ABSTRACT
In vivo, the vascular endothelial cell is exposed to a hydrostatic pressure which is the net sum of plasma osmotic and plasma oncotic pressures, tissue osmotic and tissue oncotic pressures, and a component of the “blood pressure” (as measured using sphygmomanometry). The blood pressure measured by a sphygmomanometer represents a stagnation pressure which is a conversion of the dynamic, unidirectional pressure which drives blood flow (and applies fluid shear stress to the endothelial cells) into a static, omnidirectional pressure (which contributes to the hydrostatic pressure to which the endothelial cells are exposed). Therefore, the hydrostatic pressure vascular endothelial cells are exposed to is proportional to, but not equal to, the sphygmomanometric blood pressure. For example, in the rat, abdominal aortic pressure ranges from 132-172 cm H2O but the range of tissue interstitial pressure in the kidney is from 4-29 cm H2O (Skarlatos et al., 1994). This relation also implies that variations in blood pressure (such as transient changes due to body posture and/ or vascular tone, or chronic changes due to hypertension and
atherosclerosis) can alter the net hydrostatic pressure to which endothelial cells are exposed. Additionally, anatomical parameters (e.g., height of the vascular bed and rigidity of tissue support) expose endothelial cells at different sites of the vascular tree to different hydrostatic pressures; for example, in the upright human body, the veins of the neck are maintained at atmospheric pressure (Guyton, 1986), the veins of the skull are maintained at subatmospheric pressure (Guyton, 1986), and in the large vessels of the feet, pressure may exceed 100 cm H2O above atmospheric pressure (Guyton, 1986).
