Reflex Stimulation Research Articles

Neurally mediated renal vasoconstriction during isometric muscle contraction in cats.

The aim of this study was to determine if the reflex increase in renal sympathetic nerve activity (RSNA) during static (isometric) muscle contraction evokes renal vasoconstriction and decreases renal blood flow. RSNA, renal blood flow velocity, and arterial pressure were measured simultaneously during isometric contraction of the hindlimb triceps surae muscle in eight chloralose-anesthetized cats. A 1-min contraction was evoked by stimulating the peripheral ends of the cut L7 and S1 ventral roots. RSNA and mean arterial pressure (MAP) increased 41 +/- 14% (SE) and 50 +/- 10 mmHg during static contraction, whereas mean renal blood flow velocity (MRBV) decreased 14 +/- 5%. Calculated renal vascular resistance increased 73 +/- 20% during the contraction. The increase in RSNA preceded the decrease in MRBV by 20 s. Passive mechanical stretch of the muscle increased RSNA 21 +/- 12% but did not alter MRBV. Renal denervation abolished the decrease in MRBV during isometric contraction but only attenuated the rise in MAP. Cutting the L4-S1 dorsal roots or muscle paralysis abolished the MRBV and MAP responses. Thus reflex stimulation of RSNA from the contracting muscle can induce renal vasoconstriction and decrease renal blood flow.

Therapeutic targets in ischaemic heart disease.

The adequate treatment of a disease syndrome is dependent upon a clear definition of the symptomatic, pathological, physiological and prognostic targets against which therapy is to be deployed. The syndromes of ischaemic heart disease, including angina pectoris, are complex in origin, pathology, pathophysiology and natural history, and a complete clinical profile is difficult, if not impossible, to achieve in individual patients. The prime goals of pharmacotherapy in ischaemic heart disease are easy to define, but difficult to accomplish in practice. Relief of pain, breathlessness and fatigue are the prime clinical targets for pharmacotherapy. In view of their sinister significance, the electrophysiological indications of myocardial ischaemia, whether symptomatic or silent, are also crucial targets towards which therapy must be directed. Ischaemic heart disease is accompanied by a wide variety of regional and global abnormalities of myocardial contractile function associated with widespread reflex stimulation of the peripheral vascular system and neuroendocrine systems. Primarily, drug therapy must be directed at correction of these pathophysiological components of the syndrome. Longer term but no less essential goals in the treatment of ischaemic heart disease are the prevention of the clinical sequelae of the syndrome and its progression. A natural sequel of coronary artery obstructive disease is successive thrombotic events and loss of myocardium. Calcium antagonists, by preventing the increase in myocardial cytosolic calcium during acute ischaemic episodes, defer cell necrosis; in this respect, they are unique among currently available antianginal drugs. With regard to progression, the prime pathological cause of ischaemic heart disease is coronary atheroma.(ABSTRACT TRUNCATED AT 250 WORDS)

Association of radiolabeled urogastrone binding with regenerating intestinal mucosa and epidermal growth factor/ urogastrone producing organs in rat

In the present study, we have tested the hypothesis that the regeneration of intestinal epithelium is regulated by changes in the uptake of radiolabeled recombinant human urogastrone ( 125I rhUG) in the regenerating mucosa and epidermal growth factor/urogastrone (EGF/URO) producing organs in the rats. Operations were performed on rats to approximate the ileal mucosa to the serosal surface of the cecum. This procedure allows the regeneration of ileal mucosa onto the serosal surface of the cecum. Groups of 5 rats were killed on the 2nd, 4th, 8th and 12th post-operative days. Two hours before autopsy, rats were given 0.5 ml (50 μCi with 30 μgm protein) of 125I rhUG intravenously and the following tissues were removed: regenerating mucosa, salivary gland, duodenum, liver and kidney. Results indicated that the uptake of 125I rhUG was significantly greater in the salivary gland and duodenum on the 2nd post-operative day which gradually tapered with increasing time after surgery. A similar pattern in the uptake of 125I rhUG was also evident in the regenerating mucosa. Further analysis revealed a significant correlation between the uptake of 125I rhUG in the salivary gland and duodenum vs rate of epithelialization and uptake of 125I rhUG in the regenerative mucosa. These results suggested that the endogenous EGF/URO produced in the salivary gland and duodenum may be a factor in the regulation of intestinal regeneration; however, the mechanism responsible for reflex stimulation of EGF/URO production in these organs is not known.

Parotid secretion of fluid, amylase and kallikrein during reflex stimulation under normal conditions and after acute administration of autonomic blocking agents in man

The purpose of this work was to study the effect of graded mechanical and gustatory stimulation on the secretion of the acinar products fluid and amylase and the ductal product kallikrein from the human parotid gland (n = 9). The involvement of parasympathetic and sympathetic nerves in the salivary reflexes was subsequently examined using receptor blocking agents (n = 4). Chewing elevated the secretion of all products as compared to rest (P less than 0.013). When increasing the length of the chewing object, secretion of fluid (P less than 0.013), but not enzymes, further increased. The shift from mechanical to gustatory stimulation with 0.5% citric acid enhanced significantly the secretion of amylase and kallikrein (P less than 0.009), while application of 5.0% citric acid increased the secretion of both acinar products (P less than 0.009) more than kallikrein. A differentiated reflex control of salivation both with regard to input and output was thereby indicated. The muscarinic-cholinergic antagonist oxyphencyclimin reduced median fluid secretion between 54 and 76% depending on the stimuli. During citric acid stimulation, but not during chewing, fluid secretion was reduced about 40% by the beta 1-adrenergic antagonist metoprolol, and about 20% by the alpha 1-adrenergic antagonist prazosin. Median amylase secretion was reduced 30% during chewing and 75% during gustatory stimulation by metoprolol. It was concluded that the masticatory-salivary reflex mainly activated parasympathetic pathways producing saliva of low protein content.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence for functional alpha 2-adrenoceptors on vascular sympathetic nerve endings in the human forearm.

The role of alpha 2-adrenoceptors on vascular sympathetic nerve endings in modulating release of the sympathetic neurotransmitter norepinephrine (NE) in humans was examined by measuring the regional rate of appearance of NE in forearm venous plasma (forearm NE spillover [FSO]) in 32 healthy volunteers during intra-arterial infusion of drugs acting at adrenoceptors or directly on vascular smooth muscle. Simultaneous intra-arterial infusions of tracer amounts of [3H]NE were used to calculate the extraction rate of NE in the forearm. Methoxamine or propranolol with epinephrine (PRO + EPI) was used to stimulate alpha-adrenoceptors, yohimbine was used to inhibit alpha-adrenoceptors, and sodium nitroprusside (NIP) was used to produce increases in forearm blood flow directly. Sympathetic efferent activity was manipulated by systemic intravenous infusions of NIP or trimethaphan. Yohimbine and NIP increased and PRO + EPI and methoxamine decreased NE FSO, without effects on systemic blood pressure, heart rate, or arterial levels of catechols. Changes in FSO were flow dependent; therefore, the slope of the relation between the changes in FSO and forearm blood flow was used to evaluate the effects of each drug on regional sympathoneural activity. During administration of yohimbine, the mean slope of the relation between the change in estimated FSO and the change in forearm blood flow was about four times that of the mean slope during administration of NIP (F = 6.35, p less than 0.05). The slopes of the relations between changes in FSO and forearm blood flow were unaffected by systemic trimethaphan or NIP infusion, indicating that the activity of alpha 2-adrenoceptors was not altered during inhibition or reflexive stimulation of sympathetic outflow. The results suggest that alpha 2-adrenoceptors modulate release of NE from vascular sympathetic nerve endings in humans and that the function of these receptors is unchanged during acute changes in junctional NE concentrations.

Immediate and short-term cardiovascular effects of fosinopril, a new angiotensin-converting enzyme inhibitor, in patients with essential hypertension

Immediate and short-term cardiovascular effects of a new angiotensin-converting enzyme inhibitor, fosinopril, were assessed in 10 patients with mild to moderate essential hypertension. Administration of a 10 mg oral dose of fosinopril reduced mean arterial pressure (p < 0.001) as a result of a 24% fall in total peripheral resistance (p < 0.001). Short-term therapy (12 weeks) maintained the decrease in mean arterial pressure (p < 0.05) by decreasing total peripheral resistance (p < 0.01), without reflexive cardiac stimulation or expanding intravascular volume.Renal vascular resistance decreased (p < 0.05) while renal blood flow, glomerular filtration rate and filtration fraction remained unchanged. The response pattern to mental, isometric and orthostatic stress was similarly unchanged. Left ventricular mass diminished by 11% (p < 0.01); myocardial contractility was unaffected. Afterload was reduced (p < 0.05), and velocity of circumferential fiber shortening and stroke volume increased (p < 0.05).Thus, arterial pressure reduction produced by fosinopril was associated with improved systemic and renal hemodynamics and reduced left ventricular mass.

A comparative quantitative histological investigation of atrophic changes in the major salivary glands of liquid-fed rats

Adult male rats were maintained on a wholly liquid diet for 9 days. The three pairs of major glands were removed, weighed, histologically sectioned and examined by stereological and morphometric techniques. The results were compared with the same glands from control rats maintained on normal hard diet and water, and the extent of the differences was compared between the three different types of gland. Up to 50% of the serous acinar volume in the parotid glands, but only 15% in the submandibular glands, was lost after liquid feeding. There was no loss of the mucous acinar tissue in the sublingual gland. Mean acinar diameters were reduced by 33% in parotids and 15% in submandibular glands after liquid feeding, whereas the mucous acini of the sublingual gland remained unaltered. The results point to varying levels of susceptibility to the loss of masticatory reflexes between the parotid serous acini and the submandibular serous acini, and show that the morphology of the sublingual mucous acini is independent of masticatory reflex stimulation. The reductions in acinar diameters suggest that most of the glandular atrophy after liquid feeding is due to acinar cell shrinkage rather than to losses of acinar cell numbers in both parotid and submandibular glands.

Reflex and chemical responses of tracheal submucosal glands in piglets

In adult animals, airway fluid secretion is enhanced reflexly via central nervous system pathways, and locally mediators such as substance P. To evaluat the role of maturation on these regulatory mechanisms, we compared the effects of reflex stimulation and intravenous substance P administration on airway secretionin anaesthetized, paralyzed and artificially ventilated piglets, 9 to 22 days of age, and older piglets all aged 10 weeks. Airway secretion was monitored by counting the hillocks appearing in the upper trachea in an exposed field of tracheal epithelium (1.2 cm2) coated with powdered tantalum. In younger animals, mechanical stimulation of the larynx had no discernible effect on tracheal submucosal gland secretion. Neither excitation of airway irritant receptors nor stimulation of pulmonary C-fiber receptors by capsaicin caused a significant increase of fluid secretion from tracheal submucosal glands. In addition, stimulation of peripheral chemoreceptors by ventilating animals 12% O2 in N2, and 6% O2 in N2, failed to induce a substantial change in airway secretion, when compared with number of hillocks in the control period. Furthermore, administration of sodium cyanide had little or no effect on baseline secretion. In contrast, to the weak reflex responses in younger piglets electrical stimulation of the vagus nerve caused the number of hillocks to increase on average by 16.3 ± 2.3 (P < 0.01). In addition, local application of a pledget soaked in solution of methacholine caused the number of hillocks to increase by 32.1 ± 5.2 (P < 0.01). Intravenous administration of substance P also induced an augmentation in fluid secretion. Increase in concentration of substance P (10−8, 10−7, 10−6, and 10−5 M, 1 ml) was associated with a concomitant elevation in the number of activated submucosal glands 5.3 ± 2.6, 10.0 ± 4.4, 27.1 ± 4.5, 41 ± 5). In older piglets, stimulation of laryngeal mucosa, airway irritant receptors, as well as stimulation of pulmonary C-fiber receptors induced a significant increase in tracheal secretion, although stimulation of peripheral chemoreceptors had no effect on airway secretion. These data suggest that reflex responses of submucosal glands are weak during early postnatal development, however, tracheal submucosal glands do respond to exogenously administered cholinergic substances and tachykinin peptides.

Underlying mechanisms of atrophic state of brown adipose tissue in obese Zucker rats

The mechanisms involved in brown adipose tissue (BAT) atrophy in obese rats were investigated. In urethan-anesthetized adult obese (fa/fa) and lean (Fa/?) rats, colonic temperature (Tc), interscapular BAT (IBAT) temperature (TIBAT), and the TIBAT-Tc gradient were measured after microknife cut in the prepontine region and during norepinephrine (NE) infusion. The knife cut tests the neural control of IBAT since it suppresses a tonic inhibition of thermogenesis revealing a sustained reflex stimulation of BAT. The NE infusion tests the metabolic capacity of BAT. In 22 degrees C-acclimated lean rats, the cut induced marked hyperthermia, TIBAT that rose faster than Tc, and a reversed temperature gradient. By contrast, in the obese rat, the cut had practically no effect, and NE infusion caused only slight increases in Tc and TIBAT. In cold-acclimated obese rats, an almost complete response to NE infusion and a partial response to knife cut were observed. After adrenalectomy, the responses were similar in lean and obese rats. An operational model to account for these results and for the deficit in diet-induced thermogenesis in fa/fa rats is proposed.

Vibration insensitivity of a short latency reflex linking the lower leg and the active knee extensor muscles in humans

The study indirectly investigated the afferent source of a human lower limb reflex that spans two joints and may link limb muscular activity during movement. Low threshold (motor nerve threshold (MT) to 1.6 MT) single, 1 msec, pulses were delivered to the common peroneal nerve at caput fibula. Heteronymous excitatory responses were observed in the electromyogram of the knee extensor muscle vastus medialis (VM), when the latter was prior contracted. The briefest latency for the VM reflex was 24.2 msec. The distal belly and tendon of the tibialis anterior muscle were vibrated for 20 min at a frequency of 105 Hz, amplitude 1–2 mm, to inhibit the reflex potential evoked by group Ia afferent fibres from that muscle. This significantly reduced the amplitude of the group Ia mediated Hoffmann (H) reflex in TA. Such vibration did not depress the amplitude of the heteronymous reflex to VM, when initially the latter was at peak amplitude or at its mid-range for amplitude. Reflex latency, threshold, and stimulation current for peak expression suggested that group II fibres were unlikely to be the major initiators of the reflex. The results support the view that this human reflex is primarily Ib mediated.

Evidence for Elevated Glucose Threshold in Patients With Impaired Glucose Tolerance and Symptoms of Hypoglycemia During OGTT

We evaluated the relationship between hypoglycemic symptoms, glucose nadir levels, and hormone changes in patients with impaired glucose tolerance (IGT) after an oral glucose tolerance test (OGTT). The peak counterregulatory hormone response was determined at the glucose nadir identified by continuous glucose monitoring. Eight patients with IGT who had symptoms and signs typical of hypoglycemia at the glucose nadir were compared with completely asymptomatic subjects (5 IGT patients and 13 patients who had normal glucose tolerance [NGT]). The mean glucose nadir of symptomatic IGT patients was 3.50 +/- 0.46 mM, which was not statistically different from the mean of asymptomatic NGT patients (4.10 +/- 0.56 mM) but was significantly lower than that for asymptomatic IGT patients (5.10 +/- 0.81 mM, P less than 0.001). Seven of 8 symptomatic IGT patients had glucose levels that never fell below the range of glucose nadirs for asymptomatic NGT patients. However, the symptomatic IGT group had significantly higher levels of growth hormone, cortisol, epinephrine, and norepinephrine than the asymptomatic groups in response to the nadir. We conclude that patients with IGT are capable of experiencing signs and symptoms of hypoglycemia at physiological glucose levels during OGTT with reflex stimulation of counterregulatory hormone release. This may indicate that symptomatic IGT patients have a higher glucose threshold for eliciting characteristic hypoglycemic symptom episodes than individuals with NGT.

Effect of acute hypoxemia on brain blood flow and oxygen metabolism in immature fetal sheep

Studies of cerebral blood flow and oxygen metabolism during acute hypoxic hypoxia in fetal sheep have been confined to late gestation, a time when brain development in this species is largely complete. There is no systematic study of cerebral vascular responses to acute hypoxic hypoxia in immature fetal sheep or, indeed, in immature brains of any species. We studied 13 fetal sheep in utero at 93 +/- 1 days gestation (term = 145-150 days), 48 h after intravascular catheters were placed into the superior sagittal sinus, axillary arteries, and inferior vena cava. We measured brain blood flow by the microsphere method. Cerebral oxygen consumption was calculated with the use of blood flow to the cerebral hemispheres (cerebrum, diencephalon, mesencephalon) and arterial and sagittal sinus values for oxygen content. Fractional oxygen extraction was calculated as the ratio between oxygen consumption and oxygen transport. We altered fetal oxygenation by changing the mother's inspired oxygen concentration. As in the near-term fetus, acute hypoxic hypoxia resulted in increased blood flow to cerebral hemispheres, cerebellum, and pons-medulla; furthermore, the increase in blood flow was sufficient to sustain cerebral oxygen consumption. However, in contrast to near-term fetuses, the increase in blood flow to the cerebral hemispheres was not sufficient to maintain convective oxygen transport. Cerebral oxygen consumption was therefore sustained in part by an increase in fractional extraction. Blunted hypoxic vasodilation in immature fetuses might reflect either immature regulatory mechanisms or an inability of cerebral vessels to respond to the usual stimuli. It is also possible that hypoxic vasodilation was blunted by reflex stimulation of the sympathetic nervous system.

Reflex stimulation of sympathetic outflow during rhythmic exercise in humans

The aim of this study was to determine whether a chemically generated reflex arising in nonischemic skeletal muscle normally increases sympathetic outflow during rhythmic exercise. To accomplish this aim, we recorded muscle sympathetic nerve activity (MSNA, peroneal nerve) in conscious humans during exercise interventions designed to alter the relationship between muscle blood flow and metabolic demand. Under normal conditions, MSNA increased during moderate but not during mild levels of rhythmic handgrip (0.67 Hz) and one-arm cycling (0.83 Hz). MSNA remained elevated when the moderate level of rhythmic handgrip was followed by forearm vascular occlusion, a maneuver that sustains muscle chemoreflex stimulation. Complete arm vascular occlusion was needed to increase MSNA during mild arm cycling, whereas even partial vascular occlusion greatly amplified the stimulation of MSNA normally produced by the moderate level of arm cycling. We conclude that a chemically generated reflex arising in nonischemic working muscle plays an important role in the normal activation of sympathetic discharge to nonexercising leg muscles during moderate but not during mild levels of rhythmic arm exercise.

Pharmacologic profile of amlodipine

Amlodipine is a potent calcium antagonist, inhibiting Ca 2+-induced contractions of depolarized rat aorta with an IC 50 of 1.9 nM. Unlike nifedipine, it displayed very slow association and dissociation with the calcium channel. The ability of amlodipine to inhibit Ca 2+-induced contractions was strongly dependent on the K + concentration present before the contraction, suggesting marked voltage dependence of action. Radioligand-binding studies in cardiac membrane preparations suggested that amlodipine may interact directly with both 1,4-dhydropyridine and diltiazem-binding sites on the calcium channel. Hemodynamic studies In anesthetized and conscious dogs slowed that amlodipine is a coronary and peripheral vasodilator with a slow onset and long duration of effect, even when given by intravenous injection; the reflex stimulation of cardiac output, heart rate and myocardial contractility induced by amlodipine was attenuated by propranolol, but no marked negative inotropic or dromotropic effects were observed. Amlodpine was an effective oral antihyperlensive agent in rat and dog models of hypertension, and its 24-hour duration of action in hypertensive dogs correlated well with its long plasma half-life in this species. The natriuretic properties displayed by amlodipine may contribute to its use as a first-line drug for the treatment of hypertension.

Sweating patterns in atopic dermatitis patients.

Postganglionic sweat output in ten patients with atopic dermatitis was determined by a quantitative sudomotor axon reflex test in which the output results from axon reflex stimulation by acetylcholine iontophoresis. All measurements were obtained from normal skin on the volar aspect of the left wrist and dorsal aspect of the left foot of the atopic patients. Latency, sweat volume, and dynamic sweat pattern were variables included in the study. An abnormal value or configuration was found in nine of the ten patients studied. Seven of the ten patients had abnormal sweat output values. Atopic patients have abnormal sweating patterns, which may be inherently responsible for or related to their disorder.

Our changing understanding of asthma

It is now becoming clear that asthma is a chronic inflammatory disease, involving many interacting cells. These cells release a wide variety of inflammatory mediators that activate several target cells in the airway, resulting in bronchoconstriction, microvascular leakage and oedema, mucus hypersecretion and stimulation of neural reflexes. Recent evidence suggests that mast cells do not have a key role in either the late response or in bronchial hyper-responsiveness, though they may be involved in immediate responses to allergens. The possible role of other inflammatory cells and the many different mediators which have been implicated in asthma are discussed. Microvascular leakage and the role of neural mechanisms are also examined. It seems probable that there are several different types of asthma, involving different mechanisms, which may respond to different forms of therapy, but more research is needed.

Angiotensin converting enzyme inhibitors. Present and future.

The angiotensin converting enzyme (ACE)-inhibiting agents have emerged with the diuretic agents, beta-adrenergic receptor-blocking agents, and calcium antagonists as therapeutic options for major consideration during the initial treatment of hypertensive patients. These compounds antagonize a potent pressor mechanism underlying hypertensive disease. The ACE inhibitors curtail the generation of the potent octapeptide angiotensin II; in addition, degradation of the potent vasodilator bradykinin is inhibited. Hemodynamically, ACE inhibitors reduce arterial pressure through a decreased total peripheral resistance that is unassociated with reflex stimulation of the heart or expansion of intravascular volume. The arteriolar dilation accounting for the decreased vascular resistance seems to occur in each target organ of the disease. Unlike the direct-acting smooth muscle vasodilators or adrenergic inhibitors, ACE inhibitors dilate the efferent as well as the afferent glomerular arterioles and thereby reduce glomerular hydrostatic pressure and renal filtration fraction, even though renal blood flow and glomerular filtration rate are preserved. The ACE-inhibiting compounds not only reduce left ventricular afterload in hypertension but also diminish cardiac mass and wall thicknesses. The mechanism(s) for some of these actions have not yet been defined precisely, but they undoubtedly involve the autocrine/paracrine actions of the renopressor system and their effects in the cellular biologic events of vascular smooth muscle and the cardiac myocyte. It seems plausible and exciting that the "more local" renin-angiotensin systems will be exploited by those ACE inhibitors yet to be synthesized, which will result in new applications for this class of pharmacological agents.

Coronary vascular responses to chemical stimulation of abdominal visceral organs.

Topical application of bradykinin or capsaicin to abdominal visceral organs produces adrenergically mediated, reflex increases in mean arterial pressure and cardiac work. To determine the effects on coronary blood flow, the left main coronary artery of anesthetized cats was perfused at constant pressure with a servo-controlled pump. Cardiovascular parameters were measured during reflex stimulation before and after beta-adrenoceptor blockade with propranolol. Before propranolol, reflex activation led to increases in the double product and myocardial oxygen consumption, usually accompanied by increases in coronary blood flow. However, in 32% of the observations, decreases in flow were observed. During beta-adrenoceptor blockade, reflex stimulation produced increases in cardiac work, whereas the increases in coronary blood flow were attenuated. Marked decreases in average coronary blood flow were observed more frequently (42%). In the presence of propranolol, contrary to the unblocked state, increases in oxygen consumption were achieved by increased oxygen extraction. Subsequent alpha-adrenoceptor blockade with phentolamine abolished all reflex changes. These data indicate that during stimulation of abdominal visceral chemoreceptors, the major coronary response is vasodilation, but in a sizable fraction of cases, abdominal visceral reflexes can produce sympathetically mediated coronary vasoconstriction.

Stimulation of renal sympathetic activity by static contraction: evidence for mechanoreceptor-induced reflexes from skeletal muscle.

Static muscular contraction in anesthetized animals has been firmly established to reflexly increase arterial pressure. Although group III and IV muscle afferents are known to be responsible for this reflex pressor response, there is no evidence that the stimulation of muscle mechanoreceptors, many of which are supplied by group III fibers, plays a role in causing this contraction-induced reflex effect. To provide this evidence, we recorded renal sympathetic nerve activity in chloralose-anesthetized cats while contracting the triceps surae muscles. We found that static contraction tripled renal nerve activity within three seconds of its onset, an increase that was abolished by cutting the L6 and S2 dorsal roots. On average, the contraction-induced increase in renal nerve activity was observed 0.8 +/- 0.1 seconds after the onset of this maneuver. In addition, intermittent tetanic contractions synchronized renal nerve discharge so that a burst of activity was evoked by each contraction. A similarly synchronized renal nerve discharge was evoked in paralyzed cats by electrical stimulation of the tibial nerve at five times motor threshold, a current intensity that activates group III afferents. We conclude that, in anesthetized animal preparations, mechanoreceptors with group III afferents contribute to the reflex stimulation of renal sympathetic outflow evoked by muscular contraction.

Neuropathic Pain: A New Theory for Chronic Pain of Intrinsic Origin

Why is acupuncture accepted in the East, especially for the treatment of chronic pain, but not in the West? One reason is that the modus operandi of acupuncture is not fully understood; another is the enigmatic nature of chronic pain. This article introduces a new concept of chronic pain, and suggests how acupuncture may relieve it. Chronic pain may arise from sources that are extrinsic to the nervous system (for example, ongoing injury or inflammation), but it can also be intrinsic and the result of abnormal hypersensitivity (supersensitivity) in neuropathic or partially denervated structures. Neuropathic pain typically affects the musculoskeletal system, and a pivotal component of this type of pain is muscle spasm or shortening. Spasm can cause pain localised to muscle, but sustained muscle spasm or shortening mechanically overloads tendons and their attachments, and can produce pain in these structures. Since neuropathic pain is different from nociception or inflammation, its treatment is also distinct (desensitisation of supersensitivity). Most physical treatment modalities for this type of pain, such as heat, massage or transcutaneous electrical nerve stimulation (TENS), desensitise by reflex stimulation of the affected part via its intact innervation. However these modalities are passive and limited in scope. Stimulation ends when their application is terminated. In contrast, injection techniques, including acupuncture, are more effective and long-lasting, because the tissue injury that they produce can unleash the body's healing source of bioenergy through the current of injury. Tissue injury also releases the platelet-derived growth factor (PDGF), which can promote healing.