Adrenergic receptors are protein G-coupled receptors for catecholamines. Several groups of adrenergic receptors were discovered and cloned by now (α1, α2, β1, β2). β2 adrenergic receptors (ADRβ2) are considered to contribute (after stimulation) to pathogenesis of congestive heart failure and hypertension. The ADRβ2 intronless gene is located on human chromosome 5q31-32 and its protein is composed of: seven hydrophobic transmembrane domains, an extracellular amino terminus, three extracellular and three intracellular loops, with a small fourth loop before the palmitylation site. β2‑adrenergic receptors are cell surface receptors which activate adenylyl cyclase by coupling to guanine nucleotide binding proteins (G proteins). These receptors mediate vasodilation in response to adrenergic agonists in vascular smooth muscle and together with β1 take part in chronotropic and inotropic responses in healthy heart. β2 adrenergic receptors are also present on adrenergic nerve terminals in the heart, where they facilitate norepinephrine release. ADRβ2 gene is highly polymorphic. Several polymorphisms within it have previously been examined for the relationship with cardiovascular disease but the results are conflicting. We examined the A46G polymorphism of ADRβ2 which results in amino acid substitution (Gly for Arg at amino acid position 16) within the coding region. According to the literature the replacement of the arginin in codon 16 with glycin (Arg16Gly) makes the protein more susceptible to down-regulation in response to β2 agonists, may lead to decreased agonist-mediated in vivo vasodilatation and may modulate the cardiovascular risk. The aim of our study was to evaluate the influence of Arg16Gly polymorphism in an adrenergic receptor on the risk of MI among Polish, young (<45 years) population.

One hundred ninety five patients with documented myocardial infarction (MI) (age below 45 yrs.) not suffering from diabetes mellitus or hypertension were included into our study group. The control group contained 130 healthy voluntaries.

Genotype GG was predominant in studied group of patients in comparison to control group (40% vs 34%, P<0.05). Moreover, the wild type genotype AA was less frequent in patients suffering from MI compared to healthy voluntaries (14% vs 18%).

The polymorphism A46G (Arg16Gly) seems to play a role in enhancing the risk of premature MI and could be considered as a potential genetic risk factor in studied group of patients.

This work was support by Medical University grant no: 502-19-298

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