S OF PAPERS SUBMITTED TO THE AMERICAN MOTILITY SOCIETY IMMUNOLOGICALLY INDUCED ALTERATIONS IN THE INTRINSIC PROPULSIVE STATE OF GUINEA-PIG JEJUNUM. H. Alizadeh, u I&& G.A. Castro. Department of Physiology and Cell Biology, University Texas Medical School, Houston, TX. A net aboral propulsive (NAP) pattern of intrinsic fluid-propelling behavior is initiated in jejunal segments of guinea pigs during Trichinella soiralif infection. This pattern occurs 10 days after primary inoculation but as y;;zeas 2 days after secondary inoculation with infective intrinsic Since 1. soiralis induced changes in the propulsive state of the jejunum occur five times faster in previously infected as compared with uninfected animals, experiments were conducted to determine if intrinsic control systems regulating jejunal propulsive behavior can be inxnunologically programed to dire;&;y respond to the presence of I. soiralis antigen. months after guinea pigs were inoculated with 2000 1. soiralis larvae, jejunal segments were removed and attached to a propulsion evaluation system that required segments to do hydrostatic work to expel fluid in either the oral or aboral direction. Segments from previously infected (i.e. immune) animals and from nonimmune animals produced identical patterns of propulsive behavior. Arterial perfusion of segments from immune animals with 1. soiralis antigen (200 us/ml) immediately produced a different pattern of propulsive behavior that was unlike the NAP complexes observed during intestinal infection. This antigen induced pattern was not produced by segments from immune animals arterially perfused with ovalbumin nor by segments from nonimmune animals also perfused with the I. soiralis antigen. We conclude that the enteric control system of the guinea-pig jejunum can be immunologically programmed to respond directly to specific antigenic stimuli and subsequently alter propulsive behavior. Additional studies are required to characterize the inune mechanisms that program this change in intrinsic propulsive state and to determine the relation of this antigen-induced pattern of behavior to the NAP pattern observed during 1. soiralis infection. (Supported by NIH Grants AI 11261 and AM 23038). CELLULAR MECHANISMS OF THE TONE REGULATION IN THE CANINE LOWER ESOPHAGEAL SPHINCTER (LES) IN VITRO. H.-D. Allescher: -and E.E. Daniel. Department of Neurosciences, M:,O-' ML; channel antggonists ~:~~~~?a?& ~Zhe novel Ca cf!annel activator RAY-K-8644 (10 iphe :hz M) caused increased basal tension, and antagonised in a dose-dependent manner the effect of low calcium medium and of the calcium channel antagonist PN-200-110. It also increased significantly contractions caused_ky KC1 depolarisatpn. Some agonists (acetylcholine 10 M, histamin$+lO M) caused f;;;a;LJvn after removal of external Ca or in the presenchannel antagonists in concentrations which abolished basal active tension. Moreover, y$en tone was restored by these agonistsSin the presence of Ca channel antagonists (PN 200-110 2x10 M), field stimulation still elicited full relaxation. Stimulation of thE7cAMP system with the specific Rctivator Fos~~~~,~E~a~e3xl~,nc~1s',~~~4d a dose-dependent desfease of 1) A continuous Ca influx through the cell membrane ie+involved in the spontaneous tone product&. 2) The Ca channels involved are very sensitive to Ca channel activators either because the membr$nes are depolarized or because they differ from wt:;:,;; cas$annels in smooth muscle. 3) There are intrastores capable of release by agonists to.sustain contraction. 4) The non-adrenergic, non-cholinergic inhibitory mediator causes relaxation bS+a mechanism not requiring functional voltage-dependent Ca channels. 5) A presumed increase of the intracellular CAMP-level decreases the basal tone. * Supported by MRC of Canada and by Deutsche Forschungsgemeinschaft DFG AL 245/1-l.