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1. Cat spleens were perfused with Krebs-bicarbonate solution by means of a constant flow pump. The amount of noradrenaline released by an injection of potassium chloride solution (3·7M) was measured. The dependence of noradrenaline released by KCl on the ionic composition of perfusion medium was determined.

2. In normal cats, the average output was 166 ng following a low dose of KCl (0·2 ml.), and 507 ng following a high dose (0·8 ml.). After phenoxybenzamine treatment, the outputs with both doses were nearly doubled.

3. In both normal and phenoxybenzamine treated cats, removal of calcium from the perfusing solution nearly abolished the release of noradrenaline. Replacing the calcium in Krebs solution restored the output. Increasing the magnesium concentration to 20 mM also markedly reduced the noradrenaline output.

4. Lowering the sodium concentration to either 25 or 0 mM increased the noradrenaline output by nearly two- to threefold. In solutions with reduced concentrations of sodium, noradrenaline was released over longer periods following KCl injections. In phenoxybenzamine treated cats, reduction of sodium in the perfusing solution also increased the noradrenaline output by nearly twofold following either the low or the high dose of KCl.

5. It is concluded that calcium ions are necessary for the release of noradrenaline from post-ganglionic sympathetic nerves following depolarization by potassium ions. It is also suggested that sodium ions are specifically needed for the reincorporation of released transmitter into the sympathetic nerve endings.

This article has been cited by other articles:

				M. P. Blaustein and W. J. Lederer Sodium/Calcium Exchange: Its Physiological Implications Physiol Rev, July 1, 1999; 79(3): 763 - 854. [Abstract] [Full Text] [PDF]