We studied the changes in vascular smooth muscle (VSM) cell tone during the adaptation of rat common carotids to induced hypertension. Hypertension was induced in 8 week old male Wistar rats by total ligation of the aorta between the two kidneys. Mean blood pressure increased abruptly from 92 +/- 2mm Hg (mean +/- SE) to 145 +/- 4 mm Hg and remained constant thereafter. Rats were sacrificed 2, 4, 8, and 56 days after surgery and the left common carotid artery was excised for analysis. Pressure-diameter curves were measured in vitro under normal, maximally contracted, and totally relaxed VSM. The VSM tone was analyzed in terms of its basal tone (active stress at low strains) and its myogenic tone (increase in active stress at high strains). Our results show that the capacity of the VSM to develop maximal active stress is not altered in hypertension. Basal tone, however, increases rapidly in the acute hypertension phase (2-8 days postsurgery) and drops to nearly control values at 56 days postsurgery. Also, the onset of myogenic response decreases to lower strains following the step change in pressure, to be restored back to control levels at 56 days postsurgery. We conclude that VSM adaptation is most significant in the acute hypertension phase and acts as a first, rapid defense mechanism for the arterial wall. The VSM tone returns back to normal levels once the slower geometrical and structural remodeling is developed sufficiently to restore the biomechanical environment and function of the arterial wall to control levels.

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Arteries change diameters in response to BF reduction and also flow restoration to normal after flow reduction, keeping WSS at physiologically normal levels. The lack of changes in vascular elasticity suggests that there were no significant changes in major wall constituents, such as elastin and collagen. VSM may play the dominant role in observed arterial remodeling and adaptation.

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