Pre-synaptic actions of noradrenaline on the dog ciliary muscle tissue

Effects of noradrenaline (NA) on the electrical and mechanical properties of the dog ciliary muscle were investigated using microelectrode- and isometric tension recording methods. Electrical-field stimulation to the tissue evoked excitatory junctional potentials (e.j.ps) followed by twitch contractions. Both responses were abolished by tetrodotoxin (TTX, 10(-7) M) or atropine (10(-6) M), thereby indicating that these responses are cholinergic-related. Exogenously applied NA (greater than 10(-8) M) suppressed the amplitude of e.j.ps and the following twitch contraction evoked by field stimulations, with no change in the resting tension, membrane potential and input membrane resistance of the smooth muscle cells. Exogenously applied carbachol dose-dependently contracted the ciliary muscle. However, NA (10(-5) M) did not affect the carbachol-induced contraction, thereby indicating that NA acts on the nerve terminals and reduces the amount of transmitter released from the terminals. Inhibitory effects of NA on the twitch contraction were antagonized by yohimbine (10(-6) M), but not by prazosin (10(-6) M) or timolol (10(-6) M). Guanethidine (5 X 10(-6) M) had no effect on the contraction evoked by field stimulation. These results provide evidence that exogenously applied NA activates the alpha 2-adrenoceptor located on cholinergic nerve terminal, hence the excitatory neuro-effector transmission is suppressed. These actions may explain the decrease in near point of accommodation observed with clinical application of adrenergic agents.