Submitted on June 19, 2007
Accepted on October 12, 2007
Theoretical and electrophysiological evidence for axial loading about aortic baroreceptor nerve terminals in rat
Bin Feng1, Bai-yan Li1, Eric A Nauman2, and John H. Schild1*
1 Biomedical Engineering, Purdue School of Engineering and Technology, Indianapolis, Indiana, United States
2 Mechanical Engineering, Purdue University, West Lafayette, Indiana, United States
* To whom correspondence should be addressed. E-mail: jschild{at}iupui.edu.
Arterial baroreceptors are essential for neurocirculatory control, providing rapid hemodynamic feedback to the central nervous system. The pressure-dependent discharge of carotid and aortic baroreceptor afferents has been extensively studied. A common assumption has been that circumferential deformation of the arterial wall is the predominant mechanical force affecting baroreceptor discharge. However, in vivo the arterial tree is under significant longitudinal tension, leading to the hypothesis that axially directed forces may contribute to baroreceptor function. To test this hypothesis we utilized a combination of finite element modeling methods and an in vitro rat aortic arch preparation. Model formulation utilized traditional analytical constructs available in the literature followed by refinement of model material parameters through direct comparison of computationally and experimentally generated pressure-diameter curves. The numerical simulations strongly indicated a functional role for axial loading within the region of the baroreceptive nerve terminal. This prediction was confirmed through single fiber recording of baroreceptor nerve discharge under conditions with and without longitudinal tension in the vessel preparation. The recordings (n = 5) demonstrated that longitudinal tension significantly (p < 0.02) lowered both the pressure threshold (Pth, mmHg) for baroreceptor discharge and sensitivity (Sth, Hz/mmHg). The effect was nearly instantaneous and sustained, i.e. with longitudinal tension Pth was 84 ± 3 mmHg and Sth was 0.71 ± 0.15 Hz/mmHg while without longitudinal tension Pth increased to 94 ± 4 mmHg and Sth increased to 1.20 ± 0.32 Hz/mmHg. Possible explanations of how an abrupt increase in longitudinal tension could result in a synchronized increase in afferent drive of the baroreceptor reflex and the potentiating effect this could have upon neurogenically mediated orthostatic intolerance are discussed.
