Hemodynamic factors in the pathogenesis and maintenance of hypertension

Hypertension is not simply an acute elevation of arterial pressure during a laboratory experiment. It is the development of a cardiovascular disorder provoking a variety of physiological adaptions brought about by an imbalance of pressor and depressor mechanisms that serve to control arterial pressure at normal levels in the normotensive animal. These pathogenetic mechanisms include hemodynamic, volume, renal parenchymal, sodium, renopressor, catecholamine, neural, hormonal, and even depressor factors. The most common form of the disease is essential hypertension, affecting over 95% of patients with hypertension. Although not the same, the experimental animal model that best mimics essential hypertension is the spontaneously hypertensive rat (SHR). However, to state with certainty that the SHR is a true laboratory duplicate of essential hypertension is inaccurate because the causes of both diseases remain unknown. Both forms are genetically predisposed, naturally occurring, slow but progressive in development, and similar in cardiovascular and hemodynamic adaptions. Both involve arteriolar and venular constriction and myocardial hypertrophy that provide a stable hyperfunctioning adaptation of the heart for a substantial period of time but ultimately lead to cardiac failure, stroke, and other vascular impairment. At best we can conclude that they both represent genetically predisposed disease that involves the disarray of the multifactorial interplay of mechanisms that usually maintain arterial pressure at normal levels.