Physiology 3120 Lecture Notes - Lecture 6: Hyperkalemia, Vasomotor, Solitary Nucleus
9 May 2018
School
Department
Course
Professor
Physiology 3120
Dr. Woods
Lecture 6
Aldosterone
- Made by adrenal gland which sit on top of the kidney
- A steroid hormone
o Able to permeate into whatever cell it wants to except its not going to do its action
unless that cell has its receptor
- Stimulated by…
o angiotensin II
o high potassium levels
o adrenal corticotropin hormone (ACTH)
- Increases sodium reabsorption primarily in the collecting duct:
o Increases # of Na+ and K+ channels in luminal membrane – these are channels that were
already present in the cell cytoplasmically, but they are moved from the cytosol to the
luminal membrane (this is a short term effect)
o Increases the activity of Na+/K+ ATPase
o Increases gene transcription which increases expression of Na+ channels and Na+/K+
ATPase and the K+ channel (this is a long term effect – changing gene expression takes
about 4-24 hours)
Aldosterone Action
- Increasing sodium reabsorption in the collecting duct
- Note: steroids can enter any cell that they want to, they just wont do anything in those cells
unless there is a receptor
- When aldosterone binds to its receptor, we get the physical movement of more Na+ channels in
the luminal membrane
- When we have more Na+ channels, we have more opportunity for Na+ reabsorption
- We also have more K+ channels in the luminal membrane which will increase K+ secretion
- Note: usually, when we have high levels of K+, causing the release of aldosterone, we can very
quickly increase K+ secretion bc one of the effects of aldosterone binding in the collecting duct is
increasing those channels in the membrane and their gene expression so we can secrete more
K+
- This is a good thing bc high levels of K+ in your body is not a good thing
- When we have high levels of K+,
o We get paralysis – neurons stop working
o Youre heart can develop arrhythmias
- So this is a mechanism the body has to very quickly secrete excess K+
- We have the activity of the Na+/K+ ATPase increasing
o More Na+ is actively pumped into the
interstitial space and more K+ is actively
pumped into the cytosol
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Regulation of Aldosterone
- The key element in all of this is renin
- Renin is the enzyme that is limited and is only secreted into the blood in specific scenarios
- Renin is very carefully controlled
Regulation of Renin Release
- Detection of low sodium by:
o Baroreceptors
▪ Carotid sinus baroreceptors that reflex to juxtaglomerular (JG) cells
▪ JG cells are also intrarenal baroreceptors
• local pressure detectors which can distinguish bw high and low BP
locally, right at the kidney itself
• so each nephron can have its own intrarenal baroreceptor
▪ Low Na+ = low blood fluid volume = low BP
▪ When there are low Na+ levels in the body, the baroreceptors can detect those
pressure differences
▪ When the baroreceptors receive the proper information, they tell the JG cells to
release renin
o Chemoreceptors
▪ Chemoreceptors detect composition of chemicals (ex: Na+)
▪ Located in macula densa cells (part of the tubule)which release a paracrine
factor
▪ Some of those paracrine factors will stimulate renin release while others wills
inhibit it
- We have a post ganglionic neuron that is sympathetic and it releases NE (neurotransmitter)
which triggers the JG cells
- What would be the trigger from the baroreceptors to cause renin release? When the carotid
sinus is detecting low BP, there is a decrease in AP being sent up to the solitary tract nucleus,
causing release of inhibition, causing vasomotor activation, releasing renin
- Low intrarenal pressure (less stretching of the afferent arteriole) triggers renin release
- Macula densa cells detect low Na+ which triggers a specific factor that is a stimulus for JG cells
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Made by adrenal gland which sit on top of the kidney. A steroid hormone: able to permeate into whatever cell it wants to except its not going to do its action. Stimulated by unless that cell has its receptor: angiotensin ii, high potassium levels, adrenal corticotropin hormone (acth) Increases sodium reabsorption primarily in the collecting duct: Increases # of na+ and k+ channels in luminal membrane these are channels that were. Atpase and the k+ channel (this is a long term effect changing gene expression takes already present in the cell cytoplasmically, but they are moved from the cytosol to the luminal membrane (this is a short term effect) Increases gene transcription which increases expression of na+ channels and na+/k+ about 4-24 hours) Note: steroids can enter any cell that they want to, they just wont do anything in those cells unless there is a receptor.
