Aamc 7, bs#115

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dougkaye

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If you have access to this test, tell me why Norepinephrine (NE) levels in BLOOD would be any indicator of sympathetic nervous system (SNS) stimulation or down-regulation? The question is talking about nervous system response, not endocrine!
 
I don't have access to the question, but norepinephrine is a neurotransmitter (as well as a hormone), and is used by the sympathetic nervous system which binds to adrenergic receptors on SNS effectors.
 
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sympathetic nervous system is regulated by

Norepinephrine and Epinephrine

Norepi = NT
Epi = hormone (endocrine)
 
Norepi = NT
Epi = hormone (endocrine)

Where did you find that discrepancy? Not asking to be a smartass... I had been looking through my EK Bio book for a section discussing differences between the two, but they always seem to lump them together in discussing endocrine/nervous system effects.
 
Where did you find that discrepancy? Not asking to be a smartass... I had been looking through my EK Bio book for a section discussing differences between the two, but they always seem to lump them together in discussing endocrine/nervous system effects.
i'm not sure what the difference is between the two but i have been taught repeatedly that they both exert the same types of effects.

the answer to the OP's question lies in the network of connections made by the sympathetic nervous system.

http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/A/autonomic.gif

look at this image and you will see clearly that there is a direct neural connection in the SNS to the adrenal medulla. therefore, stimulation of the SNS will result in the secretions of NE and Epi from the adrenal medulla.
 
First, this question is poorly written.

Second, if one assumes that the answer is correct as written, this is what probably happens. The sympathetic nervous system uses NE as its final excitatory neurotransmitter in the efferent system that has an effect on targets (such as muscles).

So, imagine that peripheral body neuron firing and dumping NE into the synaptic cleft, with some of the NE binding to post-synaptic receptors. This causes the intended effect, which is constriction. Nonetheless, some of the excess NE is free to diffuse around extracellularly in the synaptic cleft, and may just find its way through endothelial cells and into the blood stream.

Again, I think this is a terrible answer, but considering NE is used as a NEUROTRANSMITTER by the sympathetic nervous system, I can't think of another way it would end up in the blood.
 
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