Amino acids evoke short-latency membrane conductance increase in pancreatic acinar cells.
Sodium-gradient-driven amino acid transport is regarded as an important mechanism for cellular uptake in general as well as in pancreatic acini. Electrophysiological experiments in kidney tubules and intestine have revealed that amino acids can cause sodium-dependent membrane depolarisation. The mechanism of this depolarisation is unknown as it is uncertain whether the depolarisation is accompanied by a membrane conductance increase. The pancreatic acinar tissue would seem to be an ideal system for investigating the electrophysiological mechanism of action of amino acids because (1) the pancreas is the most active amino acid-accumulating tissue, (2) the basic electrophysiology of the pancreatic acinar cells is well characterised and (3) a direct comparison can be made in the same cells between the electrical actions of the pancreatic secretagogues and the amino acids. We now show that L-alanine evokes a stereospecific membrane depolarisation accompanied by an increase in membrane conductance and this this membrane effect has a much shorter latency than the secretagogue response. The null (equilibrium) potential for the amino acid-evoked potential change corresponds to the sodium equilibrium potential.
D000109:Acetylcholine / Q000494:pharmacology; D000409:Alanine / Q000494:pharmacology; D000596:Amino Acids / Q000494:pharmacology*; D000818:Animals; D004553:Electric Conductivity; D005755:Gastrins / Q000494:pharmacology; D007536:Isomerism; D008564:Membrane Potentials / Q000187:drug effects*; D051379:Mice; D010179:Pancreas / Q000502:physiology*; D012964:Sodium / Q000378:metabolism; D013997:Time Factors
D000596:Amino Acids; D005755:Gastrins; D012964:Sodium; D000109:Acetylcholine; D000409:Alanine