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Abstract
Despite its very potent vasodilating action in vivo, acetylcholine (ACh) does not
always produce relaxation of isolated preparations of blood vessels in vitro. For
example, in the helical strip of the rabbit descending thoracic aorta, the only reported
response to ACh has been graded contractions, occurring at concentrations above 0.1
muM and mediated by muscarinic receptors. Recently, we observed that in a ring preparation
from the rabbit thoracic aorta, ACh produced marked relaxation at concentrations lower
than those required to produce contraction (confirming an earlier report by Jelliffe).
In investigating this apparent discrepancy, we discovered that the loss of relaxation
of ACh in the case of the strip was the result of unintentional rubbing of its intimal
surface against foreign surfaces during its preparation. If care was taken to avoid
rubbing of the intimal surface during preparation, the tissue, whether ring, transverse
strip or helical strip, always exhibited relaxation to ACh, and the possibility was
considered that rubbing of the intimal surface had removed endothelial cells. We demonstrate
here that relaxation of isolated preparations of rabbit thoracic aorta and other blood
vessels by ACh requires the presence of endothelial cells, and that ACh, acting on
muscarinic receptors of these cells, stimulates release of a substance(s) that causes
relaxation of the vascular smooth muscle. We propose that this may be one of the principal
mechanisms for ACh-induced vasodilation in vivo. Preliminary reports on some aspects
of the work have been reported elsewhere.