Characterization of dilatation induced by electrical field stimulation in mammalian cerebral and peripheral vessels.

The ability of electrical field stimulation in releasing transmitter from isolated blood vessels in vitro, during recordings of constrictor or dilator responses, is dependent upon an appropriate choice of stimulation parameters which avoid concomitant change in tone due to a direct effect on the vascular smooth muscle membrane. In many species, including man, small arteries such as pial arteries frequently respond to electrical field stimulation with a dilatation which is TTX-resistant. Such dilatations occur even with stimulus parameters of 7.5 V/60 mA at 0.1 ms, 6 Hz. The stimulation parameters required to induce the TTX-resistant response are just above those needed to obtain a purely neurogenic contractile or dilatory response in vessels equipped with a dense net of adrenergic nerves, such as rabbit central ear artery, and, in addition, highly sensitive postsynaptic alpha- or beta-adrenergic receptors, such as the buccal segment of the facial vein. This prompted us to characterize further the nature of the response. It was tested whether the relaxation, despite being TTX-resistant, might be neurogenic in origin. 4-Aminopyridine, in doses that usually enhance the transmitter release from nerves, did not affect the response. Blockade by a variety of dilator antagonists, the presence of excess amounts of known dilators or removal or emptying of known vasodilator nerves did not inhibit the response. Removal of extracellular calcium did not abolish the response. Therefore, it is highly unlikely that neuronal release is involved to any measurable extent in this response. The relaxation was not significantly affected by removal of endothelium, blockade of endothelium-derived relaxing factor, or interference with mast cells. At modest stimulatory parameters (12-13 V/96-104 mA at 0.1 ms, 7-8 V/56-64 mA at 0.3 ms, at 6 Hz) chlorine gas bubbles could be seen forming at the electrode or mounting hook; this gas is toxic to the musculature and relaxes a pre-contracted vessel. At stronger stimulation (greater than 12 V/96 mA, greater than 0.3 ms at 6 Hz) a relaxation supervened that was almost prevented by scavengers of oxygen free-radical metabolites. This relaxation was partly irreversible, indicating damage to the contractile elements. We conclude that when studying electrically induced release of vasodilator transmitters in vessels not equipped with an highly effective transmitter/receptor function, even a small rise in stimulatory parameters--in order to enhance transmitter release--causes relaxations that are non-neurogenic.(ABSTRACT TRUNCATED AT 400 WORDS)