Parasympathetic nervous system activation

PARASYMPATHETIC NERVOUS SYSTEM ACTIVITY + Sexual behavior (released during orgasm in both sexes)... 

Further, heart rate does not provide diagnostic information about the soitree of mental workload. O Donnell and Eggemeier (1986) define diagnosticity as the "capability of a technique to discriminate the amount of workload imposed on different operator capacities or resources" (p. 42-3). Backs (1995) offers two reasons for heart rate s limited diagnostic utility. First, heart rate is affected by physical derrtands that may be independent of mental workload. Second, heart rate does not provide information about the separation of the sympathetic and parasympathetic nervous system activity. 

Humans exposed to cedrol fumes showed significant decreases in heart rate, diastolic and systolic blood pressure, and respiratory rate. Tests indicted that cedrol inhalation also caused a reduction in sympathetic and an increase in parasympathetic nervous system activity, results supporting the alleged relaxant effect of cedar oU. In addition, a decrease in nonrapid eye movement sleep latency was found in humans exposed to cedar essence. ... 

To evaluate HRV, several measures have been proposed. These measures are roughly classifiable into time domain analysis [5], frequency domain analysis, and nonlinear and fractal analysis [5]. Time domain analysis includes tone-entropy method [6]. Nonlinear and fractal analysis include de-trended fluctuation analysis (DFA) [7]. Frequency domain analysis is based on estimation of the power spectrum of RRI series. Depending on the estimation method of power spectrum, frequency domain analysis is classified into FFT method [8], AR model method [9], maximum entropy method [10], and complex de-modulation method [11]. Akselrod et al. [3] investigated the relation between spectral component of HRV and ANS activity [12]. They classified spectral component of HRV into a high-frequency (HF) band of 0.14-0.4 Hz, a low-frequency (LF) band of 0.04-0.14 Hz, a very-low-frequency (VLF) band of 0.003-0.04 Hz, and a ultra-low-frequency (ULF) band under 0.003 Hz. They further show that LF and HF components are affected from both sympathetic and parasympathetic nervous system activity and the parasympathetic nervous system activity, respectively [12]. Furthermore, VLF and ULF components are affected by the thermoregulation system [13],... 

The sympathetic or adrenergic nervous system operates in juxtaposition to the parasympathetic nervous system to maintain homeostasis in response to physical activity and physical or psychological stress. Sympathomimetic neurotransmission is generally mediated by norepinephrine [51-41 -2] (1), CgH NO, released from presynaptic storage granules upon stimulation. A second endogenous sympathomimetic agent, epinephrine [51-43-4] (2),... 

Giolinergic drugs mimic the activity of the parasympathetic nervous system (PNS). They also are called parasympathomimetic drugs. An understanding of the PNS is useful in understanding the cholinergic dni. ... 

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of these receptors results in muscle fasciculations even greater stimulation results in blockade and muscle paralysis (Lefkowitz et al. 1996 Tafliri and Roberts 1987). Hyperactivity of central nervous system receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not... 

Automaticity of cardiac fibers is controlled in part by activity of the sympathetic and parasympathetic nervous systems. Enhanced activity of the sympathetic nervous system may result in increased automaticity of the SA node or other automatic cardiac fibers. Enhanced activity of the parasympathetic nervous system tends to suppress automaticity conversely, inhibition of activity of the parasympathetic nervous system increases automaticity. Other factors may lead to abnormal increases in automaticity of extra-SA nodal tissues, including hypoxia, atrial or ventricular stretch [as might occur following long-standing hypertension or after the development of heart failure (HF)], and electrolyte abnormalities such as hypokalemia or hypomagnesemia. 

Sinusitis symptoms typically last 7 to 1 0 days after a viral infection and are caused by activation of the immune system and parasympathetic nervous system. 

Vagal maneuvers Maneuvers that stimulate the activity of the parasympathetic nervous system and thereby inhibit atrioventricular nodal conduction. Examples of vagal maneuvers include cough, carotid sinus massage, and Valsalva maneuver. 

On the other hand, a decrease in blood pressure causes less than normal distension or stretch of the aorta and carotid arteries and a decrease in baroreceptor stimulation. Therefore, fewer afferent nerve impulses are transmitted to the vasomotor center. The vasomotor center then alters autonomic nervous system activity so that sympathetic stimulation of vascular smooth muscle and the heart is increased and parasympathetic stimulation of the heart is decreased. As a result, venous return, CO, and TPR increase so that MAP is increased back toward its normal value. The effects are summarized in Figure 15.5. 

Figure 15.5 Effects of sympathetic and parasympathetic nervous activity on mean arterial pressure. The parasympathetic nervous system innervates the heart and therefore influences heart rate and cardiac output. The sympathetic nervous system innervates the heart and veins and thus influences cardiac output. This system also innervates the arterioles and therefore influences total peripheral resistance. The resulting changes in cardiac output and total peripheral resistance regulate mean arterial pressure.

Of the following effects, which is not elicited by activation of the parasympathetic nervous system ... 

Phase 4 Hyperpolarization occurs before K+ efflux has completely stopped and is followed by a gradual drift towards threshold (pacemaker) potential. This is reflects a Na+ leak, T-type Ca2+ channels and a Na+/Ca2+ pump, which all encourage cations to enter the cell. The slope of your line during phase 4 is altered by sympathetic (increased gradient) and parasympathetic (decreased gradient) nervous system activity. 

Perhaps the most prominent and well-studied class of synthetic poisons are so-called cholinesterase inhibitors. Cholinesterases are important enzymes that act on compounds involved in nerve impulse transmission - the neurotransmitters (see the later section on neurotoxicity for more details). A compound called acetylcholine is one such neurotransmitter, and its concentration at certain junctions in the nervous system, and between the nervous system and the muscles, is controlled by the enzyme acetylcholinesterase the enzyme causes its conversion, by hydrolysis, to inactive products. Any chemical that can interact with acetylcholinesterase and inhibit its enzymatic activity can cause the level of acetylcholine at these critical junctions to increase, and lead to excessive neurological stimulation at these cholinergic junctions. Typical early symptoms of cholinergic poisoning are bradycardia (slowing of heart rate), diarrhea, excessive urination, lacrimation, and salivation (all symptoms of an effect on the parasympathetic nervous system). When overstimulation occurs at the so-called neuromuscular junctions the results are tremors and, at sufficiently high doses, paralysis and death. 

The base-catalysed racemization of the alkaloid (-)-hy oscy amine to ( )-hyoscyamine (atropine) is an example of enolate anion participation. Alkaloids are normally extracted from plants by using base, thus liberating the free alkaloid bases from salt combinations. (—)-Hyoscyamine is found in belladonna Atropa belladonna) and stramonium Datura stramonium) and is used medicinally as an anticholinergic. It competes with acetylcholine for the muscarinic site of the parasympathetic nervous system, thus preventing the passage of nerve impulses. However, with careless extraction using too much base the product isolated is atropine, which has only half the biological activity of (—)-hyoscyamine, since the enantiomer (+)-hyoscyamine is essentially inactive. 

Beside this there are some major differences with the neurotransmission in the autonomous nervous system The contractile activity of the skeletal muscle is almost completely dependent on the innervation. There is no basal tone and a loss of the innervation is identical to a total loss in function of the particular skeletal muscle. In contrast to the target organs of the parasympathetic nervous system the skeletal muscle cells only have acetylcholine receptors at the site of the so-called end-plate, the connection between neuron and muscle cell with the rest of the cell surface being insensitive to the transmitter. The release of acetylcholine results in a postjunctional depolarization which is either above the threshold to induce an action potential and a contraction or below the threshold with no contractile response at all. In contrast to the graduated reactions of the parasympathetic target organs, this is an all or nothing transmission. 

E. The effect of ganglionic blockade depends upon the predominant autonomic tone exerted within various organ systems. Since the activity of the parasympathetic nervous system predominates in the eye, the effect of ganglionic blockade is mydriasis, not miosis. Similarly, stimulation of the genital tract and urinary retention would be decreased. Since sympathetic nervous system activity predominates in blood vessels and the ventricles, vasodilation and a decreased cardiac output would follow ganglionic blockade. 

The basis for the antihypertensive activity of the ganglionic blockers lies in their ability to block transmission through autonomic ganglia (Fig. 20.2C). This action, which results in a decrease in the number of impulses passing down the postganglionic sympathetic (and parasympathetic) nerves, decreases vascular tone, cardiac output, and blood pressure. These drugs prevent the interaction of acetylcholine (the transmitter of the preganglionic autonomic nerves) with the nicotinic receptors on postsynaptic neuronal membranes of both the sympathetic and parasympathetic nervous systems. 

Stimulation of the parasympathetic nervous system modifies the organ functions by two main pathways. Firstly, the acetylcholine released from parasympathetic nerves can activate muscarinic receptors which are present in gland cells (sweat glands), smooth muscles and heart. The... 

Muscarine Muscarine, molecular formula C9H2qN02, first isolated from fly agaric Amanita muscaria, occurs in certain mushrooms, especially in the species of the genera Inocybe and Clitocybe. It is a parasympathomimetic substance. It causes profound activation of the peripheral parasympathetic nervous system, which may result in convulsions and death. Muscarine mimics the action of the neurotransmitter acetylcholine at the muscarinic acetylcholine receptors. 

It should be noticed that the activity of secondary amines like 2-benzylaminomethyl-3-(j8-benzylaminoethyl)quinuclidine (151) depends on the presence of the bicyclic quinuclidine system, in contrast to the similar action of aminoalkyl quinuclidinecarboxylate quaternary salts. In this case transition to compounds without a quinuclidine ring removes their action on ganglions of the sympathetic and parasympathetic nervous systems. 

Anticholinergic Drugs that decrease activity at acetylcholine synapses. These agents are often used to diminish activity in the parasympathetic nervous system (SYN parasympatholytic). 

Administration of muscarinic agonists, like parasympathetic nervous system stimulation, increases the secretory and motor activity of the gut. The salivary and gastric glands are strongly stimulated the pancreas and small intestinal glands less so. Peristaltic activity is increased throughout the gut, and most sphincters are relaxed. Stimulation of contraction in this organ system involves depolarization of the smooth muscle cell membrane and increased calcium influx. 

Blood vessels receive no direct innervation from the parasympathetic nervous system. However, parasympathetic nerve stimulation dilates coronary arteries, and sympathetic cholinergic nerves cause vasodilation in the skeletal muscle vascular bed (see Chapter 6 Introduction to Autonomic Pharmacology). Atropine can block this vasodilation. Furthermore, almost all vessels contain endothelial muscarinic receptors that mediate vasodilation (see Chapter 7 Cholinoceptor-Activating Cholinesterase-Inhibiting Drugs). These receptors are readily blocked by antimuscarinic drugs. 

Q6 In comparison with the sympathetic transmitter norepinephrine, the inactivation of acetylcholine by cholinesterases is rapid so that normally the activity of acetylcholine at the synapse is relatively short-lived. The choline component is taken up into the presynaptic terminal and acetylcholine is resynthesized and stored in the synaptic vesicles. Anticholinesterases function as cholinergic stimulants in the parasympathetic nervous system since they greatly prolong and so increase the actions of endogenous acetylcholine at muscarinic receptors on the effector tissue. 

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