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This study examined multifiber baroreceptor nerve activity (BNA) as a function of carotid sinus wall distension in 19 rabbits. Analysis estimated mechanical or viscoelastic properties of the sinus wall and their influence on BNA. In six sinuses, properties were altered by treatment with the enzyme protease to remove the endothelium and with nifedipine to passively relax smooth muscle. Properties were estimated from dynamic and steady state wall response to a 45 mm Hg step increase and decrease in intrasinus pressure (ISP) of 20 min. Control wall response had fast and slow (creep) portions with a viscosity increase from 1,370 N(s)/m to 17,864 N(s)/m during step-up in ISP. Wall elasticity averaged 77 N/m; which estimated the relationship of force and change in steady state response. Control BNA response also had fast and slow (resetting) portions. A BNA and wall response relationship (BNA/m) was defined as transduction-gain (T-G) with proportional and dynamic components. In the subgroup, wall creep and baroreceptor resetting were abolished by protease treatment, suggesting an endothelial mediator which influenced sinus smooth muscle. Histology data indicated enzyme damage was limited to tunica intima tissues, and nifedipine did not block Ca2+ channels on neural structures. By comparison of responses before and after treatments the proportional component of T-G was equated to an elastic influence (1/E), with E = 7.5 x 10(-6) m/BNA, while the dynamic component was equated to a viscous influence (1/V), with V = 1.53 x 10(-4) m(s)/BNA. A simple but fundamental relationship for baroreceptor-tissue linkages was estimated by BNA/m = 1/(Vs + E), a first-order transfer function.

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