Characterization of a neurogenic and a direct smooth muscle component in the contractile response to electrical field stimulation in rat tail artery

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Abstract
1 The extent to which neuronal transmitter release contributes to the contractions induced by transmural nerve stimulation of the rat tail artery at various stimulus intensities was characterized. 2 Using tetrodotoxin, which blocks conduction of the action potential along the nerves, and .omega.-conotoxin GVIA, a blocker of transmitter release from the nerve terminals, as well as chemical and surgical denervations of the perivascular sympathetic nerves, a neurogenic and a direct smooth muscle component could be clearly separated. 3 The neurogenic component was fast in onset, rise and decline (after the end of stimulus), and showed a voltage dependency only at lower stimulus intensities. The non-neurogenic component was slower in onset, rise and decline, and showed a strict voltage dependency throughout the whole stimulus range. This implies that the non-neurogenic component becomes increasingly prominent at high, non-physiological voltages. Mechanisms underlying the declining neurogenic contractile response at the stronger stimulus intensities are discussed. 4 We found no evidence supporting the existence of a possible tetrodotoxin- or .omega.-conotoxin GVIA-resistant contractile component originating from the perivascular nerves (sympathetic or non-sympathetic). Thus, in order to get a purely neurogenic response stimulus intensities should be minimized to give a contraction that is fully sensitive to these two agents. 5 Transmitter release from the perivascular sympathetic nerves was fully responsible for the purely neurogenic contractions. Activation of postjunctional .alpha.1-adrenergic receptors was mainly involved, with a substantial contribution from .alpha.2-receptors, and a minor contribution from neuropeptide Y receptors. There was no evidence for a contractile component linked to activation of so-called .gamma.-adrenergic receptors. 6 .beta.-adrenergic receptors, serotonergic, cholinergic, prostanoic or purinergic mechanisms do not appear to contribute to the neurogenic (or the non-neurogenic) response. The neurogenic contraction does not utilize potential-sensitive calcium channels.