Changes in the external diameter of active arteries, excised from the rabbit ear, were recorded following jumps in pressure within the arteries. The arteries were either spontaneously active or were constricted with noradrenaline. Active arteries dilated when the transmural pressure was jumped from 60 to 100 mmHg, but the dilatation was largely, sometimes completely, overcome by compensatory constriction within 1-2 min. Varying the constriction from 15 to 80% of the maximal constriction had no effect on the ability of the arteries to counteract distension. An average of 90 +/- 2% of the distension was overcome in 2 min and this was achieved against increases in stress (force/wall cross-sectional area) on the muscle of not less than 74%. Jumps in pressure rarely enhanced constriction and then only when constriction was slight (less than 15% of maximal). Restoring the transmural pressure to 60 from 100 mmHg produced a transient constriction when the initial constriction was less than 50% of the maximal constriction. The sequence of counteraction of distension and transient constriction on reversing the pressure jump was reproducible for many hours. Increasing constriction of the arteries first decreased and then, at maximal constriction, suppressed all transient changes in diameter. Smaller jumps in pressure produced less dilatation which was more readily prevented by increasing constriction. These results show that the wall of the ear artery possesses a pressure-sensitive, negative feed-back mechanism which minimized changes in diameter following jumps in pressure.
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