It is generally accepted that a rise in systemic flow resistance constitutes the essential background of the increased arterial blood pressure in well-established hypertension, though the early ‘labile’ phases of essential hypertension in particular may exhibit a pattern simulating a moderately intense defence reaction, with enhanced cardiac output and muscle blood flow as the most characteristic features, apart from the rise in blood pressure. With respect to the increased flow resistance in the well-established phase, it is accepted that the vessels respond readily, and apparently normally, to vasodilator substances, from which the correct conclusion has been drawn that the resistance increase cannot be ascribed to any sclerotic narrowing of the resistance vessels (Pickering, 1968).
However, this observation has also generally led to the assumption that an increased smooth-muscle tone of the resistance vessels must be the explanation of the increased flow resistance and, despite the fact that there are numerous reports of medial hypertrophy in the precapillary resistance vessels for instance (Pickering, 1968), the possible haemodynamic consequences of such a type of structural vascular adaptation has hardly been considered at all. Instead the debate has mainly been concerned about whether the assumed increase of vascular tone is due to enhanced myogenic activity, to an increased neurogenic and/or hormonal exogenous stimulation of the vascular smooth muscles or whether these muscles might exhibit an enhanced sensitivity or ‘reactivity’ to such extrinsic stimuli.
In other words, if summarized in a diagram relating the extent of active smooth-muscle shortening to the degree of resistance increase in an idealized resistance vessel (Fig. 1), an increased smooth muscle activity, whatever its background, would mean a shift from the normal resting equilibrium at point O to a point B along the curve N.
However, one cannot safely deduce levels of vascular smooth-muscle activity between different individuals, or vascular beds, by simply assuming that they are proportional to the respective levels of current flow resistance. In each individual, or vascular bed, one must first relate the actual resistance level to that present when the vascular smooth muscles are completely inactive; i.e. when the resistance vessels are maximally dilated and exposed to the same amount of distending pressure. This latter resistance value provides the necessary ‘baseline’, or an equivalent of fully relaxed muscle length for a particular vascular bed, from which its current level of smooth muscle activity has to be judged in terms of the ratio between these two resistance values. This is simple and straightforward reasoning, but surprisingly enough studies along these lines were apparently not performed systematically until our group used this approach in analyses of the level of ‘basal tone’ in different vascular beds or individuals (Celander & Folkow, 1953; Löfving & Mellander, 1956; Folkow, 1956).
Fluorescence demonstration of dipeptidyl peptidase II in skeletal, cardiac, and vascular smooth muscles.
