Parasympathetic reflexes

On contact with moist membranes, S02 forms sulfurous acid, which is responsible for its severe irritant effects on the eyes, mucous membranes, and skin. Approximately 90% of inhaled S02 is absorbed in the upper respiratory tract, the site of its principal effect. The inhalation of S02 causes bronchial constriction parasympathetic reflexes and altered smooth muscle tone appear to be involved. Exposure to 5 ppm S02 for 10 minutes leads to increased resistance to airflow in most humans. Exposures of 5-10 ppm are reported to cause severe bronchospasm 10-20% of the healthy young adult population is estimated to be reactive to even lower concentrations. The phenomenon of adaptation to irritating concentrations has been reported in workers. However, current studies have not confirmed this phenomenon. Asthmatic individuals are especially sensitive to S02. 

Parasympathetic reflexes may also regulate mediator release and lymphocyte activity (41). Furthermore, contralateral histamine release and basophil infiltration occur following ipsilateral nasal challenge with allergen (30), an event mediated by neural reflexes. 

Sympathetic and parasympathetic nerves innervate the penis. In the flaccid state, OC2-adrenergic receptors mediate tonic contraction of the arterial and corporal smooth muscles. This maintains high penile arterial resistance and a balance exists between blood flow into and out of the corpora. With sexual stimulation, nerve impulses from the brain travel down the spinal cord to the thoracolumbar ganglia.3 A decrease in sympathetic tone and an increase in parasympathetic activity then occurs, causing a net increase in blood flow into the erectile tissue. Erections may also occur as a result of a sacral nerve reflex arc while patients are sleeping (nocturnal erections). 

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. 

Low-pressure receptors. The low-pressure receptors are located in the walls of the atria and the pulmonary arteries. Similar to baroreceptors, low-pressure receptors are also stretch receptors however, stimulation of these receptors is caused by changes in blood volume in these low-pressure areas. An overall increase in blood volume results in an increase in venous return an increase in the blood volume in the atria and the pulmonary arteries and stimulation of the low-pressure receptors. These receptors then elicit reflexes by way of the vasomotor center that parallel those of baroreceptors. Because an increase in blood volume will initially increase MAP, sympathetic discharge decreases and parasympathetic discharge increases so that MAP decreases toward its normal value. The simultaneous activity of baroreceptors and low-pressure receptors makes the total reflex system more effective in the control of MAP. 

Due to parasympathetic stimulation of the salivary glands, saliva is secreted continuously at a basal rate of approximately 0.5 ml/min. Secretion may be enhanced by two types of reflexes ... 

The simple or unconditioned salivary reflex occurs when food is present within the oral cavity and causes stimulation of chemoreceptors and pressure receptors. These receptors then transmit impulses to the salivary center in the medulla of the brainstem. Parasympathetic efferent impulses are transmitted back to the salivary glands and secretion is enhanced. 

The answer is a. (Katzung, p 240.) Older therapies—all designed to favor parasympathetic control of rhythm—include digoxin, propranolol, edrophonium, and vasoconstrictors. The vasoconstrictor phenylephrine (given by intravenous bolus) causes stimulation of the carotid sinus and reflex vagal stimulation of the atria. More recently, adenosine has been favored over verapamil, which is also very effective but slower acting... 

The injection of a vasoconstrictor, which causes an increase in mean arterial blood pressure, results in activation of the baroreceptors and increased neural input to the cardiovascular centers in the medulla oblongata. The reflex compensation for the drug-induced hypertension includes an increase in parasympathetic nerve activity and a decrease in sympathetic nerve activity. This combined alteration in neural firing reduces cardiac rate and force and the tone of vascular smooth muscle. As a consequence of the altered neural control of both the heart and the blood vessels, the rise in blood pressure induced by the drug is opposed and blunted. 

The innervation of the gastrointestinal tract is complex. The myenteric and submucosal plexuses contain many interneurons. These possess a number of neurotransmitters and neuromodulators, including several peptides, such as enkephalins, substance P, and vasoactive intestinal peptide. Reflex activity within the plexuses regulates peristalsis and secretion locally. The effects of sympathetic and parasympathetic nerve stimulation are superimposed on this local neural regulation. 

Important considerations are as follows (1) The direct effect of norepinephrine on the heart is stimulatory. (2) The reflex initiated is inhibitory, that is, opposite to the direct effect. (3) The reflex varies with the level of sympathetic and parasympathetic activity just before the initiation of the reflex. (4) The distribution of sympathetic and parasympathetic nerves is not uniform in the heart. 

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. 

The direct slowing of sinoatrial rate and atrioventricular conduction that is produced by muscarinic agonists is often opposed by reflex sympathetic discharge, elicited by the decrease in blood pressure (see Figure 6-7). The resultant sympathetic-parasympathetic interaction is complex because muscarinic modulation of sympathetic influences occurs by inhibition of norepinephrine release and by postjunctional cellular effects. Muscarinic receptors that are present on postganglionic parasympathetic nerve terminals allow neurally released acetylcholine to inhibit its own secretion. The neuronal muscarinic receptors need not be the same subtype as found on effector cells. Therefore, the net effect on heart rate depends on local concentrations of the agonist in the heart and in the vessels and on the level of reflex responsiveness. 

Effects of autonomic blockade on the response to phenylephrine (Phe) in a human subject. Left The cardiovascular effect of the selective K-agonist phenylephrine when given as an intravenous bolus to a subject with intact autonomic baroreflex function. Note that the increase in blood pressure (BP) is associated with a baroreflex-mediated compensatory decrease in heart rate (HR). Right The response in the same subject after autonomic reflexes were abolished by the ganglionic blocker trimethaphan. Note that resting blood pressure is decreased and heart rate is increased by trimethaphan because of sympathetic and parasympathetic withdrawal. In the absence of baroreflex buffering, approximately a tenfold lower dose of phenylephrine is required to produce a similar increase in blood pressure. Note also the lack of compensatory decrease in heart rate. 

Neurohumoral (extrinsic) compensation involves two major mechanisms (previously presented in Figure 6-7)—the sympathetic nervous system and the renin-angiotensin-aldosterone hormonal response—plus several others. Some of the pathologic as well as beneficial features of these compensatory responses are illustrated in Figure 13-2. The baroreceptor reflex appears to be reset, with a lower sensitivity to arterial pressure, in patients with heart failure. As a result, baroreceptor sensory input to the vasomotor center is reduced even at normal pressures sympathetic outflow is increased, and parasympathetic outflow is decreased. Increased sympathetic outflow causes tachycardia, increased cardiac contractility, and increased vascular tone. Vascular tone is further increased by angiotensin II and endothelin, a potent vasoconstrictor released by vascular endothelial cells. The result is a vicious cycle that is characteristic of heart failure (Figure 13-3). Vasoconstriction increases afterload, which further reduces ejection fraction and cardiac output. Neurohumoral antagonists and vasodilators... 

Lowenfeld12 identified the components of the fight reflex that were controlled by parasympathetic and sympathetic innervation of the smooth muscles controlling pupil diameter. They concluded that the parasympathetic nervous system must be intact to observe the light reflex the sympathetic nervous system influences the shape of the reflex. For example, in the absence of sympathetic innervation, the constriction velocity is increased and the dilation velocity is decreased. Conversely, in situations of increased sympathetic tone, the constriction is sluggish and incomplete, and the pupil slowly returns to its baseline size. The effects of abused drugs on these and other components of the light reflex were studied in the experiment described below. 

Lowenstein, O. and Lowenfeld, I.E., Mutual role of sympathetic and parasympathetic in shaping of the pupillary reflex to light, Arch. Neurology Psychiatry (Chicago), 64, 341, 1950. 

FIGURE 12.1 The afferent and efferent pathways of the parasympathetic mechanism for enhancing the defecation reflex. 

However, the intrinsic defecation reflex itself is usually weak, and to be effective in causing defecation, it must be fortified by another type of defecation reflex, a parasympathetic defecation reflex that involves the sacral segments of the spinal cord, as illustrated in Figure 12.1 and Figure 12.2. 

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