Physical mapping of autonomic/sympathetic candidate genetic loci for hypertension in the human genome: a somatic cell radiation hybrid library approach

β2Adrenergic Receptor GeneArg16GlyPolymorphism is Associated with Therapeutic Efficacy of Benazepril on Essential Hypertension in Chinese

“…The sympathetic nervous system plays a key role in both blood pressure regulation (32) and the pathogenesis of essential hypertension (33,34). Therefore, variants of ADRB2, a key mediator of the function of the sympathetic nervous system, may lead to altered levels of catecholamines and abnormal blood pressure levels (35). Prior studies have shown that ACE inhibitor treatment is accompanied by a reduction in circulating catecholamine levels (36,37).…”

Sympathetic Nervous System, Genes and Human Essential Hypertension

“…A region on chromosome 2 containing ADRA2B was found linked to early-onset EH in Scandinavians (Von Wowern et al, 2004;von Wowern et al, 2003), and also linked to BP among Nigerians (Cooper et al, 2002). By performing a genome scan in sibs and families, O'Conner's research group also assigned a cluster of SNS candidate loci to chromosome 5, which harbored several significant linkage peaks for BP (Chitbangonsyn et al, 2003). SNS candidate genes in this region include ADRB2, ADRA1A and DRD1.…”

Genetic Variation Within Adrenergic Pathways Determines In Vivo Effects of Presynaptic Stimulation in Humans

“…5,22 We hypothesized that such variants and their resultant genotypes may contribute to adrenergic responses and therefore to hypertension. Using exogenous tyramine infusion to induce a sympathetic response (by norepinephrine [NE] release) 23,24 in a local vascular bed, we found that tyramine induced dose-dependent vasoconstriction (Figure 2), and the response could be predicted by common (Ͼ10% minor allele frequency) genetic variation at multiple steps within the presynaptic adrenergic pathway (Table 2).…”

“…5 Previous emphasis has been on the postsynaptic ␤ 1 -and ␤ 2 -adrenergic receptors, although efforts to link hypertension to such single-nucleotide polymorphisms (SNPs) have yielded mixed results. 6,7 Thus, we currently focus on targeted polymorphisms in relation to local activity rather than disease state.…”