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International Journal of Hypertension
Volume 2011, Article ID 216464, 9 pages
Research Article

Modulation of Tyrosine Hydroxylase, Neuropeptide Y, Glutamate, and Substance P in Ganglia and Brain Areas Involved in Cardiovascular Control after Chronic Exposure to Nicotine

1Departamento de Genetica e Biologia Evolutiva, Instituto de Biociencias, Universidade de São Paulo, Rua do Matao 277, 05508-090 São Paulo, SP, Brazil
2Departamento de Fisiologia, Instituto de Biociencias, Universidade de São Paulo, 05508-090 São Paulo, SP, Brazil
3Departamento de Neurologia, Faculdade de Medicina, Universidade de São Paulo, 01246-903 São Paulo, SP, Brazil

Received 11 February 2011; Revised 3 June 2011; Accepted 14 June 2011

Academic Editor: Thomas Unger

Copyright © 2011 Merari F. R. Ferrari et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Considering that nicotine instantly interacts with central and peripheral nervous systems promoting cardiovascular effects after tobacco smoking, we evaluated the modulation of glutamate, tyrosine hydroxylase (TH), neuropeptide Y (NPY), and substance P (SP) in nodose/petrosal and superior cervical ganglia, as well as TH and NPY in nucleus tractus solitarii (NTS) and hypothalamic paraventricular nucleus (PVN) of normotensive Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR) after 8 weeks of nicotine exposure. Immunohistochemical and in situ hybridization data demonstrated increased expression of TH in brain and ganglia related to blood pressure control, preferentially in SHR, after nicotine exposure. The alkaloid also increased NPY immunoreactivity in ganglia, NTS, and PVN of SHR, in spite of decreasing its receptor (NPY1R) binding in NTS of both strains. Nicotine increased SP and glutamate in ganglia. In summary, nicotine positively modulated the studied variables in ganglia while its central effects were mainly constrained to SHR.