The interaction between noradrenaline activation and distension activation of the rabbit ear artery

Excised, pressurized segments of the rabbit ear artery have been used to examine the interaction between the transmural pressure and constriction of arteries by extraluminal noradrenaline. The bath temperature was kept at 32-33 degrees C to suppress instability and spontaneity of constriction. Fast, reproducible jumps in pressure were obtained by using a microcomputer to control an electropneumatic transducer. The arteries did not react actively to transmural pressure changes unless already activated by noradrenaline. Active arteries responded to distension by a pressure jump with a reproducible compensatory constriction which was unaffected by tetrodotoxin. The counteraction of distension was due primarily to enhanced activation of the muscle. Distension activation decreased with increasing constriction. Utilization of the force-generating capacity of the arteries either remained unchanged at 20-30% or, in one experiment, increased slightly when constriction against a transmural pressure of 60 mmHg was increased from 20 to 75% of maximal by raising the noradrenaline concentration. When the transmural pressure was 90 mmHg, the 35-55% utilization of the force-generating capacity either remained constant or fell as constriction was increased. Most of the force-generating capacity was available for counteracting the distension of moderately constricted arteries (less than 40% of maximal) produced by a 60-90 mmHg jump. More than 78% of the maximum capacity was used in attempting to overcome the distension when it was maintained by computer-controlled increases in transmural pressure. The moderate constrictions were produced with noradrenaline concentrations which were 500-10,000 times lower than that used to maximally activate the arteries. The rabbit ear artery possesses a powerful, distension-sensitive mechanism that acts to minimize diameter changes initiated by transmural pressure jumps. The diameter of the active artery was determined by a combination of noradrenaline activation and distension activation for constrictions up to at least 75% of maximal. It is concluded that the interaction between noradrenaline activation and distension activation helps the muscle to fulfil the special functional requirements imposed by the geometry of tubes. This type of myogenic control system may be particularly well developed in those muscular blood vessels exposed to pulsatile internal pressures.