Physiology 3120 Lecture Notes - Lecture 6: Ascending Limb Of Loop Of Henle, Vasoconstriction, Proximal Tubule

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Renal Physiology
Lecture 6
Regulation of Renin Release
Detection of low sodium by:
o Baroreceptors
Carotid sinus baroreceptor that reflex to juxtaglomerular (JG)
JG cells are also intrarenal baroreceptors
o Chemoreceptors
Macula densa cells which release a paracrine factor
Detect sodium in the filtrate
Paracrine factor promote or inhibit renin release
o JG is also innervated by SNS (NT Norepinephrine)
o JG integrates the 3 info it receives to determine if Renin is released and how
much
o i.e. Low BP in SNS
Low BP in intrarenal pressure
Low Na in filtrate
Macula Densa Function: GFR
Macula densa can sense NaCl content of the lumen due to the activity of the NKCC
multi-porter
Tubuloglomerular Feedback
1. When higher levels of NaCl, macula densa cells release ATP (cleaved to
adenosine)
Adenosine vasoconstriction of afferent arteriole
GFR Decrease
2. When lower levels of NaCl, macula densa cells release nitric oxide (NO)
NO vasodilation of afferent arteriole
GFR Increase
This combination results
in the most release of
Renin
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JG Cells & Renin Release
When NaCl levels are higher, ATP is released (cleaved to adenosine)
o Both ATP and adenosine bind to JG cells via purinergic receptors to inhibit
renin release
o RAAS Pathway not activated
When NaCl levels are lower, prostaglandins are released
o Prostaglandins bind to receptors on JG cells to promote renin release
o RAAS Pathway activated
Filtrate Flow Rate
Macula densa cells also have cilia which bend in response to filtrate flow rate
o Cilia is bent more with fast flow rate
There needs to be receptors on the luminal membrane (important)
If fluid flow rate is high then:
o ATP (adenosine) released and GFR decreases and renin is inhibited
If fluid flow rate is low then:
o NO and prostaglandins released, so GFR increases and more renin is released,
respectively
Increased GFR Fast flow less things are reabsorbed
Decreased GFR Slow flow more opportunity for reabsorption
Renin Ang II and Aldosterone
Ang II GFR is decreased everywhere in the body except for the nephron where
NO is increasing the GFR (Paradox)
Atrial Natriuretic Peptide (ANP)
Produced by atrial cells
Peptide hormone
Stimulus of high BP
Stretch receptors in the atria detect increase in blood in the atria
Release ANP directly into the vasculature
Actions to reduce sodium reabsorption by:
o Inhibits aldosterone release from the adrenal cortex
o Increases GFR (ANP is a vasodilator of the afferent arteriole)
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Actions of ANP
Aldosterone release is most important bc it dictates final reabsorption in collecting
duct
More important than the increase of GFR
Discussion Point
High levels of Na+ (increased ECF volume) causes release of ANP (decreasing Na+
reabsorption)
ANP partially achieves this through increasing GFR
How is this response different than when macula densa cells encounter high levels
of tubular Na+
How do these two responses work together?
o JG locally decreases GFR (in nephron) tweaks global response (local
reg.)
o Body globally increases GFR net effect in the body (wins over JG effects)
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