Sympathetic autonomic nervous system

Anatomy of the Autonomic Nervous System Sympathetic and Parasympathetic Divisions... 

Physical dependence is demonstrated by the elicitation of a withdrawal syndrome when alcohol consumphon is terminated. The symptoms and severity are determined by the amount and durahon of alcohol consumption and include sleep disruphon, autonomic nervous system (sympathetic) activation, tremors, and in severe cases, seizures. In addition, two or more days after withdrawal, some individuals experience delirium tremens, characterized by hallucinations, delirium, fever, and tachycardia. Delirium tremens can be fatal. Another aspect of dependence is craving and drugseeking behavior, often termed psychological dependence. 

Just as the condition of your body strongly influences the status of your brain chemistry (and, consequently, your mind), the status of your mind strongly influences the condition of your body, including your brain chemistry. Your brain chemistry exercises control of your body through the neuroendocrine system, the autonomic nervous system (sympathetic and parasympathetic see Chapter i6), and through voluntary peripheral nervous systems. Brain chemistry also influences how well you think and what kind of mood you re in. The bottom line is this What you do to and with your mind is inestimably important to what happens to your hody (including your brain), which in turn feeds hack upon your cognitive status. 

A special feature of the iris is its autonomic innervation. Sympathetic activation widens the aperture of the iris whereas impulses from the parasympa thetic nervous system decrease the aperture size. Therefore adrenergic agonists and anticholinergic compounds both increase the aperture of the iris, i.e., cause mydriasis, and antiadrenergic and cholinergic agonists decrease it, i.e., cause miosis. The iris can thus be considered an excellent mirror reflecting the balance of the autonomic nervous system in the body. " ... 

Sympathetic nervous system. That portion of the autonomic nervous system that utilizes norepinephrine as a neurotransmitter at its neuroeffector junctions. 

There is a similar high prevalence of peripheral neuropathy (34%) in the pediatric population infected with HIV (Araujo et al. 2000). The frequency of IDP in the HIV-infected population is unknown but is thought to be rare (Wulff et al. 2000). In an outpatient population of HIV positive patients, mononeuritis multiplex and lumbosacral polyradiculopathy were found in less than 1% of patients with AIDS (Fuller et al. 1993). HIV-associated autonomic nervous system dysfunction is also not uncommon as up to 66% of patients have papillary involvement and 15% have sympathetic and parasympathetic involvement causing orthostatic hypotension and respiratory sinus arrhythmia (Gluck et al. 2000). 

Autonomic nervous system Parasympathetic and sympathetic nerves that control involuntary actions in the body. 

Figure 9.1 The autonomic nervous system and its effector organs. The efferent pathways of this system consist of two neurons that transmit impulses from the CNS to the effector tissue, preganglionic neuron (solid line), and postganglionic neuron (dashed line). As illustrated, most tissues receive nervous input from both divisions of the ANS the sympathetic and the parasympathetic.

Adrenal medulla. Derived from neural crest tissue, the adrenal medulla forms the inner portion of the adrenal gland. It is the site of production of the catecholamines, epinephrine and norepinephrine, which serve as a circulating counterpart to the sympathetic neurotransmitter, norepinephrine, released directly from sympathetic neurons to the tissues. As such, the adrenal medulla and its hormonal products play an important role in the activity of the sympathetic nervous system. This is fully discussed in Chapter 9, which deals with the autonomic nervous system. 

The autonomic nervous system (ANS) modifies contractile activity of both types of smooth muscle. As discussed in Chapter 9, the ANS innervates the smooth muscle layer in a very diffuse manner, so neurotransmitter is released over a wide area of muscle. Typically, the effects of sympathetic and parasympathetic stimulation in a given tissue oppose each other one system enhances contractile activity while the other inhibits it. The specific effects (excitatory or inhibitory) that the two divisions of the ANS have on a given smooth muscle depend upon its location. 

Because cardiac muscle is myogenic, nervous stimulation is not necessary to elicit the heart beat. However, the heart rate is modulated by input from the autonomic nervous system. The sympathetic and parasympathetic systems innervate the SA node. Sympathetic stimulation causes an increase in heart rate or an increased number of beats/min. Norepinephrine, which stimulates ( -adrenergic receptors, increases the rate of pacemaker depolarization by increasing the permeability to Na+ and Ca++ ions. If the heart beat is generated more rapidly, then the result is more beats per minute. 

The autonomic nervous system exerts the primary control on heart rate. Because the sympathetic and parasympathetic systems have antagonistic effects on the heart, heart rate at any given moment results from the balance or sum of their inputs. The SA node, which is the pacemaker of the heart that determines the rate of spontaneous depolarization, and the AV node are innervated by the sympathetic and parasympathetic systems. The specialized ventricular conduction pathway and ventricular muscle are innervated by the sympathetic system only. 

Figure 14.1 Effect of autonomic nervous system stimulation on action potentials of the sinoatrial (SA) node. A normal action potential generated by the SA node under resting conditions is represented by the solid line the positive chronotropic effect (increased heart rate) of norepinephrine released from sympathetic nerve fibers is illustrated by the short dashed line and the negative chronotropic effect (decreased heart rate) of acetylcholine released from parasympathetic nerve fibers is illustrated by the long dashed line.

Figure 15.4 Effects of the autonomic nervous system on mean arterial pressure. The baroreceptors, chemoreceptors, and low-pressure receptors provide neural input to the vasomotor center in the brainstem. The vasomotor center integrates this input and determines the degree of discharge by the sympathetic and parasympathetic nervous systems to the cardiovascular system. Cardiac output and total peripheral resistance are adjusted so as to maintain mean arterial pressure within the normal range.

Because baroreceptors respond to stretch or distension of the blood vessel walls, they are also referred to as stretch receptors. A change in blood pressure will elicit the baroreceptor reflex, which involves negative feedback responses that return blood pressure to normal (see Figure 15.6). For example, an increase in blood pressure causes distension of the aorta and carotid arteries, thus stimulating the baroreceptors. As a result, the number of afferent nerve impulses transmitted to the vasomotor center increases. The vasomotor center processes this information and adjusts the activity of the autonomic nervous system accordingly. Sympathetic stimulation of vascular smooth muscle and the heart is decreased and parasympathetic stimulation of the heart is increased. As a result, venous return, CO, and TPR decrease so that MAP is decreased back toward its normal value. 

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