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1 Spontaneous and nerve stimulated release of noradrenaline and dopamine from rat and guinea-pig vas deferens have been measured electrochemically after separation by high performance liquid chromatography (h.p.l.c.). 2 In the absence of nerve stimulation both noradrenaline (NA) and dopamine were released into the bathing fluid in the rat but in the guinea-pig only noradrenaline could be detected. Drugs which block neuronal and extraneuronal uptake of catecholamines had little effect on spontaneous overflow but both tetraethylammonium and phenoxybenzamine increased overflow. 3 Transmural nerve stimulation (5-10 Hz) increased catecholamine overflow in both species and dopamine release was now measurable from the guinea-pig vas. In the rat, the proportion of dopamine to NA was unchanged from that released spontaneously. The release of both amines was little affected by drugs that block neuronal and extraneuronal uptake and a monoamine oxidase inhibitor, but was inhibited by tetrodotoxin 0.2 jig ml-'. 4 In the guinea-pig tetraethylammonium 10 mm doubled overflow and phenoxybenzamine 1O-M increased it by five times but the dopamine percentage remained constant and equal to the control. 5 Following nerve stimulation the amount of dopamine released expressed as a percentage of total catecholamine release was 6% for the rat and 1.3% for the guinea-pig. These values were considerably higher than the comparable figures for dopamine: NA content of the two tissues (2% and 0.5 % respectively). Repeated periods of stimulation depleted these tissue stores and the depletion of dopamine was significantly greater than that of NA. 6 Our interpretation of these results is that both dopamine and NA are released from a common store during normal noradrenergic transmission. While all or most of the axonal dopamine is contained in this releasable pool, most of the axonal NA lies in a second, less readily released pool.

Summary. The guinea-pig uterine artery responded to acetylcholine (ACh) with vasodilatation only during pregnancy or after oestrogen treatment. Even with high doses (1 mg/day) oestradiol-17\g=b\ esters had to be administered for several days to effect sensitization to ACh, but oestradiol-17\g=b\ itself was active within a few hours. Oestriol was equipotent with oestradiol. Sensitization was prevented when protein synthesis was inhibited over the period of oestrogen administration, but was not dependent on the integrity of the cholinergic vasodilator nerve supply to the artery.

Summary. Retrograde arteriography has been used to examine the effect of pregnancy on the diameters of the main uterine, internal iliac and inferior epigastric arteries in the guinea-pig. The diameters of the internal iliac and inferior epigastric arteries were not altered during gestation. By contrast, the diameter of the main uterine artery supplying a pregnant horn of the uterus increased in diameter to a mean value of 167% of its diameter in non-pregnancy. In cases of unilateral pregnancy, the uterine artery supplying the non-pregnant horn of the uterus was not increased in diameter. Administration of atropine (0\m=.\1 to 0\m=.\5 mg/kg) to animals in late pregnancy caused constriction of the enlarged uterine arteries to a mean value of 137% of their pre-pregnant diameter, but the diameters of the internal iliac and inferior epigastric arteries were not changed. In non-pregnant animals, the diameter of the uterine arteries was not affected by atropine. The results support previous evidence for an effector r\l=o^\leof cholinergic vasodilator nerves in the production of uterine hyperaemia during pregnancy in the guinea-pig.

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