418 



8. INHIBITOR DISTRIBUTION IN LIVING ORGANISMS 



the situation represented will be that in which no inactivation of the inhibi- 

 tor occurs in the tissues and only excretion is responsible for loss of the 

 inhibitor. The effects of excretion on the intracellular inhibitor concen- 

 tration are shown in Fig. 8-6; as the excretion becomes relatively larger, 

 the maximal intracellular level reached is less, although the early rate of 

 entry into the cells is approximately the same in each case. The marked 

 influence such excretion may have on the degree of inhibition i^roduced is 

 evident. 



TIME 



Fig. 8-5. Comparison of the rates of disappearance of an inhibitor being destroyed 

 enzymically and by a first-order reaction. Curve 1: enzymic (Eq. 8-13), (I(,)o = 10 

 niilf and F,„ = 100; (A), K^ = 5 mM; (B), K^ = 10 mM. Curve 2: nonenzymic 



(Eq. 8-4); yt^ = 10. 



It is scarcely necessary to point out that there are several factors which 

 may modify this idealized behavior. The rate of entry of the inhibitor 

 into the cell may not be linearly proportional to the external concentration 

 throughout the experimental range; cells may become saturated with inhi- 

 bitor or active membrane processes may occur. Likewise, the excretion may 

 not be proportional to (I^), especially if tubular secretion or resorption of the 

 inhibitor takes place. The binding or trapping of inhibitor within the tis- 



