α2-Adrenergic Receptor Gene Polymorphism and Hypertension in Blacks

α2-Adrenergic receptors are found on presynaptic neurons of the central and peripheral nervous systems, on blood vessels, on platelets, on adipocytes, and in the kidney and pancreas. Activation of these ubiquitous adrenoreceptors results in decreased neuronal norepinephrine release, vasodilation, a fall in blood pressure, platelet aggregation, increased sodium excretion, and decreased insulin release. We hypothesized that defects in α2-adrenergic receptors, or postreceptor defects, could explain the increased prevalence of hypertension in blacks. To test our hypothesis, we first determined whether or not a polymorphism of the α2-adrenergic receptor gene was associated with pathologic elevations in blood pressure in American blacks. Dra-I identified a restriction fragment-length polymorphism (RFLP) of 6.3 and 6.7 kb of the α2-adrenergic receptor gene on chromosome 10 in humans. Of 227 patients studied, hypertensive subjects were homozygous for the 6.3-kb allele, whereas only normotensive volunteers were homozygotes (P = .008). When analyzed by race, black hypertensive subjects were homozygous for the 6.3-kb allele, whereas only normotensive blacks were homozygous for the 6.3-kb alleles (P = .02). However, only white normotensive and white hypertensive subjects were homozygous for the 6.3-kb allele (P = 1.00). Ethnic variation among blacks may explain our findings. Alternatively, a genetic polymorphism in, or near, the α2-adrenergic receptor on chromosome 10 can contribute to the development of hypertension in blacks.