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Alright so with Gitelman/Thiazides I understand that we are blocking Na+/Cl- cotransporter in the DCT. This causes the following effects according to FA 2018: Hypokalemia, Metabolic Alkalosis, Hypomagnesemia, Hypocalciuria.
My understanding so far:
Increased Na+ in DCT -->
(1) upregulated RAAS (increased aldosterone) --> increased activity of ENaC, ROMK in DCT, and Na/K ATPase in DCT --> Hypokalemia --> increased K+/H+ exchanger activity --> increased H+ secretion and increased HCO3- reabsorption --> Metabolic alkalosis
(2) increased activity of Na+/Ca+ exchanger in DCT --> Hypercalcemia / Hypocalciuria
But where does hypomagnesemia come in?
I apologize for any mistakes in the above.
My understanding so far:
Increased Na+ in DCT -->
(1) upregulated RAAS (increased aldosterone) --> increased activity of ENaC, ROMK in DCT, and Na/K ATPase in DCT --> Hypokalemia --> increased K+/H+ exchanger activity --> increased H+ secretion and increased HCO3- reabsorption --> Metabolic alkalosis
(2) increased activity of Na+/Ca+ exchanger in DCT --> Hypercalcemia / Hypocalciuria
But where does hypomagnesemia come in?
I apologize for any mistakes in the above.
