Hyperkinetic hypertension
Established hypertension, i.e. >140/90 mm Hg, is very often preceded by hyperkinetic hypertension which is normally not treated. This hyperkinetic hypertension is characterized by a raised heart rate and blood pressure. A rise in sympathetic activity is the major determinant of hyperkinetic hypertension which is prevalent particularly in young overweight persons. If hyperkinetic hypertension is not treated, a remodelling of the vasculature ensues which leads to established hypertension. A very late state is "isolated systolic hypertension" seen in the elderly. This systolic hypertension arises from a severe remodelled aorta and large arteries with greatly reduced elasticity. The loss of the elastic recoil during diastole results in a low diastolic blood pressure while systolic blood pressure is markeldy increased.
    It should be our aim to prevent a deleterious vascular remodelling as early as possible. More emphasis should be placed on hyperkinetic hypertension, an early form of hypertension. We examined whether dietary factors could account for the occurrence of hyperkinetic hypertension. We showed in rats using radio telemetry that this hyperkinetic hypertension occurs when caloric intake is increased. A diet rich in fat (47% fat calories) and sucrose (26% sugar calories) increased heart rate as well as systolic and diastolic blood pressure (1).

The hyperkinetic hypertension arises most probably from an increased sympathetic outflow of the brain. Of particular relevance is the finding that the rise in heart rate and blood pressure occured irrespective of day-night cycle. The hypercaloric diet raised systolic blood pressure at night, i.e. light phase when rats are inactive,  to a level observed during the active dark phase. This continuous rise in blood pressure and heart rate contrasts effects of psychosocial stress which occur only intermittently. We believe that the continuous rise in blood pressure contributes to the deleterious remodelling of the vasculature.

A rise in sympathetic activity stimulates renin release of the kidneys leading to enhanced angiotensin II and aldosterone influences. These factors have a major influence on the vascular remodelling and thus manifestation of high blood pressure.

Current treatment of hypertension is typically initiated when high blood pressure is established, i.e. systolic blood pressure greater 140 mm Hg and diastolic blood pressure greater 90 mm Hg. However, this hypertension is preceded by a long period of hyperkinetic hypertension which is typically not treated. Hyperkinetic hypertension is associated with sympathetic overactivity. It appears thus as a rational therapy to reduce the raised sympathetic outflow of the brain. This is achieved best currently with the selective imidazoline agonist moxonidine. Whenever a marked adverse remodeling of the vasculature has occurred in later years, often one antihypertensive drug is not sufficient for normalizing the high blood pressure. Under these conditions,  a combination with other antihypertensive drugs is useful.

Treatment targets for hypertension

1. Rupp H, Maisch B: Radiotelemetric characterization of overweight-associated rises in blood pressure and heart rate. Am J Physiol  1999;277:H1540-1545