Controlling volume

Question 1

What can the lowering of arterial BP induce?

Answer 1

A sympathetic response: which re-increases the heart rate, secretes renin and constricts bloodflow in non-vital areas

Question 2

Name 4 likely places to get an edema (if one is to occur)

Answer 2

Gravity: abdomen (ascites), legs, ankles, lower back

Question 3

What is the principal solute in the ECF? Which major ion must be controlled to maintain volume?

Answer 3

Sodium chloride, sodium is main ion that needs to be recovered

Question 4

Which channel is in all basolateral membranes? What differs on the apical/luminal membrane?

Answer 4

Na-K-ATPase

sodium transporters differ on luminal membrane

Question 5

What do diuretics do?

Answer 5

Increase sodium and water secretion

Question 6

Name 4 targets for diuretics and which diuretic you would prescribe depending on the target

Answer 6

1. ENaC channels: amiloride
2. Na/K/Cl co transporter: loop diuretics
3. Na/Cl transporter: thiazides
4. Aldosterone receptors: aldosterone antagonists

Question 7

What is the significance of the ROMK channels and where are they? Which type of diuretic affects them?

Answer 7

Thick ascending LOH/early DCT

Luminal membrane: Transport K+ into filtrate, driven by gradient generated by Na-Cl-K cotransporter (bringing ions into cell)

Loop diuretics (furosemide) target Na-2Cl-K cotransporter and ROMK (indirectly)

Question 8

Which luminal channel resorbs Na and Cl from the filtrate in the DCT? Which diuretic targets this?

Answer 8

NCC channels, thiazide diuretics

Question 9

Describe the channels present on the luminal membrane of principal cells of the DCT/CT, which diuretic can they be targeted by?

Answer 9

Luminal: Na-K ATPase
ENac channels: Na+ into cell
K+ channels: secretion

*AMILORIDE (targeting ENac also reduces K+ secretion)

Question 10

What is the primary role of alpha intercalated cells and how are they related to principle cells?

Answer 10

Acid-base balance, (secrete H+ into filtrate and resorb more HCO3-)

Use K+ gradient from Na-K ATPase in principle cells to drive H/K antiport -> H+ into filtrate

In cell: H20 and CO2 (metabolic) form H2CO3 (carbonic anhydrase) -> dissociates into H+ and HCO3

• H+ to filtrate via H+ATPase
• HCO3- into blood

Question 11

Explain the RAAS system

Answer 11

Macula densa sense low Na+ in DCT -> prostaglandins to JG (and lacis cells) -> renin; converts angiotensinogen (from liver) -> angiotensin I

Angiotensin I –ACE (produced by lungs)–> Angiotensin II, triggers

1. vasoconstriction
2. Aldosterone (adrenal) -> increases Na and water resorption
3. thirst

-> Increase BP

Question 12

What are the 3 triggers for renin?

Answer 12

Low BP, Low Na+ in the DCT, Sympathetic response

Question 13

What is a sodium appetite, which population is it prevalent in?

Answer 13

Physiological mechanism to get salt into body if [Na+] ECF too low

*elderly with dementia

Question 14

What hormone does the opposite to renin?

Answer 14

High BP/CVP: atrial cells -> ANP -> more Na+ and water excretion

Question 15

Explain the brief cycle that occurs when a healthy person ingests salts?

Answer 15

ECF osmolarity increased-> increases BP (via osmosis and by triggering thirst)

RAAS inhibited, ANP released
-> extra water and sodium excreted

Question 16

What is the consequence of having renal artery stenosis?

Answer 16

Kidneys underperfused -> mistaken this as low BP -> trigger RAAS -> increased BP puts more pressure on renal artery (and heart)

Question 17

What is Conn’s syndrome?

Answer 17

Adrenal gland secretes excessive aldosterone, too much Na+ and water is reabsorbed

Question 18

Name 4 types of drugs you might prescribe to treat hypertension

Answer 18

1. ACE inhibitor: prevents angiotensin II
2. Angiotensin 2 antagonist
3. Diuretics; excrete more fluid
4. Calcium channel antagonists promote vasodilation (reduce TPR)