β₂-Adrenergic receptors (β₂-AR) contribute to cardiovascular regulation by influencing several functions and previous studies suggest that a decreased function of the β₂-AR may be involved in essential hypertension. β₂-AR are polymorphic and certain polymorphisms of these receptors are of functional importance. We focus here on the Arg¹⁶→Gly¹⁶ β₂-AR polymorphism, which shows enhanced agonist-promoted downregulation of the receptor and which, in two recent studies, yielded opposite results in terms of association with essential hypertension: an increased frequency of the Gly¹⁶ variant in African–Caribbean hypertensives and of the Arg¹⁶ variant in offspring of Norwegian white hypertensive parents. In the current study, we genotyped 243 subjects, including both African-American and white individuals, for codon 16 polymorphism and assessed blood pressure and cardiovascular function using impedance cardiography and pressor sensitivity to phenylephrine. We found similar patterns of cardiovascular function and expression of hypertension with the two genotypes of codon 16. There was no statistically significant difference in the overall allelic distribution of the two genotypes: among African-Americans, 51% of the hypertensives and 50% of the normotensives carried the Arg¹⁶ allele, whereas among the white subjects 40% of the hypertensives and 47% of the normotensives were carriers of the Arg¹⁶ allele. Although we observed a statistically significant increase in the Arg¹⁶/Gly¹⁶ heterozygotes in the African-American population, the Gly¹⁶ allele was not significantly increased in the African-Americans compared to whites. These findings indicate that the codon 16 polymorphisms are not associated with hypertension in a mixed American study population nor do they appear to substantially impact on a variety of hemodynamic variables.