Abstract
Although there have been divergent conclusions concerning the cardiac effects of the adrenergic blocking agents, it is generally agreed that no adrenergic blocking agent specifically inhibits the chronotropic and inotropic responses to adrenergic stimuli in the mammalian heart (1). It has been found that phenoxybenzamine, a potent adrenergic blocking agent, increases the concentration of noradrenaline and ' adrenaline in urine and plasma of dogs in barbiturate anesthesia (2, 3). Holzbauer and Vogt (4), and Gey and Pletcher (5) have shown that the intravenous injection of 20 to 25 mg/kg of chlorpromazine little affects on noradrenaline content of the hypothalamus in the cat and of the brain in the rat. On the other hand, Malhotra and Prasad (6) have recently shown that the intravenous injection of 2 to 5 mg/kg of chlorpromazine greatly increases the content of noradrenaline in the central nervous system such as hypothalamus, hippocampus, frontal cortex and midbrain in the dog, while the same procedure of 10 to 25 mg/kg significantly decreases the content of the amine in these structures. Graham (7) has demonstrated that the pressor responses of the atropinized dog to a series of 2-halogenoethylamines are blocked by pretreatment of the animal with reserpine. Benfey (8) has shown that the positive inotropic, chronotropic and hypertensive effects of phenoxybenzamine are prevented by pretreatment of dogs with reserpine or guanethidine.
The inhibitory effects of the adrenergic blocking agents such as phenoxybenzamine, dibenamine, chlorpromazine, regitine, piperoxane, yohimbine and dihydroergotamine as well as guanethidine on the action of butyrylcholine and tyramine, and the potentiating effects of these adrenergic 'blocking agents on the action of noradrenaline in the isolated atrium of the guinea-pig have been presented by Ben-fey and Greeff (9). From the results cited above it seems that the effects of the adrenergic blocking agents have something in common with that of reserpine.
If the adrenergic blocking agents affect the content of noradrenaline in the atrial muscle fibers, it is expected that the drugs may give some specific effects on the transmembrane potentials of the atrium.
