Abstract
The nature of neurogenic vasodilatation was investigated in isolated segments of rabbit lingual artery. In separate experiments membrane responses to nerve stimulation were studied by use of microelectrodes. In the presence of guanethidine to block constrictor responses and noradrenaline to induce tone, field stimulation with trains of pulses (8 Hz for 0.5 to 4 s) produced vasodilatation. Atropine (10(-6) M) reduced the relaxations to about 50% of the control values while the induced vasodilatations were potentiated by physostigmine. Tetrodotoxin (TTX, 10(-7) M) blocked all nerve-evoked responses. These data suggest that there is a cholinergic and a non-cholinergic component of the vasodilatation produced by nerve stimulation in the rabbit lingual artery. Single stimuli did not evoke electrophysiological responses. With parameters similar to those used in the mechanical studies, periarterial stimulation in the presence of guanethidine evoked membrane hyperpolarizations which achieved amplitudes of up to 11 mV. The ionophoretic application of acetylcholine (ACh) produced hyperpolarization. The inhibitory junction potentials (i.j.ps) but not the ionophoretic-induced responses were blocked by TTX. The nerve-evoked and the ACh-induced hyperpolarizations were potentiated by physostigmine (5 X 10(-7) M) and totally blocked by atropine (10(-7) M). I.j.ps and hyperpolarization to ionophoresis of ACh were recorded from arteries in which the endothelium had been removed by mechanical rubbing. Mechanical relaxation to field stimulation and ACh was observed in preparations without endothelium. These data suggest that the cholinergic component of the neurogenic vasodilatation in the rabbit lingual artery is accompanied by hyperpolarization. The non-cholinergic component does not appear to possess an electrophysiological correlate. In addition, it seems that the action of nerve-released ACh is mediated by muscarinic receptors which are situated directly on the vascular smooth muscle cells.
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