BIOL 22000 Lecture Notes - Lecture 19: Diuresis, Renal Function, Macula Densa
2 Aug 2018
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o On the left side, vasopressin level is high, which means there is a increase number
of aquaporin in collecting duct
▪ Water can diffuse down it concentration gradient, going from lumen of
collecting duct into interstitial fluid
▪ As the glomerular filtrate go down the collecting duct, it encounters
interstitial that has a higher osmolarity, this means there will always be a
driving force for the water from collecting duct to interstitial
o On the tight side, there is no vasopressin, which means the collecting duct is not
expressing aqua porin on the apical membrane
▪ As the glomerular filtrate go down the collecting duct, the surrounding
osmolality becomes higher, but there is no diffusion because there is no
aqua porins presented
• Diabetes Insipidus
o Loss of ability to produce AVP and/or the loss of vasopressin receptors
o Results in a constant H2O diuresis
o Kidney is unable to reabsorb enough water, so there is a increase in urine
production
o NOT the same as an osmotic diuresis (occurs in type I and II diabetes)
▪ H2O diuresis is NOT due to excessive solute loss
▪ Osmotic Diuresis: H2O loss is due to excessive solute loss
▪ The reason why there is a problem with water reabsorption in type I and II
is because glucose is present as a solute in glomerulus filtrate, therefore it
makes it difficult for the organism to reabsorb water because it cannot
establish a osmotic gradient
o Result of type I and II diabetes are increase in urine volume
o Osmotic diuresis is due to problem with reabsorption of solute while water
diuresis which is due to problem with reabsorption of water
o Type I and II diabetes individual can reabsorb water just fine with aqua porin
channels present, but the problem is osmolarity of glandular filtrate is higher than
normal because presence of glucose solute
o Vasopressin open existing aqua porin channels, or doe it inserts new aqua porin
channels?
▪ Aqua porin is sitting inside vesicle, vasopressin causes those vesicles to
fuse with the membrane, making the channels in the membrane
▪ Inserting new channels in the membrane
• Diabetes Mellitus (T1 or T2DM)
o Hyperglycemia
o Glucosuria
o Polyuria
▪ Osmotic diuresis
o Polydipsia
o Polyphagia
• RAAS: Renin-Angiotensin-Aldosterone System
o
o Kidney produces a key enzyme call reinin
o Renin is a peptide enzyme and it is synthesized by cells in the kidney called
granular cells
o Renin is needed to catalyze initial step in RAAS which is important for
maintaining blood pressure and sodium reabsorption
o There are three types of stimulus that produces increase section of reinin
▪ If there is a decrease in blood pressure, the decrease in blood pressure
means decrease in glomerulus filtration rate, which leads to decrease in
transport in the tubule system, which then affect the macula densa cells in
the distal tubule, and this will activate the granular cells in the afferent
arterioles to release renin into the blood stream
▪ Another stimulus is the direct affect of blood pressure on granular cells
• The granular cells are sitting right next to the afferent arteriole,
they are responding directly to change in blood pressure
▪ An indirect stimulus is when blood pressure decreases, it activate the
cardiac vascular system to cause increase heart rate and vasoconstriction
medicate by the activation sympathetic nervous system
• One of the target for the sympathetic nervous system are granular
cells
