One might strictly recognize the essential hypertensive state as a form of evolving influence, itself both a cause and an effect of integral pathways of etiopathogenesis in vascular myofiber hypercontractility and vascular myofiber ischemia.  Indeed, perhaps it is in terms of a circulatory hemodynamic disturbance that evolves both in terms primarily of myocardial hypertrophy and of vascular smooth myofiber hypercontractility that one would best understand the sustained series of both phasic and tonic responses to various systems of influence in inducing progression of the hypertensive state. Even in terms that would go beyond simple threshold considerations of such myofiber responsiveness or of myofiber contractility, the essential hypertensive state might primarily arise and evolve simply as one pathway of ischemic events that somehow progresses as positive feedback systems.  Indeed, ischemia in hypertension would beget even more ischemia that evolves in terms of parameters that are themselves inherently not related to the hypertensive state.  Indeed, ischemic organ events in arterial hypertension might evolve via systems ranging from hypercontractility of the vascular myofiber to fibrinoid necrosis of vessels, to specific vascular bed organ systems in renal failure and as systems also of intracranial hemorrhage, myocardial hypertrophy and of accelerated atherosclerosis and aneurysm formation.