ACUTE ETHANOL INHIBITS CALCIUM INFLUXES INTO ESOPHAGEAL SMOOTH BUT NOT STRIATED-MUSCLE - A POSSIBLE MECHANISM FOR ETHANOL-INDUCED INHIBITION OF ESOPHAGEAL CONTRACTILITY

In both humans and cats, EtOH administered in vivo and acutely decreas es contractility of smooth muscle of lower esophageal sphincter (LES) and lower esophagus (LE), but not striated muscle of upper esophagus. To see if these effects are associated with perturbation of Ca++ homeo stasis, esophageal muscle slices were incubated in vitro with EtOH and then Ca-45(++). At steady-state Ca++ uptake, some slices were exposed to 1 mu M carbachol (CCH). Although 100 mM EtOH had no effect on Ca+ uptake into resting or stimulated striated muscle of upper esophagus, it significantly inhibited Ca++ uptake into smooth muscle of LES and LE. For unstimulated LE and resting LES, 100 mM EtOH significantly inh ibited both initial uptake and steady-state levels, whereas lower dose s had no significant effect. EtOH at 100 mM also affected changes in C a++ content induced by CCH stimulation. CCH increased total exchangeab le tissue Ca++ content in LE, whereas it decreased Ca++ content in LES . EtOH at 100 mM blunted these CCH-induced effects in both LES and LE. In contrast to resting muscle, inhibition of CCH-stimuiated LE muscle was not limited to 100 mM ROH, because substantial and significant in hibition was also seen at EtOH doses of 25 and 50 mM, doses which are relevant even in social drinking. Thus, EtOH inhibition of Ca++ influx into esophageal muscle is selective for smooth muscle, can occur at p harmacologically relevant EtOH doses and could be the underlying mecha nism for EtOH's inhibition of contractility of esophageal smooth muscl e.