Atropine potentiates neurogenic vasodilatation of the feline infraorbital artery: possible mechanisms.

After treatment with guanethidine to inactivate sympathetic nerves, the feline infraorbital artery (IOA) relaxes in response to activation of periarterial nerves in vitro. This response was 60-65% greater in magnitude and 50% longer in duration in the presence of atropine, thus revealing a significant non-adrenergic, non-cholinergic (NANC) dilator response which is potentiated by blockade of muscarinic receptors. Nerve-mediated dilations and the potentiating effect of atropine were endothelial cell-independent. In the presence of atropine the resting membrane potential (-51 +/- 2 mV) of infraorbital vascular smooth muscle cells was not changed by activation of nerves, nor by exogenously applied vasoactive intestinal polypeptide (VIP). Electrical stimulation caused release of VIP from this artery, but atropine did not measurably enhance the degree of release of VIP. Therefore, although presynaptic, muscarinic inhibition of release of a NANC transmitter probably occurs in the IOA, either VIP is not the transmitter involved in this response or the changes in release of VIP are too slight to be detected by the in vitro techniques employed in this study.