Role of the caudal pressor area in the regulation of sympathetic vasomotor tone

Full cite: Campos, R.R., Carillo, B.A., Oliveira-Sales, E.B., Silva, A.M., Silva, N.F., Futuro Neto, H.A., Bergamaschi, C.T. Role of the caudal pressor area in the regulation of sympathetic vasomotor tone  (2008) Brazilian Journal of Medical and Biological Research, 41 (7), pp. 557-562.

Role of the caudal pressor area in the regulation of sympathetic vasomotor tone

R.R. Campos¹, B.A. Carillo¹, E.B. Oliveira-Sales¹, A.M. Silva¹, N.F. Silva²,

H.A. Futuro Neto^3,4 and C.T. Bergamaschi⁵

1Departamento de Fisiologia, Disciplina de Fisiologia Cardiovascular e Respiratória, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brasil

2Laboratório de Neuromorfologia,

3Programa de Pós-Graduação em Ciências Fisiológicas, Universidade Federal do Espírito Santo, Vitória, ES, Brasil

4Escola Superior de Ciências, Santa Casa de Misericórdia de Vitória (EMESCAM), Vitória, ES, Brasil

5Departamento de Biociênicas, Universidade Federal de São Paulo, Campus Baixada Santista, Santos, SP, Brasil

This review examines how the Caudal Pressor Area (CPA) controls sympathetic outflow. The CPA is a relatively undefined region that is located at the caudal end of the Caudal Ventrolateral Medulla (CVLM). This region has shown to illicit sympathoexcitatory responses when it is directly stimulated, suggesting that the CPA either contains SPNs or innervates SPNs via a direct or indirect pathway. The CPA is not widely considered to be one of the main contributors to SPN innervation, however, there is quite a bit of ambiguity as to where the SPNs receive their excitatory drive from. One of the main statements of this paper is that the CPA provides a significant source of tonic excitatory drive to the RVLM, which I find that surprising considering this is one of the very few times I have read about the CPA, so there must be some complication to the CPA that I simply do not know yet. Apparently the effect of the CPA is mediated through the RVLM, suggesting some direct projection from CPA to the RVLM. According to this review, the CPA projects to the CVLM as well, and that inhibition of the CPA neurons has the greatest effect on the slow frequency neurons in the RVLM, not the fast ones. This response may suggest that the CPA has a selected enhancement of C₁ neurons. It would be interesting to see how the CPA relates to our model, especially if it does have as significant of an effect on RVLM neurons as this review suggests. It would also be interesting to see if the Caudal Pressor Area is stimulating the RVLM via glutamate or a different excitatory agonist. Also the CPA could be selectively innervating particular neuronal beds in the RVLM which could account of the differential control of nerve activity results that we have shown previously. It is certainly possible those different brain regions are responsible for stimulating different subsets of RVLM neurons and that these brain regions are stimulated by different phenomena throughout the body. That being said, I do not necessarily know of any evidence of preferential control of RVLM in regards to different brain regions, however, I believe that it is certainly possible given the fact that the RVLM has to manage MANY inputs and I do not believe that it is sophisticated enough to act as an integration center as well as a delivery center without some help from its neuronal circuitry.  - M.T.L.