why does excessive aldosterone secretion decrease muscle contraction?

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super linrondo

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can someone explain why increased aldosterone secretion decrease muscle contraction? i know that aldosterone increase Na+ reabsorption and K+ secretion so K+ is leaving the cell, making it more negative. But wouldn't increased Na+ reabsorption cause Na+ to flow into the cell, making it more positive, so the two effects cancel? or maybe its the fact that K+ leave faster than Na+ go into the cell?

thanks guys!
 
Is this really an MCAT question? Aldosterone does a bunch of things, but basically in the collecting duct of the kidney haa a net effect of favoring sodium reabsorpton and potassium secretion. This is all part of a system to help regulate volume status as well as electrolyte concentrations, which im sure you know. Essentially, the absorbed sodium will drag water along with it (which is the main purpose of sodium reabsorpton here), which will dilute sodium to an extent, and there exists other mechanisms (ADH, ANP, etc...) which help to further regulate sodium and bring it back to normal. Potassium on the other hand, will be abnormally low, so this person in your question is quite likely to be hypokalemic without necessarily being hypernatremic. Hypokalemia in general causes increased flow of potassium out of the cell which decreases the resting membrane potential, making firing an action potential more difficult. At a muscle, this will cause weakness. Derangements of other ions will also affect this finely-tuned process. Read about hypocalcemia, hypercalcemia, and hypomagnesemia as well, which along with others may also cause similar neuromuscular symptoms (weakness, tetany, seizure, lethargy, paraesthesias, etc...)
 
or maybe aldosterone is somehow connected to calcium secretion. Calcium helps in muscle contraction. I am not exactly sure though.
 
or maybe aldosterone is somehow connected to calcium secretion. Calcium helps in muscle contraction. I am not exactly sure though.

Actually, this would result in excessive unwanted muscle contraction. Extracellular calcium is very important with regard to neurotransmission, exerting its effect by blocking sodium channels and essentially increasing the threshold for creating an action potential. In hypocalcemia, there is no dampening effect of calcium on these sodium channels and action potentials are created more easily. The calcium used by a muscle cell in calcium-coupled contraction is intracellular calcium being released from the sarcoplasmic reticulum; different than the extracellular calcium being discussed in the question. Also important with regard to this question however is that aldosterone does not have a role in the regulation of calcium (something done by PTH and others...), but I think that is probably beyond the point this MCAT question is trying to get into your head
 
perhaps the excessive excretion of K+ lowers the muscle cells ability to re polarize and fire again.
 
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