Nasonasal reflexes, the nasal cycle, and sneeze

The nasal mucosa is a complex tissue that interacts with its environment and effects local and systemic changes. Receptors in the nose receive signals from stimuli, and respond locally through afferent, nociceptive, type C neurons to elicit nasonasal reflex responses mediated via cholinergic neurons. This efferent limb leads to responses in the nose (eg, rhinorrhea, glandular hyperplasia, hypersecretion with mucosal swelling). Anticholinergic agents appear useful against this limb for symptomatic relief of a “runny nose.” Chronic exposure to allergens can lead to hyperresponsiveness of the nasal mucosa. As a result, receptors upregulate specific ion channels to increase the sensitivity and potency of their reflex response. Nasal stimuli also affect distant parts of the body. Nerves in the sinus mucosa cause vasodilation; the lacrimal glands can be stimulated by nasal afferent triggers. Even the cardiopulmonary system can be affected via the trigeminal chemosensory system, where sensed irritants can lead to changes in tidal volume, respiratory rate, and blink frequency. The sneeze is an airway defense mechanism that removes irritants from the nasal epithelial surface. It is generally benign, but can lead to problems in certain circumstances. The afferent pathway involves histamine-mediated depolarization of H1 receptor-bearing type C trigeminal neurons and a complex coordination of reactions to effect a response.     

Sacral reflexes

Sacral reflexes consist of motor responses in the pelvic floor and sphincter muscles evoked by stimulation of sensory receptors in pelvic skin, anus, rectum, or pelvic viscera. These responses may be elicited by physical or electrical stimuli. They have been used in research studies of the pathophysiology of pelvic floor and anorectal disorders and many have been recommended for diagnostic use. These reflexes are described and discussed in this review. More rigorous evaluation of their value in the clinical assessment and care of patients with pelvic floor and sphincter disorders is required. Currently direct comparisons of the value of particular responses are generally not available, and few of these reflexes have proven validity for use in clinical diagnosis.     

Dyspnea and respiratory reflexes]

It has been suggested that afferents from intercostal muscles may play a role in the genesis of dyspnea. In this study, lower intercostal muscles were tapped or vibrated to induce a reflex, evoked potentials, and sensation. The tapping stimulus induced H reflex in the same muscle with a latency of 12 msec. Also the same stimulus induced evoked potentials in the cerebral cortex (N1: 19.8 +/- 1.2 msec). This suggests projection of the intercostal muscle spindle afferents to the cerebral cortex. 100 Hz vibration induced a later component, presumably an event-related potential, at 250 msec after the onset of both the inspiratory and expiratory phase. Thus, it may be possible that intercostal muscle spindle afferents project to the cerebral cortex and play a role in respiratory sensation. It has been suggested that dyspnea is reduced by increasing inspiratory and expiratory intercostal muscle spindle afferents during the inspiratory and expiratory phases, respectively. Thus, stretching the inspiratory and expiratory intercostal muscles during the respective muscular contraction phase may be effective in reducing dyspnea.     

Mucosal secretory reflexes

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Upper airway reflexes

It is usually assumed that upper airway pressure receptors mediate the reflexes involved in sleep apneas, but many other receptors may be involved, including those responding to chemical stimuli. The reflexes to upper airway negative pressure have been further studied, and the timing of their inputs shown to be important. Their effects on the cardiovascular system, including cerebral blood flow, have been emphasized. The central nervous pathways for the upper airway reflexes and their relationship to the neuronal circuits of the respiratory rhythm generator are being analyzed, but no clear pattern has emerged. Many neurotransmitters have been identified, usually on the motor pathways, which points to possible therapeutic approaches. The central nervous pharmacology and the neuronal pattern for the cough reflex have been described, and a similar approach to other upper airway reflexes, especially those involved in sleep apneas, would be valuable.     

Atrial reflexes and renal function.

Distension of small balloons in the venous-atrial junctions results in an increase in heart rate, urinary flow and sodium excretion. Two types of atrial receptors are described: one type, histologically known, discharging into myelinated fibers, and a second type, discharging into nonmyelinated ("C") fibers. These responses are mediated by the myelinated fibers. Experiments have shown that simulation of receptors discharging into the large myelinated vagal fibers is responsible for a reflex increase in heart rate mediated only by sympathetic nerves and for an increase in urinary flow. The efferent pathway of the diuretic response is shown to be nervous and hormonal. Stimulation of atrial receptors causes (1) a reduction of activity in nerves to the kidney, causing an increase in both urinary volume and sodium excretion, and (2) the release of a blood-borne agent, possibly diuretic, that increases urinary volume but does not affect sodium excretion.     

Digitalis and baroreceptor reflexes in man

Data in animals indicate that large amounts of digitalis potentiate arterial baroreflexes and that this factor may be important for the cardiovascular effects of the drug. To determine if arterial baroreflex potentiation also exists after administration of therapeutic doses of digitalis in man, we studied how stimulation and deactivation of arterial baroreceptors by phenylephrine and nitroglycerin injection affect heart rate and how stimulation and deactivation of carotid baroreceptors by neck suction and pressure affects blood pressure and heart rate. The study was performed in 29 normotensive or hypertensive subjects before and after injection of Lanatoside C (0.8 mg i.v.). Baroreceptor stimulation reduced heart rate and blood pressure, while baroreceptor deactivation increased both of these variables. The bradycardic and hypotensive effect of baroreceptor stimulation increased significantly after digitalis both in normotensive and hypertensive subjects. However, the tachycardic and hypertensive responses to baroreceptor deactivation were not affected by digitalis. Thus, therapeutic doses of digitalis in man enhance baroreceptor reflexes, and both the heart rate and the blood pressure reflex effects are involved. However, the enhancement occurs to a marked degree only with baroreceptor stimulation and is not evident with baroreceptor deactivation.     

Coronary pressor reflexes.

The heart differs from other cardiovascular reflexogenic structures because it has two prominent inputs to the central nervous system. On input is spinal and is mediated by afferent cardiac sympathetic nerve fibers. The other is medullary and is mediated by afferent vagal fibers. The number of fibers projecting centrally appears to be similar in the two systems. The reflex effects produced by excitation of the two inputs are complicated and can be either pressor or depressor. However, reflex pressor effects seem to be more prominant for the spinal input and reflex depressor effects more prominent for the medullary input.