Abstract
Nicotine, one of the most widely used drugs in human society, has been implicated as a risk factor in many cardiovascular diseases. The mechanisms by which nicotine evokes cardiovascular responses are not clear. This lack of information may be partially attributed to our incomplete understanding of cardiovascular actions of this substance even under normal physiological conditions. The results of several investigators indicate that the effects of nicotine on cardiovascular function are variable. Our results indicate that the cardiovascular actions of nicotine may be variable because it evokes different responses from different regions of the brain. For example, it induces an increase and decrease in blood pressure when microinjected into the pressor and depressor areas of the ventrolateral medulla, respectively. Heart rate and resistance in major vascular beds are increased when nicotine is microinjected into the pressor area. Opposite effects on these parameters are observed when it is microinjected into the depressor area. Other investigators have shown that nicotine induces depressor and bradycardic effects when microinjected into the dorsal medulla. Thus, the net effect of nicotine on cardiovascular function depends on the accessibility of different cardiovascular neuronal pools to sufficient concentration of this substance. Specific brain cholinergic nicotinic receptors and the sympathetic nervous system are involved in these actions of nicotine. The cardiovascular actions of nicotine are comparable to those evoked by other cholinergic agonists such as carbachol and physostigmine.
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© 1987 Plenum Press, New York
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Sapru, H.N. (1987). Control of Blood Pressure by Muscarinic and Nicotinic Receptors in the Ventrolateral Medulla. In: Martin, W.R., Van Loon, G.R., Iwamoto, E.T., Davis, L. (eds) Tobacco Smoking and Nicotine. Advances in Behavioral Biology, vol 31. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1911-5_18
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DOI: https://doi.org/10.1007/978-1-4613-1911-5_18
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