1. When the splanchnic nerves were stimulated in the cat for periods of up to 2 hr, the amount of adrenaline taken up by the nictitating membrane was very small; the highest figure was 0.37 mug/g, corrected for losses.2. The noradrenaline (NA) stores of the isolated medial muscle of the nictitating membrane were labelled with [(3)H]NA, and field stimulation of single muscles was carried out in a small organ bath. A stimulation period of 5 min with supramaximal shocks delivered at a frequency of 25/sec produced a mean release of NA into the bath fluid of 0.46 +/- 0.13 mug/g (uncorrected). Phenoxybenzamine, 10 mug/ml., increased this figure by a factor of 2-3.6. When corrections were made for the amount of transmitter metabolized before it could be collected, 47% of the tissue content of NA were shown to be released during the 5 min stimulation of the normal membrane, and about 55% in the presence of phenoxybenzamine. Prolonged stimulation of a phenoxybenzamine-treated membrane was apt to lead to loss of tissue stores of NA.3. Calculation of the degree of labelling of the NA in the tissue, and of NA released by stimulation, indicated that about 21% of endogenous NA had been replaced by labelled compound both in the tissue and in the overflow.4. Transmitter release per pulse was estimated by applying 720-1330 shocks at frequencies of 4 or 6/sec to membranes exposed to phenoxybenzamine. Mean release of NA per shock and per g tissue was 1.3 ng (corrected for losses). This represents 3.5 x 10(-4) of the tissue content determined at the end of the experiment.