Are neuronal uptake mechanisms responsible for the difference in sensitivity to noradrenaline between human arteries and veins?

1. The sensitivity of human metacarpal veins and digital arteries obtained post-mortem to noradrenaline and phenylephrine has been tested. 2. pED50 values for noradrenaline were significantly higher in the veins (6.99, s.e.m. = 0.08) than in the arteries (6.56, s.e.m. = 0.09), whereas pED50 values for phenylephrine in the two tissues were not significantly different (arteries: 6.24, s.e.m. = 0.09; veins: 6.26, s.e.m. = 0.05). 3. The addition of propranolol (4 x 10(-6) mol/l) alone, or in combination with hydrocortisone (4 x 10(-5) mol/l), did not affect the responses to either noradrenaline or phenylephrine. The further addition of cocaine (3 x 10(-5) mol/l) slightly shifted the noradrenaline and phenylephrine concentration-effect curves to the left in both arteries and veins, but veins were still found to be more sensitive than arteries to noradrenaline whilst there was still no difference in the sensitivity of veins and arteries to phenylephrine. 4. Cocaine also slightly potentiated responses to barium chloride, potassium chloride and serotonin. 5. It is concluded that the difference in sensitivity to noradrenaline between arteries and veins cannot be explained by differences in neuronal uptake and it is possible that there may be differences in the properties of the postsynaptic alpha-adrenoreceptors of the two tissues. It is also concluded that the potentiation of the contractile effect of noradrenaline produced by cocaine is not solely due to inhibition of neuronal uptake of amines.