ALPHA(2)-ADRENERGIC RECEPTOR GENE POLYMORPHISM AND HYPERTENSION IN BLACKS

alpha(2)-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 u biquitous adrenoreceptors results in decreased neuronal norepinephrine release, vasodilation, a fall in blood pressure, platelet aggregation , increased sodium excretion, and decreased insulin release. We hypoth esized that defects in alpha(2)-adrenergic receptors, or postreceptor defects, could explain the increased prevalence of hypertension in bla cks. To test our hypothesis, we first determined whether or not a poly morphism of the alpha(2)-adrenergic receptor gene was associated with pathologic elevations in blood pressure in American blacks. Dra-I iden tified a restriction fragment-length polymorphism (RFLP) of 6.3 and 6. 7 kb of the alpha(2)-adrenergic receptor gene on chromosome 10 in huma ns. Of 227 patients studied, 13/107 hypertensive subjects were homozyg ous for the 6.3-kb allele, whereas only 3/120 normotensive volunteers were homozygotes (P = .008). When analyzed by race, 13/82 black hypert ensive subjects were homozygous for the 6.3-kb allele, whereas only 2/ 59 normotensive blacks were homozygous for the 6.3-kb alleles (P = .02 ). However, only 1/61 white normotensive and 0/25 white hypertensive s ubjects were homozygous for the 6.3-kb allele (P = 1.00). Ethnic varia tion among blacks may explain our findings. Alternatively, a genetic p olymorphism in, or near, the alpha(2)-adrenergic receptor on chromosom e 10 can contribute to the development of hypertension in blacks.