Summary. The functional importance of an increased wall/lumen ratio due to e. g. hypertrophy of the walls of the resistance vessels in hypertensive disease has been dealt with. Ito is theoretically highly probable that the mere existence of an increased wall mass must cause a proportionally bigger lumen decrease for a given smooth muscle shortening, so that a structurally based “potentiation” of the vasoconstrictor reeponse is obtained. For this reason a given level of smooth muscle tone will probably result in a higher flow resistance in hypertensive disease, where vascular wall hypertrophy has taken place, as compared with the normal vascular bed, provided that the maximally dilated vessels do not show an increase of the lumen as a result of the hypertrophic change. Experimental evidence suggests that this is not the case; if anything the maximally dilated resistance vessels seem to be slightly narrowed in cases of well‐established essential hypertension. In addition it is pointed out that a primary increase of pressure may in many haemodynamically important regions raise the vascular tone, simply due to some strictly local influences on the resistance vessels, where no engagement of specific vasoconstrictor agents or increased smooth muscle sensitivity is implied. Such more chronic and acute secondary consequences of a primary rise of blood pressure may importantly contribute to the increased flow resistance, and possibly most, so in so‐called essential hypertension.