A mechanistic explanation of the effect of potassium on goldfish intestinal transport.
Partial replacement of sodium by potassium or rubidium in the solution used to perfuse isolated intestinal segments of goldfish causes an increase in transmural electrical resistance. Serosal replacements have a stronger effect than mucosal replacements. A 70% inhibition of the glucose-evoked transmural electrical current is brought about by serosal replacement of 40 mM sodium by potassium. Transmural mucosal to serosal flux of 3-O-methyl-D-glucose is also strongly inhibited by serosal potassium. These inhibitory effects of potassium do not occur when the intestinal mucosa is stripped free from the intestinal muscular layers. It is concluded that potassium-induced muscular contractures cause a decrease in transport area by pressing the mucosal folds closer against each other. Certain effects of high potassium concentrations that have been reported in mammalian intestinal preparations may involve a similar mechanism.
D000818:Animals; D004553:Electric Conductivity; D005071:Evoked Potentials / Q000187:drug effects; D005947:Glucose / Q000378:metabolism / Q000494:pharmacology; D006054:Goldfish; D007408:Intestinal Absorption / Q000187:drug effects*; D007413:Intestinal Mucosa / Q000187:drug effects; D007422:Intestines / Q000187:drug effects*; D009130:Muscle, Smooth / Q000187:drug effects; D010693:Phloretin / Q000378:metabolism; D011188:Potassium / Q000494:pharmacology*
D005947:Glucose; D011188:Potassium; D010693:Phloretin