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.