Release of [₃H]‐noradrenaline from the sympathetic nerves to bovine mesenteric lymphatic vessels and its modification by α‐agonists and antagonists

Abstract

1 Isolated segments of bovine mesenteric lymphatic vessels were loaded with [3H]-noradrenaline and its efflux in response to field stimulation examined. Vessels were attached to an isometric force transducer for the simultaneous recording of mechanical activity. 2 Field stimulation at 1, 4 and 8 Hz (0.3 ms pulses, 1 min train) increased spontaneous contraction rate and evoked 3H release up to a maximum of 4.5% of total tissue 3H at 8 Hz. Output per pulse was maximal at 4 Hz. 3 Tetrodotoxin (3 x 10-6M) blocked the release of 3H in response to field stimulation although the drug did not attenuate release evoked by high K+ (65 mM) solution. Field-evoked release of 3H was also absent in Ca2+-free solution containing EGTA (1 mM). 4 When vessels were preincubated with labelled transmitter plus cocaine (5 x 10-SM) evoked release of 3H was absent. After preloading with [3H]-noradrenaline, cocaine (10-6 M) potentiated both the mechanical response to field stimulation and evoked 3H release. 5 The relatively non selective a-adrenoceptor antagonist phentolamine (3 x 10-6M) and the a2-antagonists yohimbine (10-8M) and rauwolscine (10-6M) significantly increased evoked 3H release at both of the frequencies examined (1 and 4Hz). In contrast, the selective cz1-antagonist prazosin (IO -M) failed to alter 3H release to 4 Hz stimulation although release at 1 Hz was potentiated in the presence of the drug. 6 The postsynaptic excitatory response to field stimulation remained in the presence of prazosin

Lymphatic Innervation

“…All of the above evidence suggests that bovine mesenteric lymphatics have a norad renergic innervation and this conclusion was supported when the vessels were incubated with [3H]-noradrenaline and [3H]-efflux in response to field stimulation monitored [11]. This increased with increasing frequency of stimulation reaching a maximum at 64 Hz.…”

Mediation of excitatory neurotransmission by the release of ATP and noradrenaline in sheep mesenteric lymphatic vessels.

“…A similar explanation may account for our present results although we have no direct evidence to support it. We do know that activation of presynaptic a2-receptors in bovine mesenteric lymphatics depresses the release of noradrenaline in response to field stimulation (Allen et al 1988). It is also known that a2-agonists can inhibit the field-evoked release of ATP (Sperlagh & Vizi, 1992) and that ATP can act presynaptically on P3 receptors to inhibit the release of noradrenaline (Westfall, Kasumasa, Forsythe & Bjur, 1990).…”

β‐adrenoceptor‐mediated facilitation of [3H]‐noradrenaline release from the intramural nerves of bovine mesenteric lymphatic vessels

“…Following incubation with [3H]-noradrenaline all preparations were stimulated initially at 4 Hz for 1 min to displace extraneuronal transmitter which may have been released upon contraction of the vessel. Under these conditions subsequent field stimulation-evoked 3H-efflux reflects endogenous transmitter release (Allen et al, 1988).…”

“…Despite their relatively sparse innervation when compared to accompanying arteries or veins (Alessandrini et al, 1981) this technique has been applied successfully to isolated lympahtic vessels (Allen et al, 1988). In the latter study the a-adrenoceptor agonists clonidine, xylazine and noradrenaline were shown to depress field evoked release of labelled transmitter while the a-adrenoceptor antagonists phentolamine, yohimbine and rauwolscine increased field stimulated release.…”