Potassium-induced contraction in smooth muscle.
High K-induced contractions in the smooth muscle of rabbit aorta and guinea pig taenia coli may be described as follows: High K depolarizes the smooth muscle cell membrane and opens voltage dependent Ca channels, resulting in an influx of extracellular Ca and an activation of contractile machinery. A part of the cellular Ca is taken up by mitochondria. Oxygen consumption of the muscle increases to compensate for the ATP consumed by contraction. Hyperosmotic high K solution induces osmotic shrinkage of the cell which uncouples membrane excitation from contraction. Isosmotic high K, Na deficient solution induces swelling of the cell and also inhibits the synport of Na and glucose resulting in an ATP deficiency; both of the changes could inhibit muscle contractile tension. Na deficiency may also stimulate Ca influx coupled to Na efflux in some smooth muscle preparations although such mechanism does not seem to play an important role in rabbit aorta and guinea pig taenia coli.
D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D003106:Colon / Q000187:drug effects / Q000378:metabolism; D006168:Guinea Pigs; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects; D007537:Isometric Contraction / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects; D009119:Muscle Contraction / Q000187:drug effects*; D009130:Muscle, Smooth / Q000187:drug effects*; D009994:Osmolar Concentration; D011188:Potassium / Q000494:pharmacology*; D011817:Rabbits; D012964:Sodium / Q000494:pharmacology
D002121:Calcium Channel Blockers; D007473:Ion Channels; D012964:Sodium; D011188:Potassium; D002118:Calcium