The presynaptic regulation of noradrenaline release differs in mesenteric arteries of the rabbit and guinea‐pig.

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Abstract
Prejunctional control mechanisms of neuromuscular transmission in mesenteric arteries of the guinea pig and rabbit were compared by examining excitatory junction potentials (e.j.p.). The various agents used did not modify the membrane potential or resistance of smooth muscle cells of either tissue at the concentration used in the present experiments. In the rabbit mesenteric artery, 10-7 M-phentolamine and yohimbine had almost no effect on the amplitude of e.j.p. or on facilitation. In the guinea pig mesenteric artery, phentolamine enlarged and yohimbine reduced the amplitude of the 1st e.j.p. but both agents markedly enlarged the amplitude of the e.j.p. evoked by repetitive perivascular nerve stimulation at frequencies over 0.1 Hz. In the rabbit mesenteric artery, isoprenaline and dibutyryl cyclic AMP inhibited the e.j.p. and the facilitation evoked by repetitive stimulation, while in the guinea pig mesenteric artery, isoprenaline enhanced the amplitude of e.j.p. and the facilitation process. In the rabbit mesenteric artery, ATP inhibited the amplitude of e.j.p. with no change in facilitation and adenosine inhibited mainly the facilitation process evoked by repetitive perivascular nerve stimulation. In the guinea pig mesenteric artery, these agents had no effect on e.j.p. or facilitation. In both the rabbit and guinea pig, indomethacin enlarged the amplitude and prolonged the duration of e.j.p. Prostaglandin E2 and F2.alpha. inhibited the amplitude of e.j.p. Enlarged amplitudes of the e.j.p. following pretreatment with indomethacin were inhibited by treatment with PGE2 or ATP. In the rabbit mesenteric artery, 8-phenyltheophylline (an antagonist of P1 subtype of purinergic receptor) had no effect on the e.j.p., but these agents did reverse the inhibitory action of 2-chloroadenosine (an agonist of P1 subtype of purinergic receptor) or adenosine on facilitation of e.j.p. Theophylline did not have any direct effect on e.j.p. nor did it reverse the effects of adenosine or 2-chloroadenosine. In the rabbit mesenteric artery, ATP and adenyl-imidophosphate showed much the same potency in inhibiting the amplitude of the e.j.p. Therefore, the ATP action on nerve terminals is not due to a higher energy requiring mechanism. The control mechanisms related to noradrenaline [norepinephrine, NE] release in nerve terminals differ in the guinea pig and rabbit mesenteric arteries. In the guinea pig, activation of the .alpha.2-adrenoceptor and prostaglandin receptors inhibits NE release, while .beta.-adrenoceptor activation accelerates the NE release. In the rabbit mesenteric artery, no evidence could be found for an inhibitory feed-back mechanism involving the .alpha.2-adrenoceptor. Activation of the purinergic receptors (P1 and P2 subtypes), prostaglandin receptors and .beta.-adrenoceptors inhibit NE release from nerve terminals, but there is no evidence for a purinergic inhibitory regulation of NE release under physiological conditions.