Aldosterone

Overview

Most increases in the concentration of aldosterone however can be explained by increases in the Renin-Angiotensin-Aldosterone System and therefore angiotensin 2 and/or by increases in K⁺ concentration
Only in severe fluid loss does ACTH significantly stimulate the release of aldosterone
ANP is secreted in response to sodium/water loading and therefore inhibits aldosterone secretion

Diffuses across the cell membrane - lipophillic (essentially steroidal)
Of the principal cells of distal tubule
Binds to cytoplasmic receptors
Works by altering gene transcription and increases synthesis of proteins
- Affects ATP levels

Affects sodium entry and transport
Increases number of apical sodium channels, NaCl co-transporters and Na⁺K⁺ATPase
Increases membrane permeability
Increases sodium pump activity
Total quantity of sodium is conserved not the actual plasma concentration
- This is because water follows sodium so the volume is altered according to the amount of sodium
- Angiotensin 2 and aldosterone also affect ECF so only quantity affected not concentration
- ADH and thirst response also work together to dilute the ECF so although there is more NaCl the actual concentration is constant.

In cases of increased K⁺
Increased sodium pump activity increases the amount of K⁺ in cells to reduce plasa K⁺
Generally not excreted
However if plasma K⁺ is still high aldosterone is stimulated
Causes pottassium secretion
- Pottassium via apical leak channels in the principal cells
Very tightly regulated system
- Allows large increase in K⁺ to have a miniscule effect on plasma K⁺