Autonomic nervous system parasympathetic

The ANS is the major involuntary portion of the nervous system and is responsible for automatic, unconscious bodily functions, such as control of heart rate and blood pressure and both gastrointestinal and genitourinary functions. The ANS is divided into two major subcategories the parasympathetic autonomic nervous system (PANS) and the sympathetic autonomic nervous system (SANS). 

Parasympathetic nervous system. That portion of the autonomic nervous system that utilizes acetylcholine as the neurotransmitter at the neuro-effector 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. 

Both the G- and V-agents have the same physiological action on humans. They are potent inhibitors of the enzyme acetylcholinesterase (AChE), which is required for the function of many nerves and muscles in nearly every multicellular animal. Normally, AChE prevents the accumulation of acetylcholine after its release in the nervous system. Acetylcholine plays a vital role in stimulating voluntary muscles and nerve endings of the autonomic nervous system and many structures within the CNS. Thus, nerve agents that are cholinesterase inhibitors permit acetylcholine to accumulate at those sites, mimicking the effects of a massive release of acetylcholine. The major effects will be on skeletal muscles, parasympathetic end organs, and the CNS. 

PAM chloride - 2-pralidoxime chloride. See oxime, parasympathetic nervous system -the part of the autonomic nervous system that decreases pupil size, heart rate, and blood pressure and increases functions, such as secretion of saliva, tears, and perspiration. 

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.

Release autonomic nervous system all postganglionic neurons of parasympathetic system some sympatheticpostganglionicneurons innervating sweat glands (alpha motor neurons innervating skeletal muscle)b adrenal medulla (20% of secretion) secretion)... 

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.

The effects of the autonomic nervous system on MAP are summarized in Figure 15.4. The parasympathetic system innervates the SA node and the AV node of the heart. The major cardiovascular effect of parasympathetic stimulation, by way of the vagus nerves, is to decrease HR, which decreases CO and MAP. 

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. 

The concept of chemical neurotransmission originated in the 1920s with the classic experiments of Otto Loewi (which were themselves inspired by a dream), who demonstrated that by transferring the ventricular fluid of a stimulated frog heart onto an unstimulated frog heart he could reproduce the effects of a (parasympathetic) nerve stimulus on the unstimulated heart (Loewi Navratil, 1926). Subsequently, it was found that acetylcholine was the neurotransmitter released from these parasympathetic nerve fibers. As well as playing a critical role in synaptic transmission in the autonomic nervous system and at vertebrate neuromuscular junctions (Dale, 1935), acetylcholine plays a central role in the control of wakefulness and REM sleep. Some have even gone as far as to call acetylcholine a neurotransmitter correlate of consciousness (Perry et al., 1999). 

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