19 下列何種情況，會造成腎小管的鉀離子分泌增加？

血漿中重碳酸鹽（bicarbonate）減少 血漿中二氧化碳分壓增加

遠端腎小管管腔液的流量增加 飲食中的鉀攝取量減少

分泌 secretion, getting rid off K

ans:

血漿中重碳酸鹽（bicarbonate）減少 -?

遠端腎小管管腔液的流量增加 - increase in GFR, cause less reabsoprtion in the thick ascending loop of henle, hence more secretion of k

these are the answers

d is definitely not the answer.

why?

Although small amounts of K+ are lost each day in stool (5 to 10 meq) and sweat (0 to 10 meq), the kidney plays the major role in the maintenance of K+ balance, appropriately varying K+ secretion with changes in dietary intake (normal range is 40 to 120 meq/day). The primary event in urinary K+ excretion is the secretion of K+ from the tubular cell into the lumen in the distal nephron, particularly in the principal cells in the cortical collecting tubule and in the cells in the adjacent connecting segment and outer medullary collecting tubule [1-3].

SEGMENTAL POTASSIUM HANDLING

The sequential handling of filtered K+ by the different nephron segments is depicted in the micropuncture experiments in Figure 1 (figure 1) [3,4]. The clearance of K+ is compared to that of inulin, which is filtered and then is neither reabsorbed nor secreted. As a result, a fall in the CK+/Cin ratio indicates that K+ has been removed from the tubular fluid (or reabsorbed), and an elevation in the ratio indicates that K+ has been added to the tubular fluid (or secreted). Almost all of the filtered K+ is reabsorbed in the proximal tubule and the loop of Henle, so that less than 10 percent of the filtered load is delivered to the early distal tubule (CK+/Cin <0.1). href="http://www.uptodate.com/patients/content/abstract.do?topicKey=%7EBWnhjv.1K79fOkh&refNum=5" class="abstractLink" style="color: rgb(51, 102, 51); text-decoration: underline; ">5], whereas reabsorption in the thick ascending limb of the loop of Henle is mediated by the Na+-K+-2Cl- carrier in the luminal membrane (figure 2) [2].

In comparison to these reabsorptive processes, K+ is secreted by the connecting segment, the principal cells in the cortical and outer medullary collecting tubule (figure 3), and the papillary (or inner medullary) collecting duct (as shown by the rising CK+/Cin ratio in figure 1) [1,3,6]. Secretion in these segments can be varied according to physiologic needs and is generally responsible for most of urinary K+ excretion.

Distal secretion can be partially counteracted by K+ reabsorption by the intercalated cells in the cortical and outer medullary collecting tubules [7,8]. This process may be mediated by an active H+-K+-ATPase pump in the luminal membrane, which results in both H+ secretion and K+ reabsorption (figure 4) [9-11]. The activity of this pump is increased with K+ depletion [9,11,12] and is reduced with K+ loading [13]. The former adaptation is probably responsible for the observation that net K+ reabsorption, not secretion, appropriately occurs in the distal nephron with K+ depletion [4,7,10]. Selective inhibition of the H+-K+-ATPase pump in the setting of K+ depletion abolishes distal K+ reabsorption