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

AVP是一种主要参与水运的激素。这种作用已被证明是通过刺激肾集合小管中的受体，即所谓的V2受体介导的。本研究旨在确定精氨酸抗利尿激素（AVP）是否在维持正常人钾酸碱平衡中起生理作用。具体来说，我们希望验证以下假设：(a) AVP通过刺激集合小管中的V2受体增加肾钾和酸的排泄；(b)饲粮钾负荷和胆碱铵负荷刺激AVP分泌，而饲粮缺钾则相反；(c)钾缺乏会削弱AVP的尿钾反应，而膳食钾负荷会增强AVP的尿钾反应。因此，AVP分泌的改变及其肾脏作用的增强/抑制被认为是一种以前未被认识到的机制，在改变钾和酸的饮食摄入的情况下，钾和酸碱平衡得以维持。为了验证这一假设，我们将在肾功能正常的健康受试者中进行三期研究。首先，我们将确定AVP是否会增加钾排泄和远端尿液酸化，并探讨这些影响的机制。其次，通过评估急性渗透刺激下AVP的分泌，评估缺钾、钾负荷和代谢性酸中毒对AVP分泌的影响。第三，将评估钾过剩和钾剥夺对输注生理量AVP时肾脏钾排泄和酸化反应的影响。

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.