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1 Intramural nerve stimulation elicited a powerful relaxation of the longitudinal muscle of the rabbit portal vein in the presence of atropine and guanethidine, but not of the guinea-pig portal vein.2 Intramural nerve stimulation of the rabbit portal vein produced a 13 fold increase in release of 3H-adenyl compounds after preloading with [3H]-adenosine. About 50% of this release was abolished by guanethidine. All release was abolished by tetrodotoxin. No significant release of radioactive compounds was observed during intramural nerve stimulation of the guinea-pig portal vein in the presence of guanethidine, although there was a 6 fold increase in release of radioactivity in the absence of drugs. 3 Histochemical studies using quinacrine, which binds ATP showed a fine fluorescent nerve plexus, nerve bundles, and ganglion cells in the rabbit portal vein, but not in the guinea-pig portal vein. This plexus was still present after chemical sympathectomy with 6-hydroxydopamine. 4 Adenosine 5'-triphosphate (ATP) relaxed the rabbit portal vein, but usually produced a biphasic response, consisting of a contraction followed by a relaxation, of the guinea-pig portal vein. 5 Prostaglandins E1 and E2 caused contraction of the rabbit portal vein. Indomethacin, a prostaglandin synthesis inhibitor, potentiated the relaxations of the rabbit portal vein produced by both non-adrenergic, non-cholinergic nerve stimulation and ATP. 6 High concentrations of antazoline and phentolamine, which antagonize purinergic responses in the guinea-pig taenia coli, caused a loss of basal tone so that it was not possible to assess their effects on the responses of the portal vein to either non-adrenergic, non-cholinergic nerve stimulation, or ATP. 7 Comparison of the results on the portal vein of the rabbit and guinea-pig provides support for the view that: (i) quinacrine fluorescence can be used to localize purinergic nerves and that the rabbit portal vein is supplied by these nerves; (ii) ATP is released from adrenergic nerve fibres, although, based on histochemical analysis, about 3 to 7 times less than is released from purinergic nerve fibres.

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The responses of the guinea‐pig taenia coli, urinary bladder and the rabbit portal vein to ultraviolet (u.v.) light were compared to those elicited by purinergic nerve stimulation and exogenous adenosine triphosphate (ATP). In the presence of sodium nitrite, u.v. light between 340‐380 nm produced a maximum relaxation of the taenia coli. The relaxation was reversible and fast in onset. It was unaffected by atropine, guanethidine or low concentrations of phentolamine or propranolol. When the tone was low, the relaxation was usually followed by a ‘rebound contraction’ upon cessation of stimulation. Thus, the response to u.v. light closely resembles the responses to both purinergic nerve stimulation and exogenously applied ATP. U.v. light did not initiate impulses in purinergic nerves since its action was unaffected by tetrodotoxin; nor did it release ATP from nerve terminals (in contrast to its release during purinergic nerve stimulation). The adenosine‐uptake inhibitor, dipyridamole, which potentiates the responses to purinergic nerve stimulation and ATP, did not affect the response to u.v. light. Agents known to alter postjunctional responses to purinergic nerve stimulation and ATP also altered the response to u.v. light. High concentrations of the 2‐substituted imidazoline compounds, antazoline and phentolamine, which antagonize the responses to purinergic nerve stimulation and ATP, reduced the responses to u.v. irradiation. The prostaglandin synthesis inhibitor, indomethacin, which abolishes the ‘rebound contraction’ following stimulation of purinergic nerves, also blocks the ‘rebound ‘contraction’ following u.v. irradiation. Increases in the K+ concentration produced parallel changes in the inhibitory responses to u.v. light and purinergic nerve stimulation. U.v. light produced relaxation and inhibition of spontaneous activity of the rabbit portal vein (relaxed by ATP), but had no effect on the guinea‐pig urinary bladder (contracted by ATP) and ureter (unaffected by ATP). It is suggested that u.v. light is acting on some part of the purinergic receptor complex which is involved in the mediation of inhibitory responses to ATP and purinergic nerve stimulation, and may therefore provide a way of investigating the chemistry of inhibitory purinergic receptors.