Sympathetic afferents

In addition to changes within the nerve, sympathetic afferents become able to activate sensory afferents via as yet poorly characterised a-adrenoceptors. These interactions between adjacent sensory and autonomic nerve axons and between ganglion cells result in excitation spreading between different nerve fibres. These peripheral ectopic impulses can cause spontaneous pain and prime the spinal cord to exhibit enhanced evoked responses to stimuli, which themselves have greater effects due to increased sensitivity of the peripheral nerves. 

Sensory information from the stomach is relayed to the CNS by both vagal afferent fibers and sympathetic afferent fibers. The sensory receptors of the stomach consist primarily of unmyelinated nerve endings that detect mechanical (distention and touch), chemical, and thermal stimuli. Receptive fields for the... 

Causalgia is burning pain evoked by the activation of sympathetic efferent fibres. The likely mechanism underlying this syndrome involves ectopic expression of a-adrenoceptors on nociceptive afferents following peripheral injury or disease. 

In the gastrointestinal tract, drugs or toxins, as well as mechanical stimulation, induce emesis by activation of sensory receptors on afferent neurons in the vagus and sympathetic nerves. Information is relayed to the vomiting centre via the nucleus tractus solitarius... 

The neuropeptides are peptides acting as neurotransmitters. Some form families such as the tachykinin family with substance P, neurokinin A and neurokinin B, which consist of 11 or 12 amino acids and possess the common carboxy-terminal sequence Phe-X-Gly-Leu-Met-CONH2. Substance P is a transmitter of primary afferent nociceptive neurones. The opioid peptide family is characterized by the C-terminal sequence Tyr-Gly-Gly-Phe-X. Its numerous members are transmitters in many brain neurones. Neuropeptide Y (NPY), with 36 amino acids, is a transmitter (with noradrenaline and ATP) of postganglionic sympathetic neurones. 

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. 

Explain how sympathetic nerves, angiotensin II, and prostaglandins affect the resistance of the afferent arteriole... 

Sympathetic nerves. The afferent and efferent arterioles are densely innervated with sympathetic nerves. Norepinephrine released directly from the nerves or circulating epinephrine released from the adrenal medulla stimulates a, adrenergic receptors to cause vasoconstriction. The predominant site of regulation is the afferent arteriole. Under normal resting conditions, there is little sympathetic tone to these vessels so that RBF is comparatively high. As discussed previously, this facilitates glomerular filtration. 

An overall increase in sympathetic nerve activity includes an increase in sympathetic input to the kidneys. Consequently, resistance of the afferent arteriole increases, leading to a decrease in RBF. As discussed, this results in a decrease in PGC, GFR, and urine output. As such, the renal excretion of sodium and water is decreased. In other words, sodium and water are... 

Widespread vasoconstriction supplements the increase in TPR induced by the sympathetic nervous system. Angiotensin II also causes vasoconstriction of the afferent arteriole in particular, which enhances the decrease in RBF and sodium filtration. Finally, angiotensin II promotes secretion of aldosterone from the adrenal cortex. Aldosterone then acts on the distal tubule and collecting duct to increase sodium reabsorption. 

The abdominal vagus and sympathetic nerves are the most important afferent inputs involved in vomiting induced by chemotherapy and radiation [31]. The input from vestibular nerves and the cerebellum plays an important role in the motion disease [52]. The afferent inputs from vagal, trigeminal and glossopharyngeal nerves terminate eventually in the nucleus solitarius tract located in the medulla oblongata which has neuronal connections with other medullary areas involved in emesis, for example, area postrema [53]. 

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. 

Three generally accepted mechanisms are involved in the regulation of renin secretion (Fig. 18.2). The first depends on renal afferent arterioles that act as stretch receptors or baroreceptors. Increased intravascular pressure and increased volume in the afferent arteriole inhibits the release of renin. The second mechanism is the result of changes in the amount of filtered sodium that reaches the macula densa of the distal tubule. Plasma renin activity correlates inversely with dietary sodium intake. The third renin secretory control mechanism is neurogenic and involves the dense sympathetic... 

Decreased sympathetic nerve activity in afferent arteriole leads to decreased renin release. 

Most of the haemodynamic effects of opioids are related to decreased central sympathetic outflow, specific vagal effects or, in the case of morphine and pethidine, histamine release. Fentanyl and its analogues do not cause histamine release. All opioids, with the exception of pethidine, produce bradycardia by actions on the afferent fibres of the vagus and the nucleus tractus solitarius and nucleus commissuralis, which have very high densities of opioid receptors. Pethidine often produces tachycardia, possibly due to its structural similarity to atropine. In isolated heart or heart-muscle preparations, opioids produce a dose-related negative inotropic effect, but only at concentrations 100 to several thousand times those found clinically. 

A highly simplified diagram of the intestinal wall and some of the circuitry of the enteric nervous system (ENS). The ENS receives input from both the sympathetic and the parasympathetic systems and sends afferent impulses to sympathetic ganglia and to the central nervous system. Many transmitter or neuromodulator substances have been identified in the ENS see Table 6-1. ACh, acetylcholine AC, absorptive cell CM, circular muscle layer EC, enterochromaffin cell EN, excitatory neuron EPAN, extrinsic primary afferent neuron 5HT, serotonin IN, inhibitory neuron IPAN, intrinsic primary afferent neuron LM, longitudinal muscle layer MP, myenteric plexus NE, norepinephrine NP, neuropeptides SC, secretory cell SMP, submucosal plexus. 

The enteric nervous system (see Chapter 6 Introduction to Autonomic Pharmacology) is composed of interconnected networks of ganglion cells and nerve fibers mainly located in the submucosa (submucosal plexus) and between the circular and longitudinal muscle layers (myenteric plexus). These networks give rise to nerve fibers that connect with the mucosa and deep muscle. Although extrinsic sympathetic and parasympathetic nerves project onto the submucosal and myenteric plexuses, the enteric nervous system can independently regulate gastrointestinal motility and secretion. Afferent fibers present in the mucosa and muscularis connect to cell bodies in the plexuses that mediate local reflexes. 

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