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Kubo and Misu (1) have shown that guanethidine-induced blockade of adrenergic transmission in rabbit hearts is attenuated when nerves are stimulated during subsequent perfusion with a low sodium solution and is accentuated with a high sodium solution and proposed that the drug increases the permeability of adrenergic nerve endings to sodium ions, thereby leading to blockade. Guanethidine 4 x 10-4 M increased the maximum upstroke velocity of action potentials without hyperpolarization for the first 30 min after the addition, after which the value decreased concomitantly with a gradual decrease in resting potentials until 2 hr, and the changes of action and resting potentials were antago nized by tetrodotoxin in rabbit atria (2). In the present experiments, effects of calcium and guanethidine on an increase in the output and a decrease in the endogenous contents of noradrenaline induced by sodium reduction were investigated in rabbit atria. Atria were incubated for 2 hr in 10 ml Krebs solution of the following composition expressed in mM: NaCI 143.4, KCI 5.9, CaC].2 2.5, MgCI2 1.18, glucose 11.1, Iris buffer 2.0 and EDTA 0.03. The solution was bubbled with 5 CO2 in oxygen and maintained at 37'C. Sodium deficient media were prepared by replacement of NaCI with an equiosmotic amount of sucrose or choline chloride. Calcium free solution was made by elimination of CaC12 and addition of EGTA 0.5 mM. Excess calcium solution was prepared by addition of CaCI2 without compensating for changes in tonicity. The final pH of solutions was 7.1 to 7.4. Incubation medium was collected at intervals of 30 or 60 min and noradrenaline output into media and final endogenous noradrenaline contents after 2 hr incubation periods were assayed fluorometrically (3). As demonstrated in Fig. 1, when NaCI was reduced from 143 to 72, 36, 18 or 0 mM with sucrose, noradrenaline output at each incubation interval increased (upper columns) and

EFFECTS OF CALCIUM AND GUANETHIDINE ON NORADRENALINE OUTPUT INDUCED BY SODIUM REDUCTION IN RABBIT ATRIA