BARORECEPTORS are nerve endings that respond to deformation or strain of the vessel walls in which they are located. They do not respond to pressure per se because they are not activated by pressure changes in the absence of deformation (Hauss et al., 1949; Angell-James, 1971). Pressure is sensed by the baroreceptors in a multi-step process that includes pressure-mechanical deformation in the vessel wall followed by mechano-electrical transduction in the receptors themselves. The relationship between wall deformation and intravascular pressure is not direct. Wall deformation may be quantified as strain that is calculated from the ratio of the change in wall radius produced by wall stress to the initial unstressed wall radius. Wall stress is calculated as the product of the distending pressure and the radial distance over which it acts divided by the wall thickness. Wall deformation is also viscoelastic in nature, due principally to the elastin, collagen, and smooth muscle present in the vessel wall. When the wall is strained by pressure, the receptor is deformed by an unknown coupling mechanism probably located in the processes described by Krauhs (1979) and presumably viscoelastic, which influences strongly the dynamic response of the receptors. The preceding steps are the mechanical parts of a sequence linking intravascular pressure to receptor discharge. The major components are shown in Figure 1. The remainder of the sequence is electrical in nature and is determined by the electrophysiological properties of the baroreceptor membrane and axon. By analogy with other mechanoreceptors (Terzuolo and Knox, 1971), receptor deformation generates a receptor potential and thus a receptor current which flows outward across the spike-initiating zone thereby