C. ADRIAN M. HOGBEN 187 



marily because acid is secreted by the fundus rich in parietal cells. The histo- 

 chemical study from the Carlsberg Laboratory suggested that the parietal 

 cell was the locus of HCl formation (67) but the authors subsequently recognized 

 that diffusion during analysis precludes this conclusion (68). It is doubtful that 

 visualization of dye appearance in the gastric tubule (i) is sufficient to localize 

 HCl formation. Nevertheless, the balance of evidence favors a tentative view 

 that HCl is formed by the parietal cell or, in the case of amphibia, by its ana- 

 logue, the 'secretory cell'. The parietal intracellular canalicular surface under 

 the electron microscope exhibits an intricate palisade structure similar to that 

 observed in other secreting and absorbing cells (n). An alternative, noted be- 

 low, to the premise of the parietal cell locus, is transport of Cl~ by the parietal 

 cell and H+ by the surface epithelial cell (86). 



Though particular attention is being paid to electrolyte metabolism of mito- 

 chondria, several factors point to the conclusion that the definitive step in ion 

 transport occurs across the plasma membrane of the cell. The resting potential 

 is developed across the cell membrane. If the mitochondria were solely re- 

 sponsible for active transport, passive diffusion between the particles would 

 result in inefficiency under circumstances where a high order of efficiency is re- 

 quired. There is evidence (50) that the limiting step in renal transport maxima 

 is located at the cell surface. 



Our present information suggests that the chloride, univalent anion, trans- 

 port system does not have a high degree of specificity. Heinz, Obrink and Ulfen- 

 dahl (40) have shown that the gastric mucosa preferentially transports Br~ 

 in favor of C\~ even though the ratio, 1.5, of the calculated nutrient to secretory 

 rate constants does not indicate a marked degree of specificity. In considering 

 more detailed aspects of halide competition, it may not be strictly valid to 

 assume, as did these authors, that the secretory to nutrient exchange is neg- 

 ligible i)i vivo. This would be particularly the case if it were shown that Manery's 

 observation (73) of the low specific activity attained by gastric chloride were 

 attributable to exchange between cell and lumen. Davenport's study of iodide 

 secretion into gastric juice (13) suggests that iodide can also be transported by 

 the gastric anion transport mechanism. The high I~ gastric juice/plasma ratio 

 observed at very low plasma iodide levels (13, 75, 90) has not been elucidated. 

 The behavior of an ion in trace amounts may be modified by factors that are 

 not significant when the concentration is appreciable. This is recognizable in 

 the difference between the secretion of tracer Br~ and the secretion of un- 

 labelled Br~ when the latter is a significant fraction of the plasma Cl~ (40). 

 The decrease of gastric juice tracer Br~ and I~ concentrations during copious 

 HCl secretion (37, 62) might be due to the factor of blood flow limitation. 



If the chloride in the solutions bathing the isolated frog mucosa is replaced 

 by nitrate, provided that bicarbonate is also present, the mucosa will continue 

 to maintain its spontaneous potential and continuously generate a short- 



