Tubular Function and Electrolyte Balance

which tubular activity is bigger? reabsorption or secretion

reabsorption bc kidneys filter large amount of plasma (200L) but only 2L becomes urine

If: Inulin has a plasma concentration of 4mg/100ml, and inulin appears in the urine at 12mg/min, what is the clearance rate of inulin (in ml/min)?

300ml/min bc for if 100ml has 4mg

• 12 ÷ 4 = 3

• 300L for 12 mg

structure of proximal tubules for reabsorption

inside lined with villi = increase surface area = increases absorption

most important solute to be reabsorbed

sodium bc without sodium we wouldn’t reabsorb anything

how is Na+ reabsorbed

1. Na+ diffuses from filtrate into proximal tubule

2. Na+/K+ pumps on basolateral membrane of proximal tubule

3. Na+ actively pumped into interstitial fluid

4. Na+ moves into pertubular capillaries via starling forces

what does reabsorption of Na+ cause for anions

Na+ movement creates electrochemical gradient = anion (neg) follows Na+ = reabsorbed

• e.g anion = Cl-

how is water reabsorbed

Na+ and anion reabsorption creates osmotic gradient = water moves from filtrate (low solute concentration) into extracellular fluid (high solute con)

relationship between water and Na+ in proximal tubule

intrinsically linked so can’t absorb more Na+ and less water

reabsorption of K+, Ca2+ and urea

after Na+ and water reabsorption = concentration of K+, Ca2+ and urea increase in filtrate = concentration gradient = permeable solutes reabsorbed by diffusion

overview of reabsorption steps

1. Na+ reabsorbed - involves ATP in pump

2. anions follow Na+ - electrochemical gradient

3. water then follows - osmotic gradient

4. permeable substances - concentration gradient

what is reabsorbing substances from proximal tubule

peritubular capillaries - extension of efferent arteriole

Which of these solutes are actively reabsorbed? 1. amino acids 2. glucose 3. sodium 4. lactate

all of them

glucose reabsorption

1. Na+ uses SGLT co-transporter to pull glucose against concentration gradient from filtrate into proximal tubule cells

2. glucose enters interstitial fluid via GLUT facilitated diffusion

3. Na+ actively pumped out by Na+/K+-ATPase pump

how much of glucose in filtrate is reabsorbed under normal conditions

100% is reabsorbed = no glucose in urine

how does diabetes affect Na+ reabsorption and glomerular capillaries

increased blood glucose = increase glucose reabsorb = bc glucose needs Na+ to reabsorb Na+ reabsorb also increases = mascula densa detects decreased NaCl- and thinks GFR is low = dilates afferent arteriole = increase glomerular capillary pressure too high = damages capillaries

how does SGLT-2 inhibitors help both diabetes and too much Na+ reabsorption

bc SGLT-2 is used to transport glucose with Na+ inhibiting them decreases glucose and Na+ reabsorption to more normal levels

Glucose appears in the diabetics urine because diabetes?

1. reduces Na/K ATPase activity

2. reduces Na/gluc cotransport

3. reduces GLUT activity

4. none of the above

none of above bc increase blood glucose increases glucose reabsorption until SGLT co-transporters becomes saturated = some glucose left in urine

tubular maximum

highest rate renal tubules can reabsorb or secrete a specific substance

• reached when transporters are saturated = can’t reabsorb anymore

reabsorption of bicarbonate (HCO3-)

1. proximal tubule cell secretes H+ into filtrate via Na+/H+ exchanger

2. H+ and bicarbonate form CO2 and water via carbonic anhydrase

3. CO2 diffuses into proximal cell

4. inside CO2 combines with water so split into H+ and bicarbonate by carbonic anhydrase

5. bicarbonate reabsorbed into blood

6. H+ reused to repeat process

almost 100% bicarbonate reabsorbed

ischemia

where reduced blood flow restricts oxygen and nutrients to organs and tissues

effects of aldosterone in collecting duct

increases Na+ absorption from duct by

• increase activity of Na+/K+ pump

• adds epithelial sodium channels (ENaCs) to luminal membrane = pulls Na+ from filtrate

• increase activity of hydrogen ATPase on luminal membrane = secrete H+ into filtrate = prevent from becoming too acidic

problem of increasing sodium/potassium pump in collecting duct

K+ builds up in collecting tubule cells - fixed by having potassium channel secreting K+ into filtrate

hyperaldosteronism

adrenal glands make too much aldosterone

• increases Na+ and water reabsorption = increase blood volume = increase blood pressure

• increase K+ secretion = hypoalemic

• H+ increase = alkalotic pH

sodium balance

• sodium input = diet

• output = urine (main), faeces and sweat (small)

output needs to match input

positive sodium balance

Na+ input is greater than Na+ output = increased Na+ retention = increased water retention = increase body weight

negative sodium balance

Na+ output is greater than input = increased Na+ and water loss = decrease body weight

Infusion of 1 L of normal saline will cause a change in blood volume of :

1. 1 L

2. 0.5 L

3. 0.25 L

4. 0.1 L

5. <0.1 L

0.25L bc saline is isotonic = stays in extracellular fluid and plasma only makes up 25% of ECF

which receptors detect sodium balance

• carotid baroreceptors

• renal arterial pressure receptors

• cardiac atrial baroreceptors

bc Na+ effects blood volume - monitor blood volume or pressure

where does fine tuning of Na+ reabsorption occur

collecting ducts as Na+ and water are reabsorbed thru separate methods

what triggers renin-angiotensin system

renin release triggered by volume depletion bc

• decreased pressure at afferent arteriole - detected by pressure receptors in vessel

• reduced NaCl- at macula densa

• SNS activation