502 5. QUINONES 



and Liidde, 1947). However, j)-benzoquinone at 0.6 mM acts more slowly 

 than the hydroquinone, although the effect is superficially similar. This 

 was explained by a slower penetration of the quinone form, whereas the 

 hydroquinone enters rapidly but must be oxidized inside the tissue to be 

 active. The reason for the slow penetration of the quinone was given as its 

 tanning power, that is, its reaction with membrane proteins, presumably. 

 These explanations are not entirely satisfactory: (1) there is no evidence 

 in any case that the hydroquinone penetrates better than the quinone, and 

 indeed one might predict the opposite; and (2) the role of the external pH 

 is ignored, since presumably it would not markedly affect the oxidation of 

 the hydroquinone inside the cells. The different intestinal muscles vary in 

 susceptibility to p-benzoquinone: the longitudinal muscle is paralyzed 

 first, following which there may be a brief period of stimulation of the cir- 

 cular muscle before both muscles are paralyzed and arrest occurs, no con- 

 tracture being observed at any time. A study of the effects of the quinones 

 on the responses of intestine, and other smooth muscles, to nerve stimula- 

 tion and autonomic transmitters might provide interesting information. 

 The isolated rat uterus is stimulated by 0.053-0.53 mM phthiocol with 

 respect to motility but the tonus is unchanged (Supniewski et al., 1936), 

 and the guinea pig uterus is also stimulated by 0.063 mM 1,2-napthoquin- 

 one-4-sulfonate, this being mainly with respect to the tonus (Obo, 1941 c). 

 Blood vessels respond erratically: phthiocol contracts the intestinal vessels 

 but dilates those in muscle, while menadione contracts both types of vessel 

 (Supniewski et al., 1936). We noted in the previous section that juglone 

 dilates the coronaries. Leech muscle is stimulated by 0.9 mM p-benzo- 

 quinone, and a similar response is given to the hydroquinone as long as 

 the pH is neutral or higher and oxygen is present, indicating that the qui- 

 none is the active form (Labes, 1930; Bergstermann, 1944). Because of 

 this, Bergstermann suggested that reaction with SH groups might be in- 

 volved in the action, rather than participation in oxidation-reduction 

 processes in the cells. 



Responses at Sympathetic junctions 



In discussing the actions of the quinones on various tissues it is impor- 

 tant to consider the possible interference with the formation, release, ac- 

 tion, or metabolism of the catecholamines. The clinical use of the quinones 

 in hypertension and how this may relate to sympathetic mechanisms will 

 be discussed later (page 514), and here we shall confine ourselves to isolated 

 tissue responses. Several likely mechanisms of action present themselves: 

 (1) direct oxidation of catecholamines by quinones, (2) prolongation of the 

 actions of catecholamines by hydroquinones by preventing their oxidation 

 or inhibiting enzymes involved in their metabolism, (3) depression of the 

 synthesis or release of the catecholamines, and (4) blockade of the catechol- 



