Here is an essay on the ‘Autonomic Nervous System’ for class 11 and 12. Find paragraphs, long and short essays on ‘Autonomic Nervous System’ especially written for college and medical students.
Essay # 1. Introduction to Autonomic Nervous System:
The autonomic nervous system supplies the viscera. The viscera include the gastrointestinal tract, the respiratory and urogenital systems, the heart and blood vessels, the intrinsic muscles of the eye and the endocrine and exocrine glands.
The autonomic system consists of two division – the sympathetic and the parasympathetic system. The two divisions control homeostatic functions that are primarily involuntary. The autonomic neurons located in the ganglia outside the central nervous system give rise to the postganglionic autonomic nerves that innervate the viscera. The activity of autonomic nerve is regulated by central neurons.
Responses to the sympathetic and the parasympathetic stimulation are frequently antagonistic as exemplified by the in opposing effects on the heart rate and gut motility.
The transmission of the nerve impulse across junctions such as synapses occurs through the release of humoral (chemical) messenger from the prejunctional nerve endings, which bridges the gap at the synapses, and thus activates a receptor in the organ supplied or in another nerve cell. The chemical transmitters involved differ in sympathetic and parasympathetic divisions.
Essay # 2. The Sympathetic Nervous System:
The sympathetic nervous system consists of a chain of ganglia lying on either side of vertebral column. Preganglionic sympathetic nerve fibers leave the spinal cord between the first thoracic and the second lumbar segments. Sympathetic activity is initiated from the reticular formation of the medulla oblongata and pons and from centres in hypothalamus.
The brainstem sympathetic centres, which have an intrinsic activity of their own, are regulated by many stimuli, including impulses from cortex, limbic lobes and hypothalamus, neural afferents that interact at the level of the brainstem centres and at higher centres, and changes in the physical and chemical properties of the extracellular fluid, including the circulating levels of hormones and substrates.
Noradrenaline is the neurotransmitter of postganglionic sympathetic nerve endings, which exerts its effects on the peripheral tissues. In addition, the sympathetic system releases adrenaline from the adrenal medulla, which enters the blood stream producing widespread effects throughout the body.
Noradrenaline, adrenaline and dopamine are the naturally occurring catecholamines and function as neurotransmitters within the central nervous system. Catecholamine s are synthesized from the amino- acid tyrosine, which is sequentially hydroxylated to form dihydroxyphenylalanine (dopa), decarboxylated to form dopamine and hydroxylated to form noradrenaline. In the adrenal medulla and in those central neurons utilizing adrenaline as neurotransmitter, noradrenaline is N-methylated to adrenaline. Catecholamines are stored in adrenal medulla and sympathetic nerve endings.
Catecholamines are metabolized by two enzymes:
i. Monoamine oxidase (MAO) and
ii. Catechol-O-methyltransferase (COMT).
MAO causes oxidative deamination of catecholamines and an autacoid 5-hydroxytrypyamine (5-HT or serotonin). COMT causes rapid methylation of catecholamines. Metabolism does not play an important role in terminating the action of endogenously released catecholamines. The majority of catecholamines released from nerve endings re-enter the nerve endings, thereby terminating the in action on the receptors.
Two types of adrenoreceptors are recognized on the basis of their location—α and β.
α1 receptors occur on the effecter cells and are stimulated by noradrenaline released at sympathetic nerve endings and by adrenaline, causing constriction of blood vessels, a rise in blood pressure, reflex bradycardia, dilation of the pupil and constriction of the smooth muscle around the neck of the bladder. Phenylephrine and methoxamine are selective α1 agonists while doxazosin and terazosin is selective antagonist.
α2 receptors occur on the nerve terminal from which noradrenaline is released, which stimulates the receptors. Some noradrenaline released re-enters the nerve endings limiting further release of noradrenaline, thus acting as a release control mechanism. α2 receptor agonist like methyldopa and clonidine inhibit noradrenaline release and are used in hypertension and management of opioid dependence.
β1receptors occur on the heart and kidney (juxtaglomerular cells) and cause increase in rate and excitability of the heart and release of renin resulting in increased cardiac output.
β2 receptors occur on the bronchi, blood vessels, uterus, urinary tract, eye and gastrointestinal tract. They have a higher affinity for adrenaline than for noradrenaline and are responsible for bronchial muscle relaxation, skeletal muscle vasodilation and uterine relaxation.
β3 receptor is a novel and distinct adreno-receptor, which is likely to regulate noradrenaline induced changes in energy metabolism. They are also present on adipocytes and mediate lipolysis. β3 receptors are present in cardiac muscle and depress the rate and force of contraction of the heart. The advent of β3receptor antagonist may provide useful addition to the drugs for the treatment of heart failure.
Essay # 3. The Parasympathetic Nervous System:
The parasympathetic preganglionic neurons are located in cranial and sacral portions of the spinal cord. The ganglia lie close to the innervated organ, so that the preganglionic nerves are long and postganglionic nerves are short. The parasympathetic nervous system innervates the heart, the gastrointestinal tract, the genitourinary system, iris and the salivary glands.
i. Acetylcholine (Ach):
Ach serves as the neurotransmitter at the postganglionic parasympathetic nerve endings. Ach is also the neurotransmitter at all autonomic ganglia, i.e. in both the sympathetic and parasympathetic nervous systems. In addition to autonomic nervous system, Ach is the neurotransmitter at the somatic nerves supplying the skeletal muscles (neuromuscular junction). Nerves that release Ach are said to be cholinergic.
Ach is hydrolyzed and inactivated by the enzyme acetylcholinesterase at cholinergic synapses. This enzyme (also known as specific or true cholinesterase) is present in the neurons and is concerned with the termination of the effects of Ach. A nonspecific type of enzyme, butyrocholinesterase (serum cholinesterase or pseudo cholinesterase) is present in plasma and non-neural tissues, whose physiological functions are not known.
iii. Cholinergic Receptors:
Two classes of receptors for Ach are recognized – muscarinic and nicotinic.
iv. Muscarinic Receptors:
These are located primarily on parasympathetic effecter cells in smooth muscle, cardiac muscle, and the glandular epithelium. They are selectively stimulated by muscarine and blocked by atropine. The muscarinic (M) receptors are further divided into M1,M2, and M3 receptors. These subtypes of M receptors are only of physiological importance with little role in pharmacotherapy.
v. Nicotinic Receptors:
Nicotine receptors are found in the CNS, the autonomic ganglia, adrenal medulla and skeletal muscle end plates. Nicotine, the classic agonist, first stimulates and then blocks autonomic ganglia and skeletal muscle end plates; d-tubocurarine blocks nicotinic receptors, particularly in skeletal muscles and autonomic ganglia, whereas hexamethonium preferentially blocks autonomic ganglionic receptors.