In fish, the amplified surface area and narrow diffusion distances of the gill secondary lamellae contribute to vital physiological exchange processes. Local control of blood flow within the secondary lamellae has been speculated to also play a role in regulating various exchanges. However, secondary lamellae lack vascular smooth muscle cells; the intralamellar blood space is defined by a marginal endothelium and by buttressing pillar cells. Studies have suggested both the presence of smooth muscle filaments and contractile capacity in pillar cells. To further examine the possible role of secondary lamellar hemodynamic control in gill function, the expression of smooth muscle myofilaments was investigated in largemouth bass, Micropterus salmoides. Homogenates of gill epithelial scrapings, stomach and skeletal (trunk) muscle were analyzed by SDS PAGE and Western blot. Using a monoclonal anti-smooth muscle myosin antibody, positive signals were observed for bass gill and stomach, but not skeletal muscle. A monoclonal, smooth muscle anti-α-actin antibody also yielded tissue-specific signals for bass stomach and gill. Smooth muscle α-actin in bass gill and stomach also had slower elecrophoretic mobility, implying larger molecular mass, than α-actin from the control species (guinea pig). These antibodies are now being used in ongoing immunolocalization studies intended to test the hypothesis that smooth muscle myosin and α-actin are expressed in largemouth bass pillar cells.