Abstract

With histochemical techniques, a catecholamine-specific fluorescence was observed in the tunica media of the aortae of young rabbits (1.2-1.3 kg) but not of old rabbits (>3.5 kg). The norepinephrine content of the tissues was investigated by a spectrophotofluorometric method, and the aortae of young rabbits were found to contain twice as much norepinephrine as those of old rabbits. The sensitivity of the young rabbit aortae to nicotine and tyramine was significantly greater than that of old rabbit aortae. Despite these differences, norepinephrine-induced contractions were potentiated by cocaine (10^-6-lO^-7 M) in strips of both types. After five days of cold storage at 2°C or reserpine treatment (4 mg/kg, 24 hours prior to sacrifice), these specific fluorescent substances disappeared from all layers of the tissue; such treatment was found to decrease the tissue norepinephrine content in both young and old rabbit aortae. Cocaineinduced potentiation could still be demonstrated after five days of cold storage. After incubation for 20 minutes in a Ca⁺⁺-free medium, and treatment with Mn⁺⁺, and Co⁺⁺ (both 1 mM), no cocaine potentiation of norepinephrine-induced contraction could be observed. Cocaine potentiated the Ca⁺⁺-induced contraction in a Ca⁺⁺-free medium with a high potassium content (30 mM). Cocaine (l0^-6 M), but not pyrogallol (10^-6 M), could potentiate the phenylephrine-induced contraction. Pyrogallol could potentiate the norepinephrine-induced contraction of fresh strips but not that of cold storage strips. These results suggest that adrenergic nerve fibers penetrate into the smooth muscle layer of the rabbit aortae, but that the cocaine-induced potentiation may not be dependent on these adrenergic nerve terminals in the aortic media. External Ca⁺⁺ may possibly play a significant role in the development of cocaine-induced potentiation.