A neurotransmitter role for glutamate in the autonomous nervous system was recently demonstrated in the gastrointestinal tract, and its stimulatory effect on spontaneous motility of human ureter was shown. The aim of our study was to investigate the effects of glutamate on the release of neurotransmitters from intramural nerves of the human ureter.

The effects of exogenous glutamate were tested on electric field-stimulated contractions of isolated human ureter, taken from 16 adult patients after nephrectomy. The longitudinal tension and intraluminal pressure of the isolated ureter were recorded simultaneously. The electric field stimulation was done with square wave pulses (20 V through electrodes, 400 mA, duration 1 ms, frequency 16 Hz). The pulse trains lasted for 30 s, a with 30-s pause.

Glutamate (7.9 × 10⁻⁶ M/L to 10.6 × 10⁻³ M/L) and kainic acid (6.3 × 10⁻⁸ M/L to 2.2 × 10⁻⁵ M/L) produced a concentration-dependent decrease in the electric field-stimulated activity of the isolated preparations. However, N-methyl-D-aspartic acid (9.1 × 10⁻⁸ M/L to 3.1 × 10⁻⁵ M/L), (RS)-⍺-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (7.2 × 10⁻⁸ M/L to 3.2 × 10⁻⁶ M/L) and (±)-1-Aminocyclopentane-trans-1,3-dicarboxylic acid (7.7 × 10⁻⁸ M/L to 6.5 × 10⁻⁵ M/L) were ineffective. The electric field-stimulated contractions of isolated ureter were also inhibited by lidocaine (3.70 × 10⁻⁴M/L) and atropine (1.00 × 10⁻⁶M/L).

The results of our study suggest that glutamate inhibits electric field-stimulated release of acetylcholine in the human ureter through activation of kainate ionotropic receptors, located on the intramural nerve fibers.