Physiology and pathophysiology of hypertension

The exact cause of primary hypertension is unknown. Neurohumoral, renal, metabolic, race, genetic, and environmental factors have been shown to be related to the development of hypertension; thus, the multifactorial hypothesis of the pathophysiology of hypertension. The pathophysiologic hemodynamic mechanisms of hypertension are known. However, the pathogenic processes that result in the vascular abnormalities responsible for the hemodynamic expressions of hypertension are speculative. Available data suggest that during the early phases of hypertension, when several factors may act together or independently to turn neurohumoral systems on and off, transient exacerbated alterations in pressure-flow relation are produced in subjects with a hyperresponsive cardiovascular system due to altered vascular properties. Changes in arterioles, which increase total peripheral resistance, result in an increase in diastolic and a secondary increase in systolic blood pressures in response to pressor stimuli. Changes in arteries, which decrease vascular compliance, result in an increase in systolic and a decrease in diastolic blood pressures. Initially, this response is only slightly different from that seen in the nonstimulated state. However, if the stimulation is too frequent, changes occur in vascular properties that provide hemodynamic mechanisms for additional vascular alterations. This further amplifies the increase in pressure. The relative magnitude of arteriolar to arterial vascular alterations determines the relative changes in diastolic and systolic pressures and thereby contributes greatly to the shape of the oscillatory arterial pressure wave. The height of the mean blood pressure, a weighted average of the systolic and diastolic blood pressures, is the product of cardiac output and peripheral resistance.