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Effect of Nicotine on the autonomic nervous system
A drug that affects the autonomic nervous system is nicotine. Nicotine is a stimulant drug that hastes the rate at which messages travel between the body and the brain. When nicotine consumed it increases blood pressure, myocardial contractility, and heart rate (Cardozo et al., 2020). The drug induces cardiovascular effects that are mainly a result of the stimulation of sympathetic neurotransmission. Nicotine stimulates catecholamine through the activation of receptors of nicotine acetylcholine confined on the adrenal medulla and the sympathetic peripheral postganglionic nerve endings.
The receptors are the ligand-gated cation path with a cation gate with a central pore and a pentameric that allows permeability and ion selectivity of the drug. A conformation alteration of the central pore occurs due to the binding of the drug to the external binding site that leads to the influx of calcium ions and sodium ions (Oakes et al., 2018). The binding results in depolarization of the end sympathetic nerve, which rouses calcium influx via the calcium channels to release nicotine, induced exocytotic catecholamine.
Nicotine in the intracardiac induces a beta-adrenoceptor upsurge in the contractility and heart rate. The drug also induces an alpha-adrenoceptor that causes an increase in the coronary tone vasomotor. Besides, the drug reaction causes a concurrent increase in the coronary resistance and oxygen demand that results in a damaging effect on the oxygen balance of the heart particularly in patients that have coronary artery complications.
Work Cited
Cardozo, Lais Tono, et al. “Integrating synapse, muscle contraction, and autonomic nervous system game: effect on learning and evaluation of students’ opinions.” Advances in Physiology Education 44.2 (2020): 153-162.
Oakes, Joshua M., et al. “Nicotine and the renin-angiotensin system.” American Journal of Physiology-Regulatory, Integrative, and Comparative Physiology 315.5 (2018): R895-R906.