kidney regulation

Question 1

what are the mechanism of angiotensin 2 action?

Answer 1

constriction of the efferent arteriole
increases ADH secretion from the pituitary gland
increases aldosterone secretion (acts on DCT and collecting duct, increase activity of Na+/K/H pumps = increase fluid uptake)
increases thirst
increase activity of Na/H exchanger in the PCT

Question 1

what are the effects of angiotensin 2?

Answer 1

overall effect, increasing water and Na absorption, hence also increasing blood pressure

Question 2

where does ATII bind what effect does it have?

Answer 2

Binds to AT1 receptors
AT1 receptor where ATII binds is coupled to a Gq G protein. This causes increase in IP3/DAG levels which increases Ca2+ release from intracellular stores e.g. in smooth muscle cells of the JGA and the granule cells (increase renin secretion positive feedback)

Question 3

where is angiotensinogen released from?

Answer 3

Liver and adiposites

Question 4

where is renin released from?

Answer 4

JGA cells in response to changes in effective circulation volume / blood osmolarity

Question 5

what is the role of renin?

Answer 5

converts angiotensinogen to AT1

Question 6

what is the role of ACE?

Answer 6

Angiotensin converting enzyme, converts AT1 to AT2

Question 7

where is aldosterone released from?

Answer 7

adrenal cortex (in response to AT2)

Question 8

what do macula densa cells detect?

Answer 8

changes in Na levels (cause granular cells to secrete renin)

Question 9

where are the macula densa cells?

Answer 9

cells of DCT in the JGA

Question 10

what is the JGA?

Answer 10

juxtaglomerular apparatus is the complex where the late distal tubule comes into contact with the glomerulus

Question 11

in what 4 ways can the angiotensin II system be clinically inhibited?

Answer 11

• Direct renin inhibitors e.g. (alisikiren)
  
  • Aldosterone receptor antagonists ( spironolactone)
  • AT1 receptor antagonists - block ATII from binding ( candesartan)
  • Angiotensin converting enzyme (ACE) inhibitors (captopril) - have cough side effect

Question 12

how does the sympathetic nervous system cause increase renin release in response to low blood pressure e.g. in the case of haemorrhage?

Answer 12

release of NA - binds to B1 adrenoreceptors on granular cells
increases renin secretion
also to further increase renin release sympathetic nervous system cause vasoconstriction upstream of granular cells
decreased tension in the walls as a result of less blood coming through further promotes renin release

Question 13

how is ADH secreted in response to haemorrhage what effect does this have?

Answer 13

baroreceptor reflex, decreased cardiac filling and the central actions of ATII all trigger ADH release
increases blood volume and blood pressure
however ADH doesn’t promote an increase in Na reabsorption so initial response the individual my be hyponatremia

Question 14

when is release of ANP triggered?

Answer 14

increased blood pressure
more venous return, more atrial filling

Question 15

explain the action of ANP

Answer 15

atrial natriuretic peptide
natural diuretic
binds to ANPab receptors in the kidneys and increases cGMP levels
cuases vasodilation of the afferent arteriole, increases GFR
Decrease Na/Cl cotransport in the distal tubule, decrease activity of sodium channels and Na/K ATPase activity in the collecting duct
Overall effect is an increase in Na+ excretion = acts as a natriuretic

Question 16

what is Urodilatin

Answer 16

similar to ANP already present in the kidney

Question 17

how does dopamine act as a natriuretic?

Answer 17

mainly synthesized by epithelial cells in the PCT but also released from sympathetic nerve terminals
Dopamine tonically acts via D1 receptors to increase cAMP and decrease the activity of the Na / H exchanger in the PCT

Question 18

what effect do prostaglandins have on the kidney, give examples

Answer 18

• PGE2 and PGl2 (prostacyclin) increase Na+ excretion they act as natriuretic

Question 19

why can the use of NSAIDS be problematic for those with kidney problems?

Answer 19

natriuretic effect of PG, stopped, although minor could have damaging effect on already weak kidneys
too much sodium water retained

Question 20

what other body buffer is present except HCO3, which 2 forms does it come in?

Answer 20

HPO42-(main form in blood plasma)
H2PO4- (main form in acidic environments such as urine)

Question 21

how can ammonium aid H+ excretion

Answer 21

The ammonium ion is produced in the PCT (cells) by conversion of glutamine to glutamic acid and alpha ketoglutarate
it freely diffuses across the membrane and binds to H+
to produce NH4+ which is trapped there and therefore excreted

Question 22

what are the characteristics of respiratory acidosis?

Answer 22

Hypoventilation increase in CO2, increase bicarbonate to compensate

Question 23

what are the characteristics or respiratory alkalosis?

Answer 23

Hyperventilation, decrease CO2, decrease H+, decrease HCO3 to compensate

Question 24

what are the characteristics of metabolic acidosis?

Answer 24

Renal failure, lactic acid ketoacidosis
H+ increases, HCO3 decreases, hyperventilation to compensate, decreases CO2

Question 25

what are the characteristics of metabolic alkalosis?

Answer 25

• Vomiting / contraction alkalosis
  H+ decreases, HCO3 goes up, decrease ventilation increase CO2 to compensate