- The normal structural adaptation of heart and vessels to regional changes in load or/and tissue demands is surveyed with respect to its importance for cardiovascular function in normotension as well as in physiological (giraffes) and pathophysiological (e.g. human and rat primary hypertension) variants of high pressure states.
- At the local level it implies an entirely appropriate adjustment of cardiovascular geometric design according to principles inherent in the LaPlace and Poiseuille laws. However, when generalized to all systemic circuits, as in primary hypertension, it invites to a potentially dangerous positive feedback interaction with even ordinary functional pressor influences.
- It is further emphasized how resistance vessels, besides the obvious influence of changes in: (i) vascular smooth muscle activity, are greatly affected also by changes of their (ii) geometric design, (iii) wall distensibility, and (iv) transmural pressure, how each of these four parameters can be independently altered and how they interact. Genetic reinforcements and various trophic influences may facilitate the extent and rate of 'structural upward resetting' in primary hypertension, and this resetting also encompasses the barostat mechanisms.
- Against such a background it is, in fact, from a physiological point of view, more difficult to explain how 85-90% of the population manage to maintain lifelong normotension than to explain why hypertension gradually afflicts the remaining 10-15%. It points to the presence of potentially powerful and durable, negative feedbacks that are still poorly understood (e.g. Muirhead's renomedullary depressor system).
- Considering the dominant haemodynamic influence of the structural factor in primary hypertension, it is finally stressed how the long-range goal of antihypertensive treatment should be to cause full regression of the structural upward resetting, or perhaps even to prevent its early development in subjects predisposed for hypertension.
