Abstract

Cardiovascular reactivity to stress and beta-adrenergic receptor (beta-AR) function may contribute to the development of hypertension. As Black Americans have an increased risk of hypertension, we evaluated associations between beta(1)-AR (Arg389Gly) and beta(2)-AR (Arg16Gly, Gln27Glu) gene variants and cardiovascular reactivity in 500 Black youth. Heart rate, preejection period, total peripheral resistance, and blood pressure reactivity were measured during cold and psychological stress. The Arg389Gly polymorphism in the beta(1)-AR was associated with preejection period reactivity in males but not in females. The Arg16Gly polymorphism in the beta(2)-AR was associated with diastolic blood pressure reactivity only during video game stress. An association between the Gln27Glu polymorphism in the beta(2)-AR and vascular reactivity depended on sex. Thus, specific patterns of associations emerged between genetic variations in beta-ARs and cardiovascular reactivity in young Blacks.

The Carotid Artery Atherosclerosis Burden and Its Relation to Cardiovascular Risk Factors in Black and White Africans with Established Rheumatoid Arthritis: A Cross-sectional Study

“…Indeed, in studies that included black and white populations, a different ethnic distribution of genetic polymorphisms that are associated with CVD, hypertension, and circulating lipid and CRP concentrations was found 55,56,57,58,59,60 . Further, specific patterns of associations between genetic variations in beta-adrenoreceptors and not only cold and but also psychological stress have been reported in young black individuals 61 . Finally, the potential importance of documented variations in CVD-related COX polymorphisms among white and black Americans 62 deserves further study.…”

Carotid baroreflex responsiveness in normotensive African Americans is attenuated at rest and during dynamic leg exercise

“…Although not measured in the current study, Ray and Monahan (2002) reported smaller changes in MSNA in response to lower-body negative pressure were associated with similar peripheral vascular responses in AA compared to CA, indicating potentially greater transduction from neural to end-organ responses. As well, other investigations have reported exaggerated pharmacologically-induced alpha-adrenergic responses in AA (Kelsey et al, 2010, 2012). A divergence between AAs and CAs in sympathetic vascular transduction is indeed an important consideration when comparing baroreflex control of blood pressure between groups.…”

“…Alpha-adrenergic receptor gene polymorphisms (Kelsey et al, 2012) and genetic variations in beta-adrenergic receptors (Kelsey et al, 2010) have recently been associated with cardiovascular reactivity among AAs. Additional mechanisms linked to risk for hypertension among AAs include elevated salt sensitivity (Sowers et al, 1988) via altered amiloride-sensitive epithelial sodium channel (ENaC) function (Ambrosius et al, 1999; Pratt et al, 2002), and small nuclear polymorphisms associated with blood pressure (Adeyemo et al, 2009; Fox et al, 2011).…”

Searching for genes involved in hypertension development in special populations: children and pre-eclamptic women. Where are we standing now?

“…Moreover in vitro this variant showed increased receptor down-regulation in response to β2 agonist exposure. In obese adolescents this polymorphism resulted in a lower probability of hypertension (p = 0.005) [51], whereas, when studied independently from obesity status, the same variant was associated with higher levels of SBP explaining 2.6% of the variance in European American youths [60] and with DBP reactivity to stress in black adolescents [61].…”