%0 Journal Article
%T Modulation of Tyrosine Hydroxylase, Neuropeptide Y, Glutamate, and Substance P in Ganglia and Brain Areas Involved in Cardiovascular Control after Chronic Exposure to Nicotine
%A Merari F. R. Ferrari
%A Emerson F. Coelho
%A Karen L. G. Farizatto
%A Gerson Chadi
%A Debora R. Fior-Chadi
%J International Journal of Hypertension
%D 2011
%I Hindawi Publishing Corporation
%R 10.4061/2011/216464
%X 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. 1. Introduction Cardiovascular effects of tobacco smoking are primarily attributed to the presence of nicotine in cigarettes. This alkaloid may promote decrease in baroreflex sensitivity, increase in heart rate and blood pressure, atherosclerosis, coronary heart disease, and myocardial infarction [1]. Nicotine potentiates sympathetic nervous system leading to increase in plasma and brain catecholamine levels [2, 3]. In addition, we have previously demonstrated the acceleration of onset and the exacerbation of hypertension in genetic hypertension predisposed rats after nicotine exposure [4]. The activation of sympathetic neurotransmission by nicotine may be based on its direct effect on the central nervous system, on sympathetic ganglia to increase the efferent nerve activity, and/or on peripheral sympathetic nerve endings and adrenal medulla stimulating catecholamine release [5]. Nevertheless, the activated sympathetic system might promote the reflex parasympathetic response composing an elaborated physiological effect after nicotine administration. The alkaloid instantly interacts with the central nervous system binding to nicotinic acetylcholine receptors in the hypothalamus, hippocampus, midbrain, and medulla oblongata [6, 7] modulating norepinephrine, dopamine, vasopressin, glutamate, neuropeptide Y (NPY), and other neurotransmitter systems [8]. Nicotine acts also on chemoreceptors afferents [9], enteric nervous system [10], and visceral sensory afferents (for a review about nicotinic mechanisms in the
%U http://www.hindawi.com/journals/ijhy/2011/216464/