We have recently shown that as hypertension develops in rats treated with DOCA-salt, vascular sodium pump (NaP) activity is first supressed, then elevated, and finally suppressed again in the established phase of hypertension. Such changes in vascular NaP activity could be the result of changes in levels of circulating factors affecting NaP activity, changes in density of vascular NaP molecules, or a combination. We propose studies to define the mechanisms responsible for changes in vascular NaP during development of DOCA-salt hypertension, and to determine the role of such changes. Therefore, we will determine in DOCA-salt hypertension if: 1) the plasma of rats at different stages of hypertension contain different levels of a humoral NaP effector: 2) the density of vasular NaP molecules are different at different stages of hypertension: 3) the changes in levels of a circulating humoral factor and/or changes in density of vascular NaP molecules are associated with the changes in vascular/extravascular fluid volumes during benign and malignant stages: 4) the changes in levels of a circulating humoral factor and/or changes in density of vascular NaP molecules are associated with levels of extracellular K+: and 5) integrity of the AV3V area in the brain is required for the mechanism responsible for the changes in vascular NaP activity. We also propose to examine these questions in other types of experimental hypertension such as the Goldblatt and genetic (New Zealand strain) models.
