ECF

Question 1

what are the three major edematous states?

Answer 1

CHF, cirrhosis and nephrotic syndrome

Question 2

ECF volume is closely linked to what other regulated substance?

Answer 2

sodium

Question 3

what category of disease states results in the sustained increase in ECF?

Answer 3

edematous states

Question 4

what’s the critical factor for determining sodium handling by the kidneys?

Answer 4

EABV (effective arterial blood volume)

Question 5

what two things must be sensed to determine EABV? where are the body’s sensors for those criteria? (5)

Answer 5

salt intake and cardiovascular performance

1) high pressure baroreceptors in the carotid arch and aorta
2) low pressure baroreceptors in the great veins, atria and lungs
3) intrarenal sensors
4) hepatic volume receptors
5) CNS volume receptors

Question 6

does sodium excretion depend on volume or concentration of sodium in the body?

Answer 6

volume - because it is related to ECF volume

Question 7

what’s the mechanism of action for the low pressure baroreceptors in the atria/great veins

Answer 7

modulation of sympathetic system via the central integrative centers. Afferent signal carried from the vagus nerve to the brain; can also alter ADH and renin-angiotensin-aldosterone (RAA) system

Question 8

what’s the mechanism of action for the high pressure baroreceptors found in the ventricles/aorta/carotid sinus?

Answer 8

modulation of sympathetic centers via CN X and IX

Question 9

what’s the mechanism of action for the three types of intrarenal sensors?

Answer 9

myogenic reflex: autoregulation (adaptation to altered pressure); leads to AFFERENT arteriolar constriction
TG feedback system: NaCl sensing system than can affect the AFFERENT arteriole
JG feedback system: Long-term NaCl sensing system that alters RAA system to adapt to long-term changes (decreased EABV -> increased JG system)

Question 10

what two types of receptors does the kidney have in them?

Answer 10

chemoreceptors and mechanoreceptors

Question 11

what are the two types of receptors in the liver (hepatic sensing mechanism?) what is their mechanism of action?

Answer 11

they have osmosensing receptors and naturietic sensors; they affect the nucleus of the solitary tract via the vagus nerve and can be shut off via vagotomy or denervation of the liver

Question 12

what are the cerebral sensing sensors and mechanisms?

Answer 12

there are cerebral NaCl sensors that can affect the renal system via sympathetic/renin and direct control of the afferent arteriole; they are more effective than peripheral sensors

Question 13

define glomerulo-tubular balance

Answer 13

relative maintenance of sodium excretion despite changes in the GFR

Question 14

what is the mechanism by which the Starling forces are changed when EABV expands? is there any change when EABV shrinks? where is the main effect of this action located?

Answer 14

1) EABV expansion -> inc. RPF -> no change in GFR (autoregulation) -> dec. FF -> more dilute (dec. conc.) filtrate -> dec. oncotic pressure
2) EABV expansion -> inc. RPF -> inc. hydrostatic pressure in PCT

Inc. Starling forces -> decreased backleak -> inc. excretion -> mitigates inc. EABV

when EABV shrinks, the system works in reverse with the addition that Angiotensin II will constrict the efferent arteriole in order to maintain GFR despite the loss of RPF

this system’s main effect is in the proximal tubule -> reabsorption happens where the backleak is greatest; if the EABV has expanded then proximal reabsorption is minimal (distal delivery will therefore be high)

Question 15

what’s the mechanism of action for regulating absorption in the loop of Henle?

Answer 15

regulation of the medullary concentration gradient; washout leads to no oncotic pressure gradient meaning that water does not passively diffuse into the medulla (from the descending loop of Henle) meaning that the concentration of salt in the ascending loop is increased

Question 16

how is kaliuresis avoided? where is this a potential problem? why? example when EABV is high

Answer 16

kaliuresis (potassium excretion) can be a problem in the collecting tubule where sodium reabsorption (regulated by aldosterone) can cause an electrical gradient to exist across the epithelium; this is avoided by directing the majority of sodium reabsorption regulation activities to the proximal tubule such that the potential to create a gradient in the collecting tubule is diminished;
e.g. when EABV is high; sodium levels are high in the collecting tubule, but aldosterone levels are low so there is no reabsorption occurring

Question 17

which sympathetic neurons are involved in the renal response?

Answer 17

postganglionic fibers from the celiac trunk and paravertebral fibers from T6-L4

Question 18

what are the effects of increased sympathetic activity to the renal salt/water balance?

Answer 18

broadly, acts as an anti-naturietic;

1) directly acts on the Eff and Aff arterioles
2) increased salt reabsorption in the PCT, LH and DT
3) increased renin-A-A system
4) vasoconstriction

Question 19

what can activate the RAA system?

Answer 19

nerves, prostaglandins, salt balance in DT

Question 20

Angiotensin II effects? (5 total - 2 super-categories)

Answer 20

1) constriction of the efferent arteriole
2) direct effects on the proximal tubule
- the above two both regulate absorption in the proximal tubule
1) stimulation of the sympathetic system (potentiation of Norepinephrine)
2) increased aldosterone
- increases sodium reabsorption in the distal tubule
1) peripheral vasoconstriction

Question 21

what’s the pathway for angiotensin II activation? what converts it to aldosterone?

Answer 21

angiotensinogen produced by the liver is converted to angiotensin I (ATI) by renin mediated enzyme; ATI is converted to ATII in the endothelium (esp. in the lung) and enters circulation; this can be converted to aldosterone in the ZG of the adrenal cortex

Question 22

what regulates ADH release? how is it controlled? what happens when EABV is low? where does ADH have its effect?

Answer 22

ADH regulated by the high and low pressure baroreceptors; these act on the tonically inhibited central system and release the inhibition in cases of lowered EABV; affects the collecting tubule

Question 23

broadly, what role do prostaglandins in the kidney play? how do they carry out this effect?

Answer 23

paracrine counteraction of the systemic EABV response, in order to maintain kidney function - naturesis; vasodilation of the afferent arterioles and the arterioles that service the medulla and upper cortical regions; this dilutes the medullary interstitium and causes less water to be reabsorbed in the descending loop of Henle; they also vasodilate the efferent arteriole thereby lowering the FF

Question 24

what are the major players in the prostaglandin game?

Answer 24

PGI2 and PGE2

Question 25

ANP has what effects on the kidney? (3)

Answer 25

increased GFR - due to afferent dilation and efferent constriction; inhibition of Na absorption in the collecting tubule (opposite of aldosterone); increases medullary blood flow - dilution of sodium into the thin ascending limb; (Decreases renin and aldosterone directly)

Question 26

what are the other natriuretic peptides?

Answer 26

ANP; BNP - brain natruiretic peptide - released from the cardiac ventricles; CNP which is a receptor and urodilatin (urodilatin is a paracrine stimulator)