Mechanical and biochemical effects of individual co-transmitters in rat tail arteries

1. The effects of (1) nerve stimulation (NS, 0.5 ms, 1-16 Hz, supramaximal voltage, 20 s) upon vasoconstriction, as measured by changes in perfusion pressure and (2) exogenously added co-transmitters noradrenaline (NA) and alpha, beta,-methylene ATP (alpha, beta, MeATP) upon polyphosphoinositide (PPI) breakdown, and vasoconstriction, were studied in rat tail perfused arteries or arterial rings. The interaction between NA and ATP upon contraction of artery rings and inositol phosphate (IP) accumulation was also studied. 2. Nerve stimulation evoked vasoconstriction in rat tail arteries. These pressor responses were largely (approximately 80%) blocked by the alpha 1-adrenoceptor antagonist, prazosin (10(-6) M), but not significantly affected by desensitization of P2x-purinoceptors by prior, repeated (five times) addition of alpha, beta, MeATP (10(-6) M). 3. Noradrenaline evoked a prazosin (10(-6) M)-sensitive, concentration-dependent, increase in both perfusion pressure and total inositol phosphate (IP) accumulation over the same concentration range (10(-6)-10(-4) M). The amplitude of the pressor responses to NA were about 80% of those obtained to nerve stimulation (0.5 ms, 1-16HZ 20s supramaximal voltage). 4. alpha, beta,-methylene ATP (10(-7)-10(-5) M) evoked a concentration-dependent increase in perfusion pressure which, at maximum, was equivalent in amplitude to approximately 20% of that obtained to nerve stimulation. Concentrations of the nucleotide greater than 10(-5) M were required to stimulate total IP accumulation. 5. The effects of NA (10(-6) M) and alpha, beta, MeATP (10(-5) M) upon contraction of artery rings and IP accumulation were additive and no evidence of synergism between them, on either parameter, was obtained.(ABSTRACT TRUNCATED AT 250 WORDS)