122 O. F. HUTTER 



ingly small under the influence of acetylcholine, indicating that the anion 

 does not participate in the conductance increase. Furthermore, a rough 

 estimate of the relative fluxes of potassium and bromide in the sinus venosus 

 may be made from the rate constants applying to the outflow of each isotope 

 and the relative concentrations of the two ions in the cell; it also shows that 

 we are not dealing with a highly anion-permeable tissue. There is no reason 

 then to suppose that an additional anion permeability of similar magnitude 

 to the additional potassium permeability would pass unnoticed and we are 

 inchned to conclude that acetylcholine inhibits the sinus venosus by causing 

 a great and specific increase in potassium permeabihty. In keeping with this 

 conclusion is the observation that the presence of small anions is not essential 

 for the arrest of the sinus venosus by acetylcholine. 



It should be added that it is not implied that the movement of potassium 

 through the channels opened by acetylcholine necessarily obeys the same laws 

 as the movement through normally patent channels. Recent experiments 

 (Hutter and Noble, 1960a) have shown that in heart muscle, as in skeletal 

 muscle (Katz, 1949; Hodgkin and Horowicz, 1959; Hutter and Noble, 1960b) 

 the potassium conductance declines when the fibres are depolarized by an out- 

 ward current. Such rectification need not hold for the potassium conductance 

 added by acetylcholine. The movement of potassium in the chemically opened 

 channels may rather obey the constant field equations (Hodgkin and Katz, 

 1949) in which case their contribution to the membrane conductance would 

 increase as the preparation is depolarized. 



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