Parasympathetic activity responses

Reserpine s strong inhibition of sympathetic activity allows increased parasympathetic activity to occur, which is responsible for side effects of nasal stuffiness, increased gastric acid secretion, diarrhea, and bradycardia. 

Autonomic outputs. Hypoglycaemia and hypothermia both lead to snstained sympathetic responses. Subjects feel hungry and eat if possible, bnt they refine their other actions to suit the circumstances. Hypoglycaemia requires hepatic glycogenolysis and glnconeogenesis, while hypothermia requires increased heat prodnction and a redistribntion of blood flow. Sympathetic activity is controlled by the hypothalamns, which instrncts the adrenal medulla to secrete adrenalin. This is a rather blunt control, and so localised sympathetic responses (such as blood flow regulation) are mediated by individnal nerves. Parasympathetic activity can also respond to the hypothalamus, which controls the nnclens of the solitary tract. 

The time course of sympathetic activity is significantly slower than that of parasympathetic activity, taking 10 to 40 seconds to reach its maximum effect. In contrast, parasympathetically mediated responses are completed in approximately 1 to 2 seconds for normal visual environments. 

According to another model, proposed by Schleifer Ley (1994), stress-induced hyperventilation decreases peak CO levels and increases the blood pH-level (beyond 7.45 = alkalosis). This contributes to elevated muscle tension and a suppression of parasympathetic activity. The sympathetic dominance may amplify the responses to catecholamines. 

The autonomic system is responsible for the moment-to-moment modification of practically all functions of the body. Although there are intrinsic plexi that promote normal activity, the sympathetic and parasympathetic systems enhance or retard function. Auerbach s and Meissner s plexi become activated by intraluminal distension and initiate peristalsis in an anterograde fashion. Increased parasympathetic activity, primarily from the vagus nerve in the cranial axis, increases gastrointestinal motility. The same can occur from microbial and chemical irritation of the inner walls. The effects are decreased transit time and decreased water absorption, among other effects. The person may also have other symptoms including discomfort, nausea, oating, and irritation. 

In this hypothetical mechanistic scheme, it is postulated that electrocardiographic alterations produced by exposure to air pollutants will result partly from central nervous system (CNS)-mediated changes in cardiac autonomic tone. This supposition is based on the fact that the main cytokines that are released in response to air pollution can alter CNS activity. Also subjecting the lungs to noxious stimuli may elicit powerful cardiac reflexes that can alter sympathetic and parasympathetic activity. This is a critical consideration, because it is well established that both divisions of the autonomic nervous system exert a profound influence on the repolarization properties of the heart. These potential changes may play a vital role in the culminative response of inhaled particles on the cardiopulmonary system. 

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),... 

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. 

Figure 19.17 The biochemistiy and physiology responsible for penile erection. Sexual activity itself begins with a state of arousal that leads to erection. Arousal results in part from stimulation of the sense organs. The hypothalamus coordinates the sensations and activates the autonomic nervous system. Sensory nerves from the skin of the penis and other erogenous zones stimulate the parasympathetic system. This activates nitric oxide synthase and the resultant nitric oxide, via cyclic GMP, causes vasodilation of the arterioles. This increases blood flow through the corpora cavernosa which then expands producing an erection. Pheromones secreted by the female can stimulate the odour detecting system in the nasal cavity of the male (Chapter 12 and see above). Stress, however, activates the sympathetic system releases cyclic AMP which can result in vasoconstriction of the arterioles. Other factors that can interfere with an erection are physical fatigue and alcohol.

The ANS has sympathetic and parasympathetic branches. Both are made up of centrifugal (efferent) and centripetal (afferent) nerves. In many organs innervated by both branches, respective activation of the sympathetic and parasympathetic input evokes opposing responses. 

Responses to activation of the parasympathetic system. Parasympathetic nerves regulate processes connected with energy assimilation (food intake, digestion, absorption) and storage. These processes operate when the body is at rest, allowing a decreased tidal volume (increased bronchomotor tone) and decreased cardiac activity. Secretion of saliva and intestinal fluids promotes the digestion of foodstuffs transport of intestinal contents is speeded up because of enhanced peristaltic activity and lowered tone of sphincteric muscles. To empty the urinary bladder (micturition), wall tension is increased by detrusor activation with a concurrent relaxation of sphincter tonus. 

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. 

In a normal resting subject who is receiving no drugs, there is a moderate parasympathetic tone to the heart, and sympathetic activity is relatively low. The ventricular muscle receives little, if any, parasympathetic innervation. As the blood pressure rises in response to norepinephrine, the baroreceptor reflex is activated, parasympathetic impulses (which are inhibitory) to the heart increase in frequency, and what little sympathetic outflow there is may be reduced. Heart rate is slowed so much that the direct effect of norepinephrine to increase the rate is masked and there is a net decrease in rate. Under the conditions described, however, the impact of the reflex on the ventricles is very slight because there is no parasympathetic innervation and the preexisting level of sympathetic activity is already low. A further decrease in sympathetic activity therefore would have little further effect on contractility in this subject. Thus, a decrease in heart rate and an increase in stroke volume will occur, and cardiac output will change very little. 

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