Alteration by vanadate of contractility in vascular and intestinal smooth muscle preparations.
Intestinal muscle was more sensitive than vascular muscle to vanadate. Vanadate caused a biphasic response in intestinal muscle; inhibition of spontaneous contractile activity was followed by a return of phasic contractions and a sustained increase in baseline tension. Then inhibitory response appeared to be due to vanadate-induced release of an inhibitory transmitter from intramural nerve endings. The excitatory response appeared to be due to the action of vanadate at an intracellular site, possibly by inhibition of a Ca-ATPase that controls intracellular Ca2+ levels. Vanadate did not alter intracellular Na+ and K+ levels in isolated longitudinal muscle. Thus, inhibition of intestinal muscle NaK-ATPase cannot account for the alterations in contractility.
D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D066298:In Vitro Techniques; D007422:Intestines / Q000187:drug effects; D009119:Muscle Contraction / Q000187:drug effects*; D009130:Muscle, Smooth / Q000187:drug effects*; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism; D011817:Rabbits; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014638:Vanadates; D014639:Vanadium / Q000494:pharmacology*
D014639:Vanadium; D014638:Vanadates; D010042:Ouabain; D012964:Sodium; D000252:Calcium-Transporting ATPases; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium