BIOL 031 Lecture Notes - Lecture 18: Cirrhosis, Osmoreceptor, Aquaporin 2

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Normal physiologic responses to changes in ecf volume, and how these control mechanisms serve in the long term regulation of blood pressure. Honestly this should all follow really obviously from the past 4 page learning objective. He also only really addresses a loss of ecf volume. Disorders with a deficit of total body na. Affects the loop of henle (can be an issue with pretty much any channel: nkcc2, romk, clcnkb) Mutation is a loss of function in ncct (na/cl cotransporter) Makes the enac (sodium reabsorbing) channel more active. Aldosterone should be in much lower levels than cortisol. Messes up the regulation and makes it the same. If you give cortisol, negative feedback will kick in and turn it off. Mutation is in 11-b-hydroxysteroid dehydrogenase which inactivates cortisol in the cell. Cortisol can then go into the cell and act like aldosterone. The control of extracellular fluid osmolality is called osmoregulation.

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