Physiology 3120 Lecture Notes - Lecture 5: Vasoconstriction, Baroreceptor, Collecting Duct System

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Renal Physiology
Lecture 5
Clinical Note: Gout and Kidney Stones
Increased levels of uric acid (urate) in the blood is called hyperuricemia
o How uric acid exists in the blood
o High levels = hyperuricemia which causes physiological problems
o Nucleotide (purines) metabolized uric acid urate
Both gout and kidney stones can be caused by hyperuricemia
Much (90%) of the filtered uric acid is reabsorbed in the proximal tubule due to its
function as an antioxidant in the body
o Purpose for a waste product
If in excess in the blood, uric acid is secreted back into the tubule via transporters
o Balance mechanism happens at the level of secretion
o Known 12 transporters in proximal tubules
o Mutation in any will cause imbalance of uric acid in blood
Causes of Increased
Uric Acid
Decreased secretion (problems w/ transporters in
nephron)
Increased purine intake (red meat, beer, wine, etc)
Describe Gout
Urate start to crystallize and deposit in your joints
Inflammation of joints
Fingers and toes (big toe esp) are most affected
Describe the
Symptoms of Kidney
Stones
Most are made from urate
More pain associated with them than birth lollllll
Typically form stones in the tubules of your nephron
Symptoms depend where they’re lodged (can be
asymptomatic if little)
Ureter (pain) Bladder (no pain) Urethra (pain)
Hormonal Regulation of Sodium Balance
Two hormone systems to regulate body levels of sodium:
1. Renin-Angiotensin-Aldosterone System (RAAS)
Sodium levels are low
2. Atrial Natriuretic Peptide (ANP)
Sodium levels are high
Usually activating this pathway (even with normal diet)
When sodium levels are high, the ECF volume increases as does blood pressure
Influences water retention also
Have receptors to detect changes in blood pressure and filtrate composition to
activate these pathways
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RAAS Pathway (Description in study guide)
Multi-organ/enzyme/hormone pathway
Involves the Liver, Vasculature, Endothelial cells, Adrenal glands (cortex), & Kidney
Liver:
o Produces lots of proteins (i.e. albumin)
o Angiotensinogen
Large protein
Constitutively produced
In the vasculature no known function
Kidney (Juxtaglomerular cells):
o Renin
Only secreted when Na+ levels are low
Peptide (10 aa in length)
In the vasculature no known function
Endothelial cells:
o Angiotensin II
Ang I Ang II via ACE
ACE is embedded in the endothelial cells (high in pulmonary capillary
beds)
Guarantee mechanism because all blood will go through pulmonary
circulation and exposed to ACE
Hormone (8 aa in length)
In the vasculature changes cellular function
Adrenal glands:
o Aldosterone
Very outside of cortex glomerulosa layer
Cells are stimulated to release aldosterone
Steroid hormone
In the vasculature changes cellular function
Change how kidneys reabsorb Na+
ACE-Angiotensin Converting Enzyme
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