VASOPRESSIN, POTASSIUM EXCRETION AND ACID-BASE BALANCE

AVP是一种主要参与水运输的激素。 这种效应 已经证明是通过刺激肾脏中的受体介导的 集合小管，也就是所谓的V2受体。 拟议的研究旨在 确定精氨酸加压素（AVP）是否在 维持人体内的钾和酸碱平衡。 我们特别 我想检验这样一个假设：（a）AVP增加肾钾 和通过刺激收集的V2受体的酸排泄 （B）膳食钾负荷和氯化铵负荷 刺激AVP分泌，而饮食缺钾则 相反的效果;和（c）钾剥夺将损害钾尿 对AVP的反应，就像它损害对AVP的水渗透反应一样。 AVP，而膳食钾负荷将增强它。因此， 在AVP分泌和放大/抑制其肾脏作用中， 被认为是钾和酸碱平衡的可能机制 可以维持的条件下，饮食摄入的钾和 酸被修改。 为了验证这一假设，我们将在健康人群中进行一项三阶段研究。 肾功能正常的受试者 首先，我们将确定AVP是否 增加钾排泄和远端尿酸化， 这些影响的机制。其次，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，前期钾素盈余和前期 缺钾对肾脏钾排泄和酸化的影响 将评估对生理量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.