A mathematical model has been developed that relates wall tension in resistance vessels to changes in both distending pressure and flow; the effect of alterations in wall: lumen ratio is taken into account. The model indicates that increased autoregulatory activity in the forearm circulation of patients with primary hypertension could result from an increased response of the vascular smooth muscle to increased intraluminal pressure, but it could be accounted for by an increase in wall:lumen ratio from about 0.2 to 0.3. When the effect of the same increase in wall:lumen ratio on response to dilator agents is examined, it appears that the enhanced response to verapamil could be accounted for by structural change and there is no need to postulate a functional change. If this view is correct, however, it becomes necessary to assume a reduced response of the vascular smooth muscle to sodium nitroprusside in patients with hypertension if the unchanged dilator effect of this drug is to be explained.
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