Human Physiology Past Exam Q

[seretide]

Hey people,

Just wanted to see if anyone can give me a hand with this question (if curious it's the 2011, Semester 2 paper).

Question asks about locally mediated (no input from the nervous/endocrine systems) mechanisms by which arterioles change their diameter.

Can't seem to think of anything that isn't using a hormone or taking use of the nervous system....

[ferrsal]

I think it's autoregulation. The smooth muscle cells that surround the arterioles are sensitive to conditions in the extracellular fluid. So for example if there are low O2 and high CO2 levels, the smooth muscles relax. This causes vasodilation in the arterioles and therefore increase in blood flow through the arterioles in order to increase O2 delivery, CO2 removal and waste product removal.

I feel stupid answering a non-first year's question but I was just revising the cardiovascular system and I think this is the answer you're looking for

[simpak]

Yup it's about metabolites produced locally in the tissues, you should have some information on this somewhere in your slides?

[seretide]

I think it's autoregulation. The smooth muscle cells that surround the arterioles are sensitive to conditions in the extracellular fluid. So for example if there are low O2 and high CO2 levels, the smooth muscles relax. This causes vasodilation in the arterioles and therefore increase in blood flow through the arterioles in order to increase O2 delivery, CO2 removal and waste product removal.

I feel stupid answering a non-first year's question but I was just revising the cardiovascular system and I think this is the answer you're looking for

Yup it's about metabolites produced locally in the tissues, you should have some information on this somewhere in your slides?

Went through everything.. even re-listened to some lectures but couldn't find it. I think it may have been one of these sort of on the side notes. Thanks for your responses, was going to kill myself if I didn't find the answer!

[simpak]

Interesting but may have something to do with the change in co-ordinator this year!

[seretide]

Nah Charles is pretty awesome... Besides when ferrsal mentioned it, I remembered he spoke about it, just couldn't find it

[jinny1]

Charles is perfection personified.....

[simpak]

Omg that's not what I meant!  I love Charles!  I just meant maybe he cut it from your lectures so won't examine it, it is a past exam written when another person was running the subject.  BUT APPARENTLY NOT IF HE SPOKE OF IT.

[jinny1]

Omg that's not what I meant!  I love Charles!  I just meant maybe he cut it from your lectures so won't examine it, it is a past exam written when another person was running the subject.  BUT APPARENTLY NOT IF HE SPOKE OF IT.

hehe i know what you meant

[seretide]

Don't EVER speak against him again!

[jinny1]

Could someone tell me what venous constriction results in??

Does it affect GFR? Or EDV,TPR etc...

Thanks

[Russ]

It'll affect all those things, some more than others. Venous constriction will increase TPR (variably, depends on how much constriction etc.). This increases venous return to the heart (increased preload, increased EDV). Frank Starling curve says that as EDV increases, SV/CO will subsequently increase and GFR will temporarily increase before autoregulation restores it to normal.

[jinny1]

It'll affect all those things, some more than others. Venous constriction will increase TPR (variably, depends on how much constriction etc.). This increases venous return to the heart (increased preload, increased EDV). Frank Starling curve says that as EDV increases, SV/CO will subsequently increase and GFR will temporarily increase before autoregulation restores it to normal.

Thanks!!!

I don't understand how venous constriction increases venous return. If the veins are constricted, doesn't that mean less blood??

Like in arterioles, dilation means more blood to the muscles/organs and constriction means less blood. So why is it the other way around for veins?

[seretide]

Does anyone know features of the neuromascular junction that results in end plate potentials having higher amplitudes than excitatory post synaptic potentials??

[pi]

Thanks!!!

I don't understand how venous constriction increases venous return. If the veins are constricted, doesn't that mean less blood??

Think of it as pushing blood back to the heart. It makes more sense if you think about dilated vessels with the blood moving slowly back to IVC/SVC, if you suddenly compressed that vein all the blood would flow a lot faster back, ie. inreased return. It only flows one-way (to the heart) due to valves.

For example when the soleus muscle contracts it compresses veins causing that blood to travel back to the heart (ie. increased return).

It's all about reducing the pressure gradient and making it easier for the blood to get back to the heart