考古重點

1. TGF & GBF

2. Ang II

 Angiotensin II causes the kidneys to retain both salt and water in two major ways:
a. Angiotensin II acts directly on the kidneys to cause salt and water retention.
One major effect is to constrict the renal arterioles, thereby diminishing blood flow through
the kidneys. The slow flow of blood reduces the pressure in the peritubular capillaries, which
causes rapid reabsorption of fluid from the tubules.(chapter19)
First, efferent arteriolar constriction reduces peritubular capillary hydrostatic pressure,
which increases net tubular reabsorption, especially from the proximal tubules. Second,
efferent arteriolar constriction, by reducing renal blood flow, raises filtration fraction in the
glomerulus and increases the concentration of proteins and the colloid osmotic pressure in
the peritubular capillaries; this mechanism increases the reabsorptive force at the
peritubular capillaries and raises tubular reabsorption of sodium and water.
Angiotensin II directly stimulates sodium reabsorption in the proximal tubules, the loops of
Henle, the distal tubules, and the collecting tubules. One of the direct effects of angiotensin
II is to stimulate the sodium-potassium ATPase pump on the tubular epithelial cell
basolateral membrane. A second effect is to stimulate sodium-hydrogen exchange in the
luminal membrane, especially in the proximal tubule. A third effect of angiotensin II is to
stimulate sodium-bicarbonate co-transport in the basolateral membrane (Figure 28-18).
 b. Angiotensin II causes the adrenal glands to secrete aldosterone, and the aldosterone in turn
increases salt and water reabsorption by the kidney tubules.
 Change with pressure

3. ADH
 測 copeptin 的量檢測 ADH 的問題
 Set point: 275-290 mOsm/kg
 1%Posm 的改變可使 ADH 分泌量增加 7 倍=BP 或 ECF 的數值變化 5-10%
 

Receptor Location Function

V1a Extrarenal vasculature vasoconstricts
Prostaglandin synthesis↑(CD & interstitial cell)
Blood vessel
Vasa recta vasoconstricts
V1b
V2 Renal tubule (DCT & CD) Sodium reabsorption↑(CD→NKCC & TAL→ENaC)
Water and urea permeability↑(CD)
 AQP
Principle cell
利用 PKA→AQP2 & AQP3 表現量上升
4. ANP

5. 攝取高鈉>ECF 增加
 Activation of low-pressure receptor reflexes:右心房和肺臟
 Suppression of Ang II formation:藉由增加動脈壓和 ECF
 Stimulation of natriuretic systems:ANP
 Small increases in arterial pressure:藉由增加 ECF

6.
7.
Bartter syndrome is a rare but interesting condition that is due to defective transport in the thick ascending
limb. It is characterized by chronic Na+ loss in the urine, with resultant hypovolemia causing stimulation of
renin and aldosterone secretion without hypertension, plus hyperkalemia and alkalosis. The condition can be
caused by loss-of-function mutations in the gene for any of four key proteins: the Na–K–2Cl cotransporter,
the ROMK K+ channel, the ClC–Kb Cl – channel, or barttin , a recently described integral membrane
protein that is necessary for the normal function of ClC–Kb Cl – channels.
The stria vascularis in the inner ear is responsible for maintaining the high K + concentration in the scala
media that is essential for normal hearing. It contains both ClC–Kb and ClC–Ka Cl – channels. Bartter
syndrome associated with mutated ClC–Kb channels is not associated with deafness because the Clc–Ka
channels can carry the load. However, both types of Cl – channels are barttin-dependent, so patients with
Bartter syndrome due to mutated barttin are also deaf.
8. 組織電顯圖