1
The result in both cases was a significant increase in extracellular acetylcholine.
2
This decrease was not affected by concomitant treatment with acetylcholine receptor antagonists.
3
Menthol produced significant potentiation of peak contractions at each concentration of acetylcholine.
4
Vasoconstrictor responses to these doses of acetylcholine are considered to be abnormal.
5
Inhibitors for these enzymes have potential to prolong the availability of acetylcholine.
6
It works to stimulate production and release of acetylcholine in the brain.
7
A dopamine-independent way seems also to be involved in the histamine-evoked acetylcholine release.
8
Endothelial function was determined by quantitative coronary analysis after acetylcholine challenge.
9
Finally, adaptations in nicotinic acetylcholine receptor function are also involved in nicotine dependence.
10
Accumbens dopamine and acetylcholine decreased, with signs of tolerance to the dopamine effect.
11
Acetylcholinesterase is an enzyme that regulates the activity of acetylcholine, a vital neurotransmitter.
12
The postsynaptic geometric arrangement and function of acetylcholine receptors were normal.
13
Too much acetylcholine, not enough serotonin, and you've got a depression.
14
Acute morphine increased the responses to acetylcholine of the isolated mouse urinary bladder.
15
Incremental doses of acetylcholine were then injected into the coronary artery.
16
There was a statistically significant correlation between the acetylcholine-induced contractions and blood pressure.
