Metabolic modulation of neurotransmitter release--adenosine, adenine nucleotides, potassium, hyperosmolarity, and hydrogen ion.
Evidence has accumulated that several factors, which have been proposed as mediators of exercise hyperemia, can modulate adrenergic neurotransmission in blood vessels. Adenosine and the adenine nucleotides depress the response of isolated blood vessels of the dog to nerve stimulation more than that to exogenous norepinephrine; this difference is explained by a decreased release of the neurotransmitter. Potassium, hyperosmolarity, and acidosis also depress adrenergic neurotransmission in isolated veins. These results are consistent with the hypothesis that metabolic changes in the vicinity of the adrenergic neuroeffector junction are capable of decreasing the output of neurotransmitter to the blood vessels in the exercising muscle.
D000227:Adenine Nucleotides / Q000378:metabolism*; D000241:Adenosine / Q000378:metabolism*; D000818:Animals; D004285:Dogs; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000378:metabolism*; D009994:Osmolar Concentration; D011188:Potassium / Q000378:metabolism*; D012501:Saphenous Vein / Q000502:physiology
D000227:Adenine Nucleotides; D018377:Neurotransmitter Agents; D000241:Adenosine; D011188:Potassium