The present study was aimed at investigating possible transmitter mechanisms in the endothelial cell layer in regulating the tone of the vascular smooth muscle. The thoracic aorta was isolated from the anesthetized male white rabbits and its
helical
strips were prepared. Electrical field stimulation was delivered to platinum wire electrodes positioned parallel to the vessel segment preconstricted with phenylephrine (3.5×10E-6 mol/L) at a distance of 1.5~2.0 mm. The electrical stimulation
(70V, 5
msec, 0.5~200Hz) caused either relaxation only (34%) or a biphasic response (prolonged relaxation following a weak and transient contraction, 66%). The relaxation response was frequency-dependent, and at 200Hz a complete relaxation was noted.
Mechanical
rubbing of the endothelial layer abolished or greatly attenuated the relaxation. The relaxation was also markedly attenuated in the presence of N-G -nitro-L-arginine methyl ester (10E-3 mol/L) or procaine hydrochloride (3.5×10E-4 mol/L).
Tetrodotoxin,
guanethidine, atropine or indomethacin failed to block or enhance the relaxation response to electrical field stimulation. It is concluded that the vascular endothelium in the aorta contains diffusible substances that regulates the function of
the
smooth muscle layer, in which relaxation is more prominent than contraction. Their release by the electrical stimualtion in vitro may not involve classic neuronal transmitter release mechanisms or metabolism of arachidonic acids by
cyclooxygenase.
The
release of the relaxing agents may require an increase in cytosolic calcium level. The chemical nature of the relaxant may be, to a large extent, nitric oxide.
(Korean J Thorac Cardiovasc Surg 1995;28:742-6)
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