VASCULAR NA PUMP ACTIVITY AND HYPERTENSION

我们最近的研究表明，当高血压发生在用 DOCA盐，血管钠泵（NaP）活性首先受到抑制，然后 最后，又在既定的阶段被压制， 高血压 血管NaP活性的这种变化可能是 影响NaP活性的循环因子水平的变化， 血管NaP分子的密度，或其组合。 我们建议进行研究，以确定负责变化的机制， DOCA盐性高血压发展过程中的血管NaP，并确定 这种变化的作用。 因此，我们将在DOCA盐中确定 高血压，如果： 1)处于高血压不同阶段的大鼠血浆中含有不同的 体液NaP效应物的水平： 2)不同时期血管NaP分子密度不同 高血压： 3)循环体液因子水平的变化和/或 血管NaP分子密度的变化与 良性和恶性阶段的血管/血管外液体体积： 4)循环体液因子水平的变化和/或 血管NaP分子的密度与 胞外K+：和 5)该机制需要大脑中AV 3V区域的完整性 负责血管NaP活性的变化。 我们还建议在其他类型的实验中研究这些问题。 高血压，如Goldblatt和遗传（新西兰株）模型。

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.