Neuronal and Extraneuronal Outflow of3H‐Noradrenaline Induced by Electrical‐Field Stimulation of an Isolated Blood Vessel

The adrenergic neuronal selectivity of3H‐outflow elicited by electrical‐field stimulation of rabbit isolated pulmonary artery preloaded with3H‐(‐)‐noradrenaline (3H‐NA) was examined. Following incubation (45 min) of arterial rings at 37°C with3H‐NA (10‐6M) and a 100 min wash‐out period, the sympathetic neurones were stimulated selectively and supramaximally, as regards tension development, with a constant current (250 mA; 300 monophasic pulses; 10 Hz; 0.3 ms). The initial stimulation‐induced3H‐outflow was higher than the subsequent 5 outflows, which remained almost constant (39, 20, 19, 17, 16 and 16 pmol g‐1, respectively).3H‐NA and3H‐O‐methylated plus deaminated metabolites constituted 11% and 74%, respectively, of the total3H‐outflow induced during the initial stimulation period, but 38% and 38%, respectively, during the second stimulation period. Omission of Ca2+in the physiological salt solution reduced the 6 stimulation‐induced outflows to 67, 40, 35, 24, 21 and 21%, respectively, of the untreated preparations. Bretylium (3 × 10‐5M) or tetrodotoxin (10‐6M) reduced the3H‐outflow to approximately the same extent. Stimulation‐induced outflows from artery rings preloaded with3H‐NA in the presence of cocaine (10‐3M) or in the cold (3°C) approximated the Ca2+, bretylium and tetrodotoxin‐insensitive release. These treatments all completely blocked the neurogenic contractile response. When artery rings were preloaded with3H‐NA in the presence of normetanephrine (10‐4M), the stimulation‐induced Ca2+‐insensitive outflows were markedly reduced. The results suggest that the field stimulation‐induced release of3H‐NA is in part of extraneuronal origin.