Hypertension is a serious disease with a genetic association. It is currently diagnosed by an elevated arterial blood pressure. In addition to the elevated blood pressure, microvascular studies over the past three decades have brought to light a plethora of vascular and cellular complications in hypertension. Many of these complications not only encompass the abnormal adjustment of the arterial blood pressure, but also involve an array of tissue functions that have no direct association with the arterial blood pressure elevation. In addition to chronic organ pathologies, hypertensives exhibit diabetic complications, immune abnormalities and an extraordinary sensitivity to acute blood pressure reduction, conditions, which may indicate the presence of a systemic complication in hypertensives. No conclusive evidence has been advanced to suggest that the elevated blood pressure in the arteries serves as the primary event in the complications that arise from the hypertensive syndrome. There is a need to better understand the mechanisms for lesion formation and end-organ injury in hypertension and to analyze the enhanced propensity for organ damage associated with chronic hypertension. Hypertension is a challenging problem to medicine and to bioengineering. A systematic analysis is required. Our past work was designed to find the mechanisms for the elevation of the blood pressure in hypertensives. Our recent research is designed to uncover the mechanisms that lead to an inflammatory reaction in hypertension, to oxygen free radical formation, to leukocyte-endothelial-interaction, and to cell death.

Bright field and fluorescent in-vivo images of neutrophil adhesion to endothelium in rat postcapillary venule before (Panel A) and after stimulation with the inflammatory mediator, platelet activating factor (PAF) (Panel C). The fluorescent images show cell death (red nuclei) as detected with the life/death indicator propidium iodine (right panels). The neutrophil adhesion to the endothelium can be inhibited with an antibody against P-selectin (PB1.3) (Panel D) which inhibits also the parenchymal cells death. The antibody itself has no significant effect on cell adhesion without stimulation (Panel B). (For details see Delano et al., 1997).