VASOPRESSIN, 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 已被证明是通过刺激肾脏中的受体来调节的 收集小管，即所谓的V2受体。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 人体内钾和酸碱的维持。具体来说，我们 想要验证这样的假设：(A)AVP增加了两个肾脏的钾 和通过刺激收集中的V2受体排酸 (B)膳食钾负荷和氯化铵负荷 刺激AVP的分泌，而饮食中缺钾有 相反的作用；和(C)缺钾会损害利尿剂 对AVP的反应，与它损害水渗透反应的方式大致相同 AVP，而膳食中的钾负荷会提高AVP。因此，更改 AVP的分泌及其对肾脏的放大/抑制作用是 被认为是钾和酸碱平衡的可能机制 可以在以下条件下保持：饮食中钾的摄入量和 酸是经过修饰的。 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 负荷、缺钾和代谢性酸血症对AVP分泌的影响 将通过血浆AVP分泌对渗透压的反应来评估 刺激。第三，优先补钾和优先补钾的效果 缺钾对肾脏钾排泄和酸化的影响 将评估对生理剂量AVP输注的反应。

AVP is a hormone primarily involved in water transport. This effect has been shown to be mediated by stimulation of receptors in the renal collecting tubule, so called V2 receptors. The proposed study aims to determine whether arginine vasopressin (AVP) plays a physiologic role in maintaining potassium and acid-base in human subjects. Specifically, we wish to test the hypothesis that (a) AVP increases both renal potassium and acid excretion by stimulation of V2 receptors in the collecting tubule; (b) dietary potassium loading and ammonium chloride loading stimulate AVP secretion while dietary potassium deprivation has the opposite effect; and (c) potassium deprivation will impair the kaliuretic response to AVP, much the same way it impairs the hydroosmotic response to AVP, while dietary potassium loading will enhance it. Thus, alterations in AVP secretion and amplification/suppression of its renal actions are postulated as possible mechanisms whereby potassium and acid-base balance can be maintained under conditions where dietary intake of potassium and acid are modified. 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. Secondly, the effect of potassium loading, potassium deprivation and metabolic acidemia on AVP secretion will be assessed by the response of plasma AVP secretion to an osmotic stimulus. Thirdly, the effect of prior potassium surplus and prior potassium deprivation on the renal potassium excretory and acidification responses to the infusion of physiologic amounts of AVP will be assessed.