Transmembrane action potentials were recorded from embryonic rat hearts at ages between 10& days of gestation and birth (21 to 22 days). The resting potential averaged 30 to 40 mv at IOJ2 days and increased to around 80 mv by birth. Two periods of rapid increase in resting potential were noted: 1) from 10^ to 13& days and 2) from 19M days of gestation to birth. The maximal upstroke velocity of the action potential increased as the resting potential increased. The duration of the ventricular and atrial action potentials was inversely related to heart rate, and their rate sensitivity decreased with age. The atrial action potential lost its rate sensitivity by 13M days of gestation and the ventricular action potential lost its by birth. At IOJ2 days diastolic depolarization was found in the area of the ventricle proximate to the A-V junction, the left and right atria, and the sinus venosus. The velocity of the diastolic depolarization was greatest in the sinus venosus and least in the ventricle. The diastolic depolarization decreased with growth and was lost by 13/2 days of gestation. ADDITIONAL KEY WORDScardiac action potentials cardiac pacemaker cardiac electrophysiology diastolic depolarization mammalian embryonic heart growth and differentiation• The transmembrane action potential of the embryonic and fetal heart has been studied principally in the chick embryo (1-7).In the ventricle of 6-to 8-day chick embryo hearts, Lehmkuhl and Sperelalcis (2) found resting potentials of 72 mv and action potentials of 86 mv. Potentials in the range of 30 to 50 mv were found in 37-to 67-hour chick embryos by Meda and Ferroni (3). Action potential configuration was found to be simi-

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The cholinergic innervation of the rabbit heart was studied in vitro and in vivo. An isolated preparation, which included the combined atria, S-A node, A-V node and bundle of His, was mounted so that microelectrodes could be placed in either the specialized or nonspecialized tissues. Using a roving monopolar electrode, local transmural electrical stimulation of intracardiac nerves (nerve stimulation) was applied at the A-V or the S-A node. At the A-V node it induced hyperpolarization, reduced the duration and amplitude of action potentials recorded from three regions of die A-V node and the His bundle, whether the preparation was spontaneously beating or electrically driven in either the forward or retrograde direction, and blocked membrane excitation in the nodal and nodal-His regions and to downstream structures. The depressant effects of nerve stimulation were augmented by physostigmine and antagonized by atropine. Addition of acetylcholine to die bath reduced the frequency at which the A-V node conducted, but in the concentrations used did not duplicate the effects of nerve stimulation. The behavior of the S-A node is qualitatively similar to that of the A-V node. In the presence of a sinus rhythm, nerve stimulation applied at the A-V node did not affect the activity of the S-A node, and during artificial atrial drive, nerve stimulation of the S-A node did not affect A-V nodal function, indicating that little or no neural communication exists between the two regions in die isolated preparation. Locally released acetylcholine appears to depress excitability of specialized cells in the central node, independently of the direction of propagation. ADDITIONAL KEY WORDS transmembrane potentials S-A node cholinergic neurotransmitter innervation in specialized atrial tissues conduction block driving frequency and A-V conduction rabbits• For many years attention has been directed to the influence of A-V nodal conduction on cardiac performance. The introduction of intracellular recording methods has contributed much to the investigation of A-V nodal function. From such studies Hoffman et al.(1-5) proposed that a characteristic feature of the A-V node is the phenomenon of decremental conduction, and emphasized the functional changes which occur in the isolated tissue during rapid atrial excitation combined with the application of acetylcholine. The major change in the A-V node associated with increased frequency of atrial excitation was shown to be a progressive decrease in the rate of depolarization and in the amplitude of nodal action potentials (3). Atrial excitation at a frequency higher than 6.2/sec was not followed by excitation of the A-V node (6). The application of acetylcholine caused marked depression of the amplitude of nodal action potentials during forward, but not retrograde, conduction (2, 5). The observed decrease in the duration and amplitude of atrial action potentials was regarded as an important determinant for the cholinergic block of A-V conduction (5). It was proposed that cholinergic changes in ...