Decreased beta2 adrenergic mediated venodilatation in Native Americans

A considerable body of research has been accumulated regarding the pathogenesis and treatment of hypertension in Whites (Caucasians) and in Blacks. This research has led to more effective therapies geared specifically towards these ethnic groups. Unfortunately, very little information is available regarding the pathogenesis of hypertension and the effect of antihypertensive treatment in Native Americans (North-American Indians). Ethnic variability in the response to adrenergic mediated stimulation has been previously described, and reduced compliance of the venous system has been suggested among the possible mechanisms responsible for essential hypertension. The aim of this study was to compare venous responsiveness between Native Americans and Whites to vasoactive substances.

The alpha1-adrenergic agonist, phenylephrine and the beta2-adrenergic agonist isoproterenol were studied in 10 Native American and White volunteers. The dorsal hand vein technique was used, which is a simple, relatively non-invasive method to study the response to vasoactive substances, in vivo.

The maximal venodilatory response to isoproterenol in the Native American group was 53.2+/-27.5%; while in the White group it was 103.4+/-66.0% (p<0.05). The maximal venoconstriction for phenylephrine in the Native American subject group was similar to that of the White group (85.4+/-24.0% vs. 89.4+/-10.9%) (p = n.s.).

Based on our findings, we can anticipate that Native Americans may respond differently to antihypertensive therapy. However, further investigation needs to be done with an eye towards the development of drug therapy and treatment strategies tailored to this specific population.