here's another question: if this drug is used to treat glaucoma - particularly because they inhibit the secretion of aqueous humor, whats the mechanism for it? i know for a fact that aq. humor is secreted because mainly of sodium pumping out from the cilliary body to the posterior chamber of the eye but isn't the eye unaffected by the carbonic anhydrase activity? or does the increase in sodium secretion affect the remaining sodium used to pump out the aq.humor thus disrupting the secretion of aq.humor? can someone please explain? thanks
The ciliary body also pumps Hco3- which is an important component of the aqueous humour so thereby inhibiting CA would mean a decrease in the amount of aqueous humour
I found the video to be very easy to understand, except for one part. I just don't understand why CA inhibitors cause an increase in Na+ excretion. I can very clearly see why HCO3- is excreted but the moment you mentioned Na+ excretion I just couldn't follow. Could you please explain this? Thank you!
Hey! Thanks for your reply. You see, I was thinking about this and came to the following conclusion: Acetazolamide inhibits CA IV in the lumen and so stops the dissociation of carbonic acid into H2O and CO2m tgerefore HCO3- is excreted. Inside the cell CA II is also inhibited, and so the H2O and CO2 inside the cell cannot be converted into carbonic acid. Therefore there are no protons available for the Na+/H+ exchanger. Even though there is a low concentration of intracellular Na+, due to the absence of H+, the exchanger breaks down and Na+ can't be reabsorbed, so it's excreted along with HCO3- (that results from CA IV inhibition). Sorry it is long-winded. it makes sense to me. idk about HCO3- being excreted as NaHCO3.
Increase in Sodium levels in PCT due to decreased Na+ - H+ exchanger (H+ is in decreased amount because Carbonate cannot enter due to inhibition of Carbonic anhydrase). So increased sodium will move throughout the tubule in kidney and get slight reabsorbed from principal cells where in exchange Potassium ions are released and excreted into urine decreasing the concentration of the Potassium ions intracellularly causing Hypokalemia
thank you very much
I benefited from your explanation you are really awesome
Thanks so much for this video. Life saver!
You are the man! 🙌🙌
God bless you good sir !
Can these CA inhibitors inhibit the Carbonic Anhydrase present in the RBCs and interfere with CO2 transport?
I can't find the video where you explain the mechanism of hypokalaemia and hyperchloremia, can you explain?
Where did you explain the metabolic alkalosis I can't find it please
Please what is the role of specific amino acid residues in the catalysis of carbonic anhydrase?
here's another question: if this drug is used to treat glaucoma - particularly because they inhibit the secretion of aqueous humor, whats the mechanism for it? i know for a fact that aq. humor is secreted because mainly of sodium pumping out from the cilliary body to the posterior chamber of the eye but isn't the eye unaffected by the carbonic anhydrase activity? or does the increase in sodium secretion affect the remaining sodium used to pump out the aq.humor thus disrupting the secretion of aq.humor? can someone please explain? thanks
The ciliary body also pumps Hco3- which is an important component of the aqueous humour so thereby inhibiting CA would mean a decrease in the amount of aqueous humour
great video
Sooo...should I take this before hiking at higher altitudes??
your videos are amazing ! please make more videos sir :)
I found the video to be very easy to understand, except for one part. I just don't understand why CA inhibitors cause an increase in Na+ excretion. I can very clearly see why HCO3- is excreted but the moment you mentioned Na+ excretion I just couldn't follow. Could you please explain this? Thank you!
Roberto Gonzalez because HCO3- is being excreted as NaHCO3 thats why Na+ is also excreted
Hey! Thanks for your reply. You see, I was thinking about this and came to the following conclusion:
Acetazolamide inhibits CA IV in the lumen and so stops the dissociation of carbonic acid into H2O and CO2m tgerefore HCO3- is excreted. Inside the cell CA II is also inhibited, and so the H2O and CO2 inside the cell cannot be converted into carbonic acid. Therefore there are no protons available for the Na+/H+ exchanger. Even though there is a low concentration of intracellular Na+, due to the absence of H+, the exchanger breaks down and Na+ can't be reabsorbed, so it's excreted along with HCO3- (that results from CA IV inhibition).
Sorry it is long-winded. it makes sense to me. idk about HCO3- being excreted as NaHCO3.
Hco3- is excreted mainly,but also minimal excretion of Na+ and H20 is there
best video ever!
CAI and lots, lots, lots of water.
Thank you so much :)
Really good.
Any one doing research to use metallic nanoparticles is a inhibitor??
good job
Cause of hypokalemia!?
Increase in Sodium levels in PCT due to decreased Na+ - H+ exchanger (H+ is in decreased amount because Carbonate cannot enter due to inhibition of Carbonic anhydrase). So increased sodium will move throughout the tubule in kidney and get slight reabsorbed from principal cells where in exchange Potassium ions are released and excreted into urine decreasing the concentration of the Potassium ions intracellularly causing Hypokalemia
Mouril Shah but it should be mild hypokalemia, right? because less Na is being reabsorbed. correct me if I'm wrong. this point is too confusing.
Thank u '!!
Among all the garbage posted on You-Tube, their are a small handful of videos such as this. The only problem is finding them!!!!!!!!!!!!!
Mmmmmm☺️
good job