Calcium level in blood

[Monkeymaniac]

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While going over "bones" section in EK biology, I realized that it says something like

Free calcium ion conecentration [CA2+] is what's important physiologically. Too much calcium can make membranes hypo-excitable causing lethargy, fatigue, memory loss, and too little calcium can cause colvulsion and cramps.

1. Isn't fatigue caused when action potential is triggered too often, and thus there aren't enough neurotransmitter in the pre-synaptic membrane to be able to relay the signal? How does the high concentration of CA2+ cause that?

2. How does the low [CA2+] cause cramps? Isn't cramps supposed to happen when muscles are out of ATP's, which causes myosin to be kept attached to actin filament?

Thanks in advance.

 

[DavidMD2B]

While going over "bones" section in EK biology, I realized that it says something like



1. Isn't fatigue caused when action potential is triggered too often, and thus there aren't enough neurotransmitter in the pre-synaptic membrane to be able to relay the signal? How does the high concentration of CA2+ cause that?

2. How does the low [CA2+] cause cramps? Isn't cramps supposed to happen when muscles are out of ATP's, which causes myosin to be kept attached to actin filament?

Thanks in advance.

1. Calcium (Ca2+) is a vital element in the process of neurotransmitter release; when Ca2+ channels are blocked, neurotransmitter release is inhibited. When the action potential reaches the nerve terminal, voltage-dependent Ca2+ channels open and Ca2+ rushes into the neuron terminal due to a greater extracellular concentration.

2. Deficiencies in both Ca++ and Mg++ will cause cramps. However, the lack of ATP plays a role in rigor mortis, a phenomenon associated with death.

I hope the above brief explanations will help guide you to dig deeper.

 

[Monkeymaniac]

1. Calcium (Ca2+) is a vital element in the process of neurotransmitter release; when Ca2+ channels are blocked, neurotransmitter release is inhibited. When the action potential reaches the nerve terminal, voltage-dependent Ca2+ channels open and Ca2+ rushes into the neuron terminal due to a greater extracellular concentration.

2. Deficiencies in both Ca++ and Mg++ will cause cramps. However, the lack of ATP plays a role in rigor mortis, a phenomenon associated with death.

I hope the above brief explanations will help guide you to dig deeper.

I appreciate your answers.

1. So how does the high [Ca++] block the calcium channel? and what are the situations where fatigue is caused?

2. Would you please explain further as to how the deficiencies in Ca++ or Mg++ cause cramps?

Thanks!

 

[dingyibvs]

He didn't say high [Ca2+] blocks calcium channels. High calcium ion concentrations will probably cause too much neurotransmitter release, thus exciting muscles and such too often and resulting in fatigue. I don't know this for sure tho, sometimes the body works in odd, roundabout ways.

As for cramps, I have no idea, sry 🙁

 

[DavidMD2B]

I appreciate your answers.

1. So how does the high [Ca++] block the calcium channel? and what are the situations where fatigue is caused?

2. Would you please explain further as to how the deficiencies in Ca++ or Mg++ cause cramps?

Thanks!

1. Ca++ does not block Ca++ channels as stated above by dingyibvs. Ca++ not only plays a direct role in muscle contraction (Hint: Ca2+-Troponin complex) it also facilitates neurotransmitter release. Therefore, a high [Ca++] means more neurotransmitter release --> more muscle contraction --> result in fatigue.

2. Cramps are quite complex in nature and can be something that's benign, as infrequent muscle pain to symptoms experienced by someone with ALS. Cramps related to sports are usually related to electrolyte imbalance. Hence, your favorite sports drinks. I'm sorry that I'm not familiar with the exact mechanisms.

You may want to grab a physiology text to deeper your understanding on excitation-contraction coupling. Here's a link to a great online source:

http://muscle.ucsd.edu/musintro/jump.shtml

Good luck studying.

 

[fizzgig]

seems like it might be a shift in excitability of the membranes. way too much calcium might cause desensitization, requiring a bigger depolarization to get the VgatedCa channels to open and cause NT release. way too little might cause sensitization, so the NT release gets triggerhappy

http://www.prep4usmle.com/forum/thread/13791/