Stroke Volume Q- First Aid is wrong??

[mossyfiber12]

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Hey guys, I came across a statement in FA that didn't sound right to me. It says that contractility (and SV) increases with decreases in extracellular sodum.

I thought it would be the opposite. Don't you need to increase the extracellular Na to have prolonged Ca efflux (via the Na/Ca exchanger) and thus increase the contractility and stroke volume?

 

[FlowLimited]

If calcium is leaving the cell, wouldn't that decrease the contractility? So if you've got lowered extracellular sodium, the Na/Ca exchanger won't be particularly active and more calcium will stay in the cell. More calcium in the cell means stronger contractility.

Does that make sense? If so, I think FA is right.

 

[Whatayear]

Also wouldn't an increased level in intracellular calcium lead to increased calcium sequestering in the sarcoplasmic reticulum leading to stronger and quicker contraction when the calcium is released from the SR during depolarization.

 

[hoqhuuep]

FA is right - we just covered this in class last block.

You have to remember that the Na/Ca exchanger is reversible as well. Less extracellular Na means less Ca export by this channel (3 Na in/Ca out). So you have more intracellular Ca hanging around to be sequestered into the SR via the SERCA, and thus, stronger contractility upon subsequent depolarizations.

PM me if this doesn't make sense!

 

[sincity college]

Nah, FA has it right OP.

If Na+ is decreased extracellular, via Digoxin or any cardiac glycoside, then there is an increase in intracellular Na+ due to blockage of Na/K pump. When Na+ accumulates inside, there isn't a strong concentration gradient for Na+ to further flow in the cell so that Ca2+ can flow out that would typically happen if Na+ is high outside cell. So with Ca2+ accumulating in the cell, its sequestered more by the SR and because tension (contraction) is directly related to Ca2+ concentration - it increases. This is called a positive inotropic effect.

 

[mossyfiber12]

thanks guys!