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AJP - Heart and Circulatory Physiology, Vol 257, Issue 4 1147-H1155, Copyright © 1989 by American Physiological Society
ARTICLES |
P. A. Jackson and B. R. Duling
Department of Physiology, University of Virginia, School of Medicine, Charlottesville 22908.
The magnitude of the arteriolar response to altered intraluminal pressure was assessed in isolated, cannulated vessels of the hamster cheek pouch. Microvessels were studied during various levels of smooth muscle activation, either occurring spontaneously, or resulting from the application of exogenous agonists including potassium (35 or 70 mM) and phenylephrine (1.25 or 2.50 x 10(-6) M). Diameter-pressure curves were obtained by lowering intraluminal pressure from 60 to 0 mmHg in seven steps at 3-min intervals. At an intraluminal pressure of 40 mmHg, spontaneous tone produced an average constriction to 34 +/- 2% of the maximum diameter. Step reductions in pressure typically led to reductions in the level of activation of the muscle, which resulted in a net dilation over a significant pressure range. This "myogenic response" was more effective in modifying spontaneous tone than in modifying exogenous tone. In fact, the data suggest that reduction of the intraluminal pressure to zero can result in complete inactivation of spontaneous tone. Complete inactivation was not observed when contractions were induced by exogenous agonists, however. The magnitude of the myogenic response in arterioles was consistent with a role in autoregulation, which is 2.5-fold greater than that previously reported for small arteries. The data demonstrate that in the analysis of the mechanics of submaximally activated blood vessels one must include considerations of two phenomenon: the classical stress-length behavior as determined under conditions of maximal activation, and a superimposed modification of the activation level induced by stress- or length-dependent processes. Furthermore, the findings indicate substantial differences in response when tone is spontaneous compared with the case when tone is induced by exogenous agonists.
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