Neuronal and Extraneuronal Outflow of 3H‐Noradrenaline Induced by Electrical‐Field Stimulation of an Isolated Blood Vessel

Abstract

The adrenergic neuronal selectivity of ³H‐outflow elicited by electrical‐field stimulation of rabbit isolated pulmonary artery preloaded with ³H‐(‐)‐noradrenaline (³H‐NA) was examined. Following incubation (45 min) of arterial rings at 37°C with ³H‐NA (10^‐6 M) 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‐induced ³H‐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 and ³H‐O‐methylated plus deaminated metabolites constituted 11% and 74%, respectively, of the total ³H‐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^‐5 M) or tetrodotoxin (10^‐6 M) reduced the ³H‐outflow to approximately the same extent. Stimulation‐induced outflows from artery rings preloaded with ³H‐NA in the presence of cocaine (10^‐3 M) 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 with ³H‐NA in the presence of normetanephrine (10^‐4 M), the stimulation‐induced Ca²⁺‐insensitive outflows were markedly reduced. The results suggest that the field stimulation‐induced release of ³H‐NA is in part of extraneuronal origin.