ION MOVEMENTS DURING VAGUS INHIBITION 

 OF THE HEART 



O. F. HUTTER 



Department of Physiology, University College, London 



The arrest of the heart by the vagus nerve has often entered into discussions 

 on nervous inhibition because a favourable experimental situation in this 

 case allowed physiologists to discover long ago something about the site 

 and nature of the inhibitory process. The Webers' original concept of in- 

 hibition as a phenomenon distinct from fatigue (Weber, 1846) was chal- 

 lenged for several decades by physiologists who believed that the rhythm of 

 the heart was due to the spontaneous activity of easily exhaustible vagal 

 nerve endings (Schitf, 1858). But the neurogenic theory of impulse formation 

 in the vertebrate heart lost ground as evidence for a direct inhibitory action 

 of the vagus on cardiac muscle accumulated. Thus Gaskell (1883) pointed out 

 that vagus stimulation caused not only arrest of the heart but also weakening 

 of the auricles, and MacWilliam (1883) observed that the sinus venosus of 

 the eel's heart becomes inexcitable during vagus stimulation, that is, it could 

 not be made to contract by direct electrical or mechanical stimuli. In 1887 

 Gaskell made the discovery that stimulation of the vagus nerve produces an 

 increase in the resting potential of the auricles (Gaskell, 1887). Some workers 

 had difficulty in repeating this observation, or doubted its significance, but 

 Sir William Bayliss (1915) mentions in the Principles that he used to demon- 

 strate Gaskell's effect to students of University College and he saw in this 

 phenomenon and in Biedermann's and Pavlov's work on invertebrate muscle 

 convincing evidence that muscular tissue itself undergoes a change under the 

 influence of inhibitory nerves. When the humoral theory of synaptic trans- 

 mission moved forward as resuk of Loewi's (1921) work it was therefore 

 possible to fit acetylcholine into the picture as the agent which causes the 

 changes in the heart muscle (Dale, 1937). 



A problem since then has been the mode of action of the acetylcholine 

 released by vagal stimulation. That a "mobilization" of potassium ions is 

 involved was indicated by the experiments of Howell and Duke (1908). 

 Lehnartz (1936) and Holland et al. (1952a, b). But httle progress in the 

 formulation of a coherent hypothesis was made until the general nature of 

 the excitatory synaptic action of acetylchohne was understood. With advance 

 in that field (Fatt and Katz, 1951), the concept of a change in ionic perme- 



114 



