Abstract
1. The effect of sinusoidal internal pressures on the constriction of in vitro, pressurized segments of ear arteries from rabbits has been examined. All arteries were constricted against a static transmural pressure of 60 mmHg to 35-60% of maximal, using extraluminal noradrenaline, before being exposed to the sinusoidal pressures. 2. There was a short period of adaptation when active arteries were first exposed to physiological pulsatile pressures. This adaptation had two components: a small, largely transient distension, lasting about 1 min, and sustained suppression of the distension produced by individual pressure pulses. 3. Constriction of adapted arteries was insensitive to physiological changes in pulse frequency (3-5 Hz), mean pulsatile pressure (60-120 mmHg), pulse amplitude (20-40 mmHg) and to alterations in pulse shape (sinusoidal, triangular and ramp). Over-all distension was restricted to 3.6 +/- 1.0% (S.D. of an observation) when the mean of a 3 Hz sinusoidal pressure of 30 mmHg amplitude was increased in steps from 75 to either 115 or 120 mmHg. 4. An initial distension was needed to initiate suppression of pressure pulse distension. Distension by individual pressure pulses, within a train of rectangular 60-90 mmHg pulses of 0.5 s duration, was maximally suppressed (85.6 +/- 1.3%; S.E. of mean, n = 9) at a pulse interval of 0.7 s. 5. Active ear arteries possess a myogenic mechanism capable of minimizing changes in constriction over the full physiological range of pulsatile internal pressures.