Figure 16-2 The diagram shows that adenosine triphosphate (ATP) and norepinephrine (NE) are released as cotransmitters from the sympathetic nerves supplying the vas deferens and some blood vessels. ATP acts on P₂ -purinoceptors on the smooth muscles to initiate excitatory junction potentials, action potentials, and a fast initial contraction involving electromechanical coupling through voltage-dependent calcium (Ca²⁺ ) channels. NE acts on α₁ -adrenoceptors to produce the second, slower phase of the contraction by pharmacomechanical (or at least spike-independent) coupling through receptor-operated Ca²⁺ channels. Prejunctional α₂ -adrenoceptors and P₁ -purinoceptors can reduce transmitter release when activated by NE and adenosine (AD), respectively (i.e., prejunctional neuromodulation), whereas NE and ATP enhance each other's actions (i.e., postjunctional neuromodulation). (Adapted from Burnstock G: Local mechanisms of blood flow control by perivascular nerves and endothelium. J Hypertens Suppl 8:S95, 1990.)