Abstract
It is suggested that blood viscosity remains constant through the action of an autoregulatory mechanism. The sensors and control loops correspond to two types of viscoreceptors, one sensing blood viscosity in large vessels, and another red cell rigidity in small vessels. The presence of rigid cells leads to a decrease of hematocrit to a level corresponding to below-normal blood viscosity in order to compensate for the increased peripheral vascular resistance caused by rigid cells. A malfunction of the beta system will lead to, or contribute to essential hypertension. The structure of the sensors is unknown and one can only specu late on the possible modes of function.
Get full access to this article
View all access options for this article.
