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Am J Physiol Heart Circ Physiol 293: H3659-H3672, 2007. First published October 19, 2007; doi:10.1152/ajpheart.00712.2007
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Theoretical and electrophysiological evidence for axial loading about aortic baroreceptor nerve terminals in rats

Bin Feng,1,2 Bai-yan Li,1 Eric A. Nauman,2 and John H. Schild1

1Department of Biomedical Engineering, Indiana University Purdue University, Indianapolis; and 2Weldon School of Biomedical Engineering, Purdue University, West Lafayette, Indianapolis

Submitted 19 June 2007 ; accepted in final form 12 October 2007

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 analytic 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., under longitudinal tension average Pth was 84 ± 3 mmHg and Sth was 0.71 ± 0.15 Hz/mmHg, which immediately increased to a Pth of 94 ± 4 mmHg and a Sth of 1.20 ± 0.32 Hz/mmHg with loss of axial tension. Possible explanations of how an abrupt change in axial loading could result in a synchronized increase in afferent drive of the baroreceptor reflex, and the potentiating effect this could have on neurogenically mediated orthostatic intolerance are discussed.

finite element modeling; mechanosensory afferent; orthostatic hypotension; arterial biomechanics; baroreflex



Address for reprint requests and other correspondence: J. H. Schild, Dept. of Biomedical Engineering, Indiana Univ. Purdue Univ. Indianapolis, 723 W. Michigan St., SL174, Indianapolis, IN 46202 (e-mail: jschild{at}iupui.edu)







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