Neuro-effector transmission and mechanical responses in smooth muscles of the dog iris were studied, using tension recording and microelectrode methods. Electrical stimulations evoked an initial phasic contraction followed by relaxation in both the iris sphincter and dilator muscles. Atropine selectively suppressed phasic contraction of the sphincter and relaxation of the dilator muscle, while guanethidine selectively blocked relaxation of the sphincter and contraction of the dilator muscle. Pharmacological investigations revealed distributions of alpha 1-excitatory (mediating contractions) and alpha 2-inhibitory (mediating relaxations) adrenoceptors in addition to beta-inhibitory adrenoceptors in the sphincter muscles, and alpha-excitatory and beta-inhibitory adrenoceptors in the dilator muscle. These results indicate that the iris sphincter and dilator muscles receive double reciprocal innervations by the cholinergic and adrenergic nervous systems. Norepinephrine (NE) or carbachol did not modify membrane potential of the smooth muscle cells in either muscle tissue, yet these agents evoked muscle relaxation or contraction, respectively; in the sphincter muscle. Reversed sequences of mechanical responses were observed in the dilator. Ca-free solution reduced the resting tension and blocked the agonist-induced contraction in both muscle tissues. Excess-[K]0 solution dose-dependently depolarized the muscle membrane, and evoked combined mechanical responses of relaxation and contraction which were blocked by adrenergic and cholinergic blocking agents, mainly due to NE or acetylcholine (ACh) released from the nerve terminals in both muscle tissues. In the sphincter muscle, excess-[K]0 solution evoked a phasic contraction in the presence of these blocking agents. Specific mechanical features of the dog iris in relation to excitation-contraction coupling were given attention.