Ethnic differences in stress induced sodium regulation and blood pressure

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DESCRIPTION (provided by applicant) Essential hypertension has reached epidemic proportions in the African American (AA) community. Differences in the ability to regulate sodium adequately in a high salt environment and differences in stress have been hypothesized to contribute to the differences in essential hypertension between AAs and European Americans (Eas). The objective of Project 2 is to study the interactive relationship between salt and stress in the development of the ethnic differences in essential hypertension. The general hypothesis of this proposal is as follows: AAs compared to EAs are genetically predisposed to show slower natriuresis during and following stress due to differences in the regulation of vasoactive and volume regulatory agents. This results in extended periods of elevated blood pressure. The increased blood pressure load leads to the early development of preclinical disease states. Therefore, the first three aims of the study are to contrast AAs and EAs before, during, and two hours following a 60 minute behavioral challenge on changes in sodium handling (Aim 1), hemodynamic functioning (Aim 2), and vasoactive and volume regulatory agents of the sympathetic nervous system, the renin-angiotensin-aldosterone system, and the endothelial system (Aim 3). The fourth aim of the study is to relate the response patterns to preclinical disease states of the heart (left ventricular mass), kidneys (micro albumin), and vasculature (pulse wave velocity, endothelial dependent vasodilation). The fifth aim of the study is to determine if the response pattern observed during laboratory testing is associated with blood pressure functioning during ambulatory testing. The final aims of the study are to determine the genetic polymorphism(s) associated with the hemodynamic change in blood pressure following stress. The proposed study will contribute significantly to the understanding of how salt and stress interact in the development of hypertension in AAs.