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

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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.s). The various agents used did not modify the membrane potential or resistance of smooth muscle cells of either tissue at the concentrations 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.s or on facilitation. In the guinea-pig mesenteric artery, phentolamine enlarged and yohimbine reduced the amplitude of the first e.j.p. but both agents markedly enlarged the amplitude of e.j.p.s 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.s and the facilitation evoked by repetitive stimulation, while in the guniea-pig mesenteric artery, isoprenaline enhanced the amplitude of e.j.p.s and the facilitation process. In the rabbit mesenteric artery, ATP inhibited the amplitude of e.j.p.s 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.s or facilitation. In both the rabbit and guinea-pig, indomethacin enlarged the amplitude and prolonged the duration of e.j.p.s. Prostaglandin E2 and F2 alpha inhibited the amplitude of e.j.p.s. Enlarged amplitudes of the e.j.p.s following pre-treatment 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.s, 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.s. Theophylline did not have any direct effect on e.j.p.s 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 e.j.p.s. Therefore, the ATP action on nerve terminals is not due to a high energy requiring mechanism. From these results we conclude that the control mechanisms related to noradrenaline (NA) release in nerve terminals differ in the guinea-pig and rabbit mesenteric arteries.(ABSTRACT TRUNCATED AT 400 WORDS)

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