The time courses of arteriolar responses to rapid pressure changes can be partially explained by a myogenic mechanism with static- and rate-sensitive components.
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Animal arteriolar data suggest rate-sensitive myogenesis; leaves open human autoregulation mechanisms and clinical relevance.
The arterial myogenic response may consist of both static- and rate-sensitive components. However, in a recent study of bat wing arterioles, we were unable to demonstrate rate-sensitive constrictions when luminal pressure was elevated at rates between 0.06 and 1 mmHg/s. We have now examined this response in isolated arterioles in vitro, where pressure could be elevated more rapidly. Arterioles were dissected from the hamster cheek pouch and cannulated with micropipettes. Diameters were measured using an inverted microscope and video system, while the vessels were pressurized at various rates (up to 120 cmH2O/s) without flow. Most arterioles developed spontaneous tone and vasomotion and showed myogenic responses over the pressure range 40-160 cmH2O. The magnitude and time course of the active diameter response to a rapid pressure change was highly dependent on the amplitude and direction of the pressure step; monophasic constrictions were observed in response to small-amplitude, positive-pressure steps, and biphasic constrictions were consistently observed when box pressure was elevated to values exceeding 120 cmH2O. The time courses of these responses could be partially, but not completely, explained by a myogenic mechanism with static- and rate-sensitive components. The possible mechanism and physiological significance of this behavior in a microvascular network are discussed.
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Davis et al. (1990) studied this question.
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