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The degeneration contraction of a sympathetically innervated smooth muscle in the rat after reserpine, inhibition of monoamine oxidase or tyrosine hydroxylase.

The degeneration contraction of the periorbital smooth muscle in conscious rats was measured after treatment with each of 3 different monoamine oxidase (MAO) — inhibitors, reserpine or the methylester of α-methylthyrosine. Pheniprazine (10 mg/kg), nialamide (100 or 200 mg/kg) pargyline (100 or 200 mg/kg) given at the time of denervation and pargyline (100 or 200 mg/kg) given at 10 hrs after denervation significantly increased the size of the degeneration contraction. 200 mg/kg of pargyline tended to delay the onset of the contraction. However, pheniprazine, nialamide or pargyline at 100 mg/kg started it prematurely. An injection of reserpine (1 mg/kg) given at 2–3 hrs before the expected start of the degeneration transmitter release did not induce any excitatory effect and abolished the degeneration contraction. Inhibition of the synthesis of noradrenaline by the methylester of 1-α-methyltyrosine (H 22/07) given at the time of denervation or 10–12 hrs later did not influence the size or the time course of the degeneration contraction. It is concluded that: — The degeneration transmitter release is normally influenced by functional MAO. — Since the potent MAO-inhibitors studied did not consistently delay the start of the degeneration contraction, it does not seem reasonable that bretylium, which earlier has been found both to possess MAO-inhibiting and delaying effect, induces a delay only by inhibiting intraaxonal MAO. — There is no significant contribution of newly formed noradrenaline to the degeneration contraction.