ARGININE VASOPRESSIN (AVP), POTASSIUM EXCRETION AND ACID BASE BALANCE

AVP是一种主要参与水运输的荷尔蒙。这一效果具有 已被证明是通过肾脏中受体的位置模拟来调节的 收集小管，即所谓的V2受体。这项拟议的研究旨在 确定精氨酸加压素(AVP)是否在血管紧张素转换酶中起生理学作用 维持正常人的钾和酸碱平衡。 具体地说，我们希望检验这样的假设：(A)AVP增加了 肾组织中刺激V2受体的钾和酸排泄 收集小管；(B)膳食钾负荷和胆酸铵 负荷刺激AVP的分泌，而膳食缺钾则有 相反的作用；和(C)缺钾会损害利钾作用 对AVP的反应，而饮食中的钾负荷增强了它。因此， 精氨酸加压素分泌的改变及其对肾脏的放大/抑制 行动被假定为以前未被认识到的机制， 在下列条件下维持钾和酸碱平衡 饮食中钾和酸的摄入量发生了变化。 为了验证这一假说，我们将在健康的 肾功能正常的受试者。首先，我们将确定AVP是否 增加尿钾排泄和远端尿酸的探讨 这些影响的机制(S)。第二，钾的作用 剥夺、钾负荷和代谢性酸中毒对AVP分泌的影响 将通过评估AVP分泌来评估急性 渗透性刺激。第三，钾过剩和钾的影响 剥夺对肾钾排泄和酸化反应的影响 生理剂量的AVP的输注将被评估。

AVP is a hormone primarily involved in water transport. This effect has been shown to be mediated by sitmulation of receptors in the renal collecting tubule, so-called V2 receptors. The proposed study is aimed to determine whether arginine vasopressin (AVP) plays a physiologic role in maintaining potassium and acid-base balance in normal human subjects. Specifically, we wish to test the hypothesis that (a) AVP increases both renal potassium and acid excretion by stimulating V2 receptors in the collecting tubule; (b) dietary potassium loading and ammonium cholrdie loading stimulate AVP secretion while dietary potassium deprivation has the opposite effect; and (c) potassium dperivation impairs the kaliuretic response to AVP, while dietary potassium loading enhances it. Thus, alterations in AVP secretion and amplificaiton/suppression of its renal actions are postulated as previously unrecognized mechanisms whereby potassium and acid-base balance are maintained under conditions where dietary intake of potassium and acid are altered. To test this hypothesis, we shall conduct a three-phase study in healthy subjects with normal kidney function. First, we shall determine if AVP increases potassium excretion and distal urinary acidification and explore the mechanism(s) of these effects. Second, the effect of potassium deprivation, potassium loading, and metabolic acidosis on AVP secretion will be assessed by evaluating AVP secretion in response to an acute osmotic stimulus. Third, the effect of potassium surplus and potassium deprivation on the renal potassium excretory and acidification response to the infusion of physiologic amounts of AVP will be assessed.