Nerves adrenergic Vagus

The central adrenergic system. It is only recently that immunohistochemical methods have been developed to show that adrenaline-containing cells occur in the brain. Some of these cells are located in the lateral tegmental area, while others are found in the dorsal medulla. Axons from these cells innervate the hypothalamus, the locus coeruleus and the dorsal motor nucleus of the vagus nerve. While the precise function of adrenergic system within the brain is uncertain, it may be surmized that adrenaline could play a role in endocrine regulation and in the central control of blood pressure. There is evidence that the concentration of this amine in cerebrospinal fluid... 

The adrenergic pathways that use epinephrine as a neurotransmitter, which have been explored only recently. One of these systems is also tegmental and is mixed with noradrenergic cells. The other is thalamic-hypothalamic, involved with the vagus nerve. Some adrenergic fibers are also found in the fourth ventricle and the spinal cord. 

The sinoatrial (SA) node is innervated by both the sympathetic (beta and parasympathetic (vagus) nervous systems. Sympathetic activation increases the discharge rate of the SA pacemaker cells, and thereby increases heart rate (a positive chronotropic effect). Sympathetic nerves also innervate adrenergic receptors (betaj) on cardiac ventricular cells leading to an increase in stroke volume (a positive inotropic effect). Vagal activation, on the other hand, has the opposite effect and decreases heart rate and conduction velocity. In normal adults, cardiac vagal innervation is functionally predominant, so abolition of vagal activity results in a pronounced tachycardia (increased heart rate). 

Gastrin Enteroendocrine G cells of the stomach, duodenal bulb, and other cells Induces gastric acid secretion 1. Luminal contents, especially aromatic amino acids, calcium, coffee, and ethanol 2. Vagus nerve stimulation activation of beta-adrenergic and GABA neurons 3. Somatostatin inhibits secretion... 

Bronchoconstriction results from the effects of acetylcholine, histamine, and inflammatory mediators released within the bronchial walls. The vagus nerve releases acetylcholine in response to stimulation of upper airway mucosa by irritants. Acetylcholine also triggers release of pulmonary secretions which further reduce air flow by plugging airways. Sympathomimet-ics (adrenergic agonists, cholinergic antagonists), methylated xanthines and corticosteroids reverse or reduce bronchoconstriction (Tables 5.1A and 5.1B). 

The rapid onset of the bradycardia in response to hypoxia is suggestive of a neural reflex (Fig. 2). The sensors for this reflex have been identified as the carotid chemoreceptors (27,28), which send afferent fibers in the carotid sinus nerve to a central integrating area in the brainstem (29) and whose efferent arm consists of parasympathetic cholinergic fibers to the heart carried in the vagus nerve (cranial nerve X) and a-adrenergic sympathetic fibers to resistance vessels in peripheral vascular beds (30). The absence of this bradycardic response earlier in gestation (31) is indicative of immaturity of neural reflex mechanisms. 

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