Abstract
1. Direct injury to the smooth muscle of the sheep carotid artery in vivo caused large, persistent and sharply limited annular contraction, even with tetrodotoxin 10(-5)M present to block nerves. 2. Surcose gap records from artery strips showed that mechanical injury caused slow, prolonged depolarization of the smooth muscle that spread for a few millimetres in a circular direction in relation to the intact artery wall with an apparent space constant of 1-26--3.49 mm. In the longitudinal direction, no depolarization was recorded 1 mm from the site of injury. No spikes were recorded more than 1 mm in either direction from the site of injury except when procaine, which facilitates electrical activity in the smooth muscle, was present. 3. When responses of inner and outer muscle were recorded separately, injury caused comparable contraction of both parts. 4. Clotted blood caused large contractions of intact artery strips; it contracted inner much more than outer muscle. 5. The main factors in the intact vessel's response to injury therefore seem to be inner and outer muscles' direct response to injury, reinforced by spread of depolarization round the vessel wall, and inner muscle's response to vasoconstrictor agents released by clotting blood.
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