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Autonomic Drug An autonomic drug is a chemical substance that can either inhibit or enhance the functions of the parasympathetic and sympathetic nervous systems. This type of drug can be used to treat a wide range of diseases, such as urinary, gastrointestinal and cardiopulmonary disorders [1]. Contents 1. Drugs acting on the parasympathetic nervous system 1.1  Mechanism of action 1.2 Medical uses 2. Drugs acting on the sympathetic nervous system 2.1 Mechanism of action 2.2 Medical uses 3. References Drugs acting on the parasympathetic nervous system Parasympathetic nervous system is one of the targets of autonomic drugs. By inhibiting or stimulating this nervous system, therapeutic effects can be achieved. Mechanism of action The activation of parasympathetic nervous system can bring some major physiological effects, such as a rise in glandular secretion, an increase in contraction of smooth muscle, and a reduction in both heart contractility and heart rate. To achieve the above physiological effects, two types of receptors are involved in neurotransmission, namely nicotinic receptors and muscarinic receptors [1]. These two groups of receptors can bind to the same neurotransmitter, acetylcholine, to relay the neurotransmission in the synapse [1]. At the synapse, acetylcholine is released from the presynaptic neuron. After that, acetylcholine can either bind to the receptors on the postsynaptic neuron to continue transmission of nerve signals or bind to receptors on tissues of the organ to cause a physiological response [1]. Then acetylcholine will be degraded to choline and acetate by acetylcholinesterase and this will terminate the action of acetylcholine. By acting on the receptors and acetylcholinesterase involved in transmission of nerve signals, autonomic drugs can be adopted to stimulate or inhibit parasympathetic nervous system to achieve therapeutic effects. Promoting stimulation of parasympathetic nervous system can be attained by using muscarinic agonists or anticholinesterase drugs. Muscarinic agonists can bind to muscarinic receptors and hence promote the transmission of nerve impulses to organs [1], facilitating the physiological effects brought by parasympathetic nervous system. Anticholinesterase drugs interact with acetylcholinesterase so as to prevent acetylcholine from binding to acetylcholinesterase. This hinders the decomposition of acetylcholine, maintaining neurotransmission and also the resulting physiological effects. Inhibition of parasympathetic nervous system can be achieved by utilizing muscarinic antagonists or inhibitors of acetylcholine release. Muscarinic antagonists can bind to muscarinic receptors and block the receptors [1]. Acetylcholine cannot interact with muscarinic receptors so transmission of nerve impulses cannot be passed from neurons to organs to bring about the original physiological response. For inhibitors of acetylcholine release, they can impede the release of acetylcholine from the presynaptic nerve fibre. In this way, there is a decline in neurotransmission and the corresponding physiological effect will be diminished. Medical uses Autonomic drugs are used clinically to treat diseases that are related to the parasympathetic nervous system. Bethanechol is a muscarinic agonist. It is included in the therapy for underactive bladder with poor contraction of detrusor muscle [2]. Since contraction of detrusor muscle in the bladder is controlled by parasympathetic nervous system, Bethanechol can bind to muscarinic receptors to stimulate activation of parasympathetic nervous system and restore contraction of detrusor muscle. A low dose of Bethanechol is often used in treatment as increasing the dose can cause side effects like nausea, diarrhea and headache [2]. Physostigmine is an example of anticholinesterase drugs and it is used in treating glaucoma [3]. For patients with glaucoma, a rise in intraocular pressure is usually found [3]. Physostigmine can block the action of acetylcholinesterase, reducing disintegration of acetylcholine. There is a higher availability of acetylcholine for supporting neurotransmission in parasympathetic nervous system, which promotes contraction of smooth muscle in the ciliary body. This results in an increase in outflow of aqueous humor by widening Schlemm's canal and the trabecular meshwork, lowering the intraocular pressure of patients with glaucoma [3]. The use of Physostigmine may bring about several adverse effects, such as increased pupilary block, ciliary cramps and intestinal cramps [3]. Patients with bradycardia are treated with atropine [4]. Atropine is a muscarinic antagonist, which can obstruct the muscarinic receptor and acetylcholine cannot bind to the receptor for sustaining transmission of nerve signals to the heart through the parasympathetic nervous system. This allows an increase in heart rate. Hyperthermia, dilated pupils and dry mouth are side effects associated with the use of atropine [5]. Botulinum toxin A is an example of inhibitors of acetylcholine release, which is a drug for treating overactive bladder [6]. It blocks the release of acetylcholine from the presynaptic neuron and therefore acetylcholine cannot interact with receptors in the postsynaptic neuron to carry on neurotransmission in parasympathetic nervous system. This results in a decline in contraction of detrusor muscle in the bladder and brings back a normal activity of the bladder. Adopting this therapy to treat overactive bladder can raise the risk of having urinary retention, hematuria and infections in the lower urinary tract [6]. References 1.      Becker DE. Basic and clinical pharmacology of autonomic drugs. Anesthesia Progress. 2012 December [accessed 2019 Mar 5]; 59(4):159-169.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3522494/ 2.     Kim DK. Current pharmacological and surgical treatment of underactive bladder. Investigative and Clinical Urology. 2017 December [accessed 2019 Mar 5]; 58(Suppl 2): S90-S98. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5740035/ 3.     Schmidl D, Schmetterer L, Garhöfer G, Popa-Cherecheanu A. Pharmacotherapy of glaucoma. Journal of Ocular Pharmacology and Therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics. 2015 March [accessed 2019 Mar 5]; 31(2):63-77.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4346603/ 4.     Barstow C, McDivitt JD. Cardiovascular Disease Update: Bradyarrhythmias. FP essentials. 2017 March [accessed 2019 Mar 5]; 454:18-23. https://www.ncbi.nlm.nih.gov/pubmed/28266824 5.     Jones P, Dauger S, Peters MJ. Bradycardia during critical care intubation: mechanisms, significance and atropine. Archives of disease in childhood. 2012; 97(2):139-144. 6.     Hsieh PF, Chiu HC, Chen KC, Chang CH, Chou EC. Botulinum toxin A for the Treatment of Overactive Bladder. Toxins (Basel). 2016 March [accessed 2019 Mar 5]; 8(3):59. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4810204/ DOI: 10.3390/toxins8030059.