In order to throw light on the mechanism of acute hypertensive baroreceptor resetting, we examined the relationship between aortic baroreceptor firing and aortic wall properties in anaesthetized dogs as pressure was varied in a number of ways. We recorded baroreceptor impulses from the left aortic nerve, and measured aortic pressure with a catheter‐tip transducer and external aortic diameter with ultrasonic transit‐time transducers. Narrow anticlockwise hysteresis loops were evident in the pressure‐diameter relationship of the upper thoracic aorta, both during the rapid pulsatile pressure changes of the cardiac cycle and during the slow excursions of mean pressure imposed for construction of baroreceptor pressure‐‐response curves. In contrast to the 'phase‐lag' response of diameter to pressure, the baroreceptor response was 'phaselead' in character, decreasing when stress‐induced creep occurred in the aortic wall. When the mean arterial pressure set‐point was increased from 100 to 125 mmHg for 20 min, the hysteresis loops relating mean diameter to mean pressure in the range 60‐200 mmHg were displaced along the diameter axis in the direction of wall creep. A reduction in the baroreceptor response to pressure (i.e. resetting) always accompanied this displacement. Administration of ouabain (25‐35 micrograms/kg) had no consistent effect on baroreceptor resetting. It has been suggested that acute baroreceptor resetting is akin to adaptation. To investigate the possibility that the two processes are accompanied by similar changes in aortic wall properties, we converted the aorta into a closed sac and distended it with a square wave of pressure. Like resetting, adaptation of the baroreceptor response to maintained pressure was associated with a small degree of creep of the aortic wall. Our results are compatible with the hypothesis that acute hypertensive resetting of aortic baroreceptors is similar to adaptation, both phenomena being attributable to relaxation of viscoelastic coupling elements, leading to a reduction of strain at the receptor membrane. Whether viscoelastic processes alone can account for acute resetting, or whether changes in ionic balance are involved also, baroreceptor responsiveness is a function of the stress history of the wall, the pressure‐response curve moving along the pressure axis in the direction of the prevailing set‐point. Hence, in early hypertension physiological resetting of baroreceptors will precede pathological resetting, and may even promote an upward movement of set‐point.
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