Facilitatory and inhibitory modulation by endogenous adenosine of noradrenaline release in the epididymal portion of rat vas deferens.

The present study aimed at determining the modulation by adenosine of the release of noradrenaline in the epididymal portion of the rat vas deferens. The tissues were treated with pargyline and perifused in the presence of desipramine and yohimbine. Up to four periods of electrical stimulation were applied (5 Hz, 9 min). The A1-adenosine receptor selective agonist R-N6-phenylisopropyladenosine (R-PIA; 100-900 nmol.l-1) reduced, whereas the A2A-receptor selective agonist 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine (CGS 21680; 3-30 nmol.l-1) increased the electrically-evoked noradrenaline overflow in a concentration-dependent manner. The nonselective agonist 5'-N-ethylcarboxamidoadenosine (NECA; 30-300 nmol.l-1) reduced noradrenaline overflow, but the effect did not depend on the concentration. Adenosine deaminase at the concentration of 0.5 mu.ml-1 decreased but at that of 2.0 mu.ml-1 increased noradrenaline overflow. The inhibitors of adenosine uptake, S-(4-nitrobenzyl)-6-thioinosine (NBTI; 50 nmol.l-1) and dipyridamole (3 mumol.l-1), increased the electrically-evoked noradrenaline overflow. The A1-adenosine receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX; 20 nmol.l-1) caused an increase whereas the A2-adenosine receptor antagonist 3,7-dimethyl-1-(2-propynyl)xanthine (DMPX; 0.1 mumol.l-1) caused a decrease. NBTI (50 nmol.l-1), partially antagonized the effect of both DPCPX (20 nmol.l-1) and DMPX (0.1 mumol.l-1).(ABSTRACT TRUNCATED AT 250 WORDS)