I see that this question has gone unanswered, so I'll give it my best guess (based on my past experience as a physiologist). In many cases, tests are performed on urine because they are not invasive like blood draws. And in this case, I would argue that drawing samples from brain tissue carries risk to the patient that probably makes it prohibitive, especially on a large scale basis. So, as a researcher, you'd choose the least invasive approach - under the assumption that you are not reducing the validity, nor limiting the reliability of the measurement to a degree that renders it useless.

Again, I may be off, but it seems like a reasonable assumption.

Ariel

My understanding of urine dopamine (DA) and catecholamine testing is not for a correlation with brain chemistry but to test for iatrogenic or neoplastic over-production. In other words you would expect elevated levels in an individual who had consumed L-dopa or had a phaeochromocytoma. Looking at urine DA as some form of analogue of neuronal DA would be excessively confounded by the fact that the kidneys themselves express DA and secrete it into the tubule lumen as a form of Na+ homeostasis mechanism (for a quick review see: Carey RM. Renal dopamine system. Hypertension 2001; 38: 297–302). If you want to see brain levels of DA look into microdialysis and HPLC. Not only would you be able to quantify DA levels, but isolate them to a specific region of cortex.

Thanks you very much dear Linden and Justin for your informative response,

What am I looking for is that " is the measuring of NTs in blood and urine really give us useful information to asses the disease like Parkinson?

As far as I concerned, there is no specific information about the optimum range of Dopamine concentration to be healthy.

If it is the case what we are going to do by measuring these NTs in physiology?

Cheers...

To my knowledge, there are no serological tests for Parkinson's disease (PD). You must remember that PD is not a disease of global DA deficiency. Instead, it is caused by a selective loss of a subset of DA neurons (the so called nigrostriatal dopaminergic projection neurons). There are some good hypotheses on why these neurons are susceptible to selective death, but there is not a single reason we know of as to why these particular neurons die in the disease.

Measuring blood or urine NTs is not an effective method of detecting or screening for the disease. The BBB is pretty effective at keeping NTs separated from the blood other than in a couple of specific regions like the hypothalamus to pituitary venus plexus. On top of this Neural crest cells in the PNS and endocrine system secrete enough catecholamines that any measurement made in serum would overwhelm any contribution made from the CNS.

Testing for NTs in the serum does have merit when a doctor wants to determine if a patient either has a NT expressing tumor (possibly derived from neural crest cells), or if they want to determine if a patient is surreptitiously taking or not taking a NT increasing drug.

I hope this makes what I was saying a bit more clear.

Dear Justin,

Thank you very very much again for your detailed information.

To the best of my knowledge, Measuring NTs in Urine and Blood not at all a diagnostic test for PD.

but there are numerous publications in which the authors are claiming that they can test for PD because they are able to test for NTs in Urine and Blood Serum. Is it not misleading readers...

Cheers...

While catecholamines and serotonin in the blood and urine are not derived from the brain sometimes, for reasons that are not known, they do reflect brain levels. For example, urinary dopamine is low in Parkinson's disease (http://www.ncbi.nlm.nih.gov/pubmed/13686753) even though urinary dopamine levels are thought to be derived mainly from dopamine formation in the kidney. However, urinary dopamine is not a diagnostic test for Parkinson's disease. There are many papers that measured serotonin related compounds in blood or plasma in psychiatric disorders and there is evidence that sometimes there can be a correlation between blood, or plasma, and brain measures (http://www.ncbi.nlm.nih.gov/pubmed/7680408).

Thank you very very much Dear Simon N Young for your informative response.

I agree with, but..., when we have more than one source for dopamine in the body and we dont know that from which part (brain or kidney) it is coming from, then depending on such an uncertain situation to diagnose deadly bad diseases like mentioned above really make any sense? rather misleading and in fact cheating the world (please correct me, if I am wrong)?

Cheers...

I totally agree that you cannot diagnose a brain disease with peripheral measurements. While some researchers may feel that you can obtain useful information about brain disorder with peripheral measures, and the literature is full of studies of that type, personally I think peripheral measures are usually a waste of time. You cannot know if a compound is regulated in a similar way in the brain and in the periphery..

I would not say that it is cheating the world, but I do think that sometimes papers are written with misguided science. Four instance the first paper that correlates you're in dopamine with Parkinson's patients and normal controls may not have thought through all the confounding variable's. For instance Parkinson's patients tend to have some level of dementia as well and with most movement disorders and dementias patients tend to become dehydrated which will have the effect of reducing urinary excretion of dopamine since they will be trying to retain tubular sodium. The proper controls would be to have patients with similar fluid status rather than just age matched. There have been papers that looked for secondary causes of abnormal dopamine another catecholamine levels, and found that these levels correlated better with secondary diagnoses (http://www.ncbi.nlm.nih.gov/pubmed/15949155). 

I am also glad that Dr. McGill brought up the serotonin story. Since I had forgotten about it before writing my previous answers.

I don't want to imply that there will never be an inexpensive serological test that will affectively screen for diseases like Parkinson's, but I feel we aren't quite there yet. And that's why his scientists we do experiments and try to prove hypotheses.

Thank you very much Dear Linden ,Simon and Justine for your opinions on this

As no one in RG having clear information on this particular topic (if you have please share with us)...!, I would like to conclude it as follows...

1. Researchers working on this topic must know that Dopamine in urine and blood has no direct or indirect relationship with Parkinson disease (as not yet confirmed).

2. Until we get a proof for this, we should not say or report in the misleading way.

3. I am Personally requesting the RG subject experts to please share your knowledge with as many as possible, then only "We researchers can serve the world the best science"

"LET US SHARE OUR KNOWLEDGE WITH WORLD RESEARCHERS TO MAKE OUR Scientific World  BETTER, BETTER AND THE BEST..."

I hope this will be done soon and continues for ever...

Have a day full of Knowledge and cheers...

can anyone tell me what is the normal concentration of dopamine in the human being?

According to medline plus (https://medlineplus.gov/ency/article/003561.htm)

In the blood:

• The normal range for epinephrine is 0 to 140 pg/mL (764.3 pmol/L).
• The normal range for norepinephrine is 70 to 1700 pg/mL (413.8 to 10048.7 pmol/L).
• The normal range for dopamine is 0 to 30 pg/mL (195.8 pmol/L). 

In the urine (collected over 24hrs):

• Dopamine: 65 to 400 micrograms (mcg)/24 hours (420 to 2612 nmol/24 hours)
• Epinephrine: 0.5 to 20 mcg/24 hours
• Metanephrine: 24 to 96 mcg/24 hours (some laboratories give the range as 140 to 785 mcg/24 hours)
• Norepinephrine: 15 to 80 mcg/24 hours (89 to 473 nmol/24 hours)
• Normetanephrine: 75 to 375 mcg/24 hours
• Total urine catecholamines: 14 to 110 mcg/24 hours
• VMA: 2 to 7 milligrams (mg)/24 hours (10 to 35 mcmol/24 hours)

In some cases, brain derived neurotransmitters do cross the BBB while others do not-but their metabolites do. There have been many studies that show a correlation / association between peripheral measures and whats happening in the brain, but it really comes down to the methodology used, what metabolites are measured, and to how much of an extend is it reflective of the CNS (measured usually via CSF). But all of this does need to be put into context and wont change the fundamental caveat understanding that any peripheral measures are indirect measures and are indicative in nature and reliant on the literature to establish validity / extent to which it can be used.