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1. When sheep carotid arteries had become electrically active after 30 min in Ca-free saline, noradrenaline 0·1 mM caused almost as much contraction as it did with Ca 1·25 mM present; it also caused slight electrical depolarization, usually with increased spike frequency, followed by electrical quiescence.

2. In Ca-free saline with EDTA the arteries became profoundly depolarized, and their mechanical responses greatly reduced, within a few minutes. The mechanical responses to noradrenaline that remained were accompanied by electrical repolarization or, after longer periods in EDTA, by no electrical change.

3. This residual mechanical responsiveness to noradrenaline, always tested at 36° C, declined on average 26 times as rapidly during exposure to EDTA at 36° C as at 5° C and was not reduced by increasing the concentration of EDTA from 1·25 to 12·5 mM. This temperature-sensitivity was significantly too high to be explained by a diffusion-limited process.

4. The results suggest that most of the tissue Ca responsible for contractility in simple Ca-free saline was either free in the extracellular space or in cellular stores that were discharged within a few minutes when free extracellular Ca was removed. They also indicate a small resistant Ca store which did not communicate with the exterior by diffusion, and part of which noradrenaline could utilize for contraction by means not dependent on depolarization conducted from the cell membrane.