Effects of peptide hormones and adrenergic agents on membrane potentials of target cells.
Catecholamines and a number of peptide hormones either hyperpolarize or depolarize surface membranes of target cells. For catecholamines there is no consistent relationship between alpha and beta-adrenergic action and the direction of the change in transmembrane electrical potential difference. Examples of all possible mechanisms have been reported to underlie the altered electrical potentials. The question of what roles hormone-induced altered polarization may play is linked to the question of why a large transmembrane electrical field strength is a general property of cells. It is suggested that the normal, or resting, field strength serves to maintain an array of configuration of membrane dipoles (proteins: transport systems, enzyme systems), and that hormone-induced changes in the field strength serve to command an altered array of configuration of membrane dipoles with a different set of functions. Insulin hyperpolarizes rat skeletal muscle. The mechanism is not by activation of a ouabain-sensitive electrogenic pump, but probably by reduced permeability to Na+. Insulin-induced hyperpolarization precedes other reported effects of insulin. Electrically produced hyperpolarization of a segment of whole muscle (rat), in the absence of insulin, stimulates specific D-glucose transport. Thus, it is possible that insulin-induced hyperpolarization is part of the transduction chain, signaling from the insulin-receptor complex to instruct effector responses to insulin.
D000818:Animals; D002395:Catecholamines / Q000494:pharmacology; D002463:Cell Membrane Permeability; D004058:Diffusion; D004553:Electric Conductivity; D006728:Hormones / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects*; D008565:Membrane Proteins / Q000502:physiology; D051379:Mice; D051381:Rats
D002395:Catecholamines; D006728:Hormones; D007328:Insulin; D008565:Membrane Proteins