ECF Flashcards
what are the three major edematous states?
CHF, cirrhosis and nephrotic syndrome
ECF volume is closely linked to what other regulated substance?
sodium
what category of disease states results in the sustained increase in ECF?
edematous states
what’s the critical factor for determining sodium handling by the kidneys?
EABV (effective arterial blood volume)
what two things must be sensed to determine EABV? where are the body’s sensors for those criteria? (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
does sodium excretion depend on volume or concentration of sodium in the body?
volume - because it is related to ECF volume
what’s the mechanism of action for the low pressure baroreceptors in the atria/great veins
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
what’s the mechanism of action for the high pressure baroreceptors found in the ventricles/aorta/carotid sinus?
modulation of sympathetic centers via CN X and IX
what’s the mechanism of action for the three types of intrarenal sensors?
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)
what two types of receptors does the kidney have in them?
chemoreceptors and mechanoreceptors
what are the two types of receptors in the liver (hepatic sensing mechanism?) what is their mechanism of action?
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
what are the cerebral sensing sensors and mechanisms?
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
define glomerulo-tubular balance
relative maintenance of sodium excretion despite changes in the GFR
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?
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)
what’s the mechanism of action for regulating absorption in the loop of Henle?
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
how is kaliuresis avoided? where is this a potential problem? why? example when EABV is high
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
which sympathetic neurons are involved in the renal response?
postganglionic fibers from the celiac trunk and paravertebral fibers from T6-L4
what are the effects of increased sympathetic activity to the renal salt/water balance?
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
what can activate the RAA system?
nerves, prostaglandins, salt balance in DT
Angiotensin II effects? (5 total - 2 super-categories)
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
what’s the pathway for angiotensin II activation? what converts it to aldosterone?
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
what regulates ADH release? how is it controlled? what happens when EABV is low? where does ADH have its effect?
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
broadly, what role do prostaglandins in the kidney play? how do they carry out this effect?
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
what are the major players in the prostaglandin game?
PGI2 and PGE2
ANP has what effects on the kidney? (3)
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)
what are the other natriuretic peptides?
ANP; BNP - brain natruiretic peptide - released from the cardiac ventricles; CNP which is a receptor and urodilatin (urodilatin is a paracrine stimulator)
