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PubMed1987

Changes in sensorimotor functions after spinal lesions evaluated in terms of long-latency reflexes.

Lesions of the central afferent and efferent pathways cause onset-delays of long-latency EMG responses from anterior tibial muscle after passive dorsiflection of the ankle joint in standing subjects. In 23 patients with spinal tumour or cervical stenosis and clinical signs of a medullary lesion, short-, medium- and long-latency EMG responses from distal leg muscles after ankle dorsiflection were recorded prior to and after surgical intervention. Fifteen of the patients were re-examined between 1 and 2 years after surgery. The results of the follow-up study support the hypothesis of a supraspinal pathway for long-latency EMG responses in distal leg muscles and show their significance as a quantitative measure of sensorimotor functions.

Electromyography↗
PubMed1991

Impairment of vasomotor reflexes in the fingertips of leprosy patients.

A method is described for eliciting fingertip vasomotor reflexes by inspiratory gasp and contralateral hand cold challenge. The results of the two tests are reproducible on replicate testing and, when taken together, have proved reliable for detection of impairment of autonomic reflexes in 10 newly registered leprosy patients who did not have any obvious deformity. Similar, but less severe, impairment of vasomotor reflexes was noted in a group of 10 fully treated, apparently cured ex-leprosy patients, none of whom showed clinically obvious neuropathy. Both the new patients and the ex-patients were significantly different from healthy contacts and from healthy Europeans, who were indistinguishable by this test. Evidence is presented suggesting that impairment of these vasomotor reflexes is mainly due to damage to the efferent pathway in the peripheral nerves. The method might prove valuable for investigation of early nerve damage in new patients or during reversal reactions in leprosy at a stage before irreversible damage is done.

Adult↗
PubMed1998

Chronic cough in the Holmes-Adie syndrome: association in five cases with autonomic dysfunction.

The Holmes-Adie syndrome consists of unilateral or bilateral tonic pupils with near light dissociation and tendon areflexia. It is associated with autonomic disturbances affecting sudomotor and vasomotor function. Five such patients are reported on who also had a troublesome chronic dry cough, which was of unknown aetiology and was resistant to a range of treatments. The cough may be related to involvement of afferent or efferent pathways in the vagus. Chronic cough may be an accompaniment in the Holmes-Adie syndrome, like other forms of autonomic dysfunction.

Adie Syndrome↗
PubMed1995

Post-typhoid anhidrosis: a clinical curiosity.

A 19-year-old girl developed generalised anhidrosis following typhoid fever. Elaborate investigations disclosed nothing abnormal. A skin biopsy revealed the presence of atrophic as well as normal eccrine glands. This appears to be the third case of its kind in the English literature. It is postulated that typhoid fever might have damaged the efferent pathway of sweating.

Adult↗
PubMed1985

Mechanisms of action of sodium cromoglycate.

The effects of sodium cromoglycate (SCG) on cardiovascular and pulmonary responses to phenylbiguanide, capsaicin, and vagal stimulation were studied in anesthetized guinea pigs. Phenylbiguanide had no bronchospastic activity but induced reflex changes in arterial blood pressure which were reduced or abolished by SCG. Capsaicin induced nonreflex bronchospasm, and decreases in arterial blood pressure that were unaffected by SCG. Sodium cromoglycate, given before or after atropine, had no effect on the bronchospasm and cardiovascular responses to unilateral or bilateral stimulation of the vagus nerves. We conclude that SCG may influence both the afferent and efferent pathways of responses to drugs.

Animals↗
PubMed1981

Neural influences on oscillations in basal plasma levels of insulin in monkeys.

The effects of cholinergic and adrenergic blocking agents on the period and amplitude of sustained oscillations in plasma levels of insulin and glucose were studied in 16 overnight-fasted conscious rhesus monkeys. Blood samples were withdrawn at 2-min intervals before and during or following administration of drugs that affect neurotransmission. Cholinergic blockade with atropine had no effect on the oscillations. alpha-Adrenergic blockade with phentolamine caused a rise in plasma insulin that lasted less than 10 min and was followed by a slight, although not consistent, decrease in mean insulin and a consistent small decrease in glucose. There was a sustained increase in heart rate, but no effect on the oscillations of insulin or glucose. beta-Adrenergic blockade induced by propranolol led to persistent decreases in mean plasma insulin 60% below the base line, small but variable decreases in glucose, and a sustained decrease in heart rate, but no change in period or relative amplitude of the oscillations in plasma levels of either insulin or glucose. General anesthesia with pentobarbital did not eliminate these oscillations. Our observations on the failure of the blockade of certain putative efferent pathways or depression of higher cortical centers to alter the period of the oscillations of insulin reduce the likelihood that the oscillations are transmitted from a pacemaker in the central nervous system.

Animals↗
PubMed2006

Ghrelin acts on the dorsal vagal complex to stimulate pancreatic protein secretion.

Ghrelin receptors are present in the central nervous system. We hypothesized that ghrelin released from the stomach acts as an endocrine substance and stimulates brain stem vagovagal circuitry to evoke pancreatic secretion. In an in vivo anesthetized rat model, an intravenous infusion of ghrelin at doses of 5, 10, and 25 nmol increased pancreatic protein secretion from a basal level of 125 +/- 6 to 186 +/- 8, 295 +/- 12, and 356 +/- 11 mg/h, respectively. Pretreatment with atropine or hexamethonium or an acute vagotomy, but not a perivagal application of capsaicin, completely abolished pancreatic protein secretion responses to ghrelin. In conscious rats, an intravenous infusion of ghrelin at a dose of 10 nmol resulted in a 2.2-fold increase in pancreatic protein secretion over basal volume. Selective ablation of the area postrema abolished pancreatic protein secretion stimulated by intravenous infusion of ghrelin but did not alter the increase in pancreatic protein secretion evoked by diversion of bile-pancreatic juice. Immunohistochemical staining showed a marked increase in the number of c-Fos-expressing neurons in the area postrema, nucleus of the solitary tract, and dorsal motor nucleus of the vagus after an intravenous infusion of ghrelin in sham-lesioned rats; selective ablation of the area postrema eliminated this increase. In conclusion, ghrelin stimulates pancreatic secretion via a vagal cholinergic efferent pathway. Circulating ghrelin gains access to the brain stem vagovagal circuitry via the area postrema, which represents the primary target on which peripheral ghrelin may act as an endocrine substance to stimulate pancreatic secretion.

Animals↗
PubMed1987

Cardiac receptor modulation of blood flow and fluid transport in feline jejunum.

The aim of the study is to determine the effects of selective cardiac receptor unloading on vascular resistance and net fluid transport in the small intestine. In anesthetized cats, cardiac receptors were unloaded by positive pressure ventilation (PPV). Arterial baroreceptor activity was artificially maintained constant. To test if the observed responses were due to a vagal reflex, experiments were performed both in animals with intact vagal nerves (n = 9) and after bilateral cervical vagotomy (n = 8). PPV-induced decreases in central blood volume (CBV) significantly increased intestinal vascular resistance (IVR) and net fluid absorption rate and decreased the transmural potential difference (PD). Cervical vagotomy per se also increased IVR and absorption rate and decreased PD. In vagotomized animals, decreases in CBV had no consistent effects on IVR, net fluid absorption rate, or PD. The results are compatible with cardiac receptor modulation of both blood flow and fluid absorption rate in the feline jejunum. Differences in the response patterns for the vascular and absorptive effects suggest that they may be mediated by separate efferent pathways.

Absorption↗
PubMed1988

TRH analogue, RX 77368, injected into dorsal vagal complex stimulates gastric secretion in rats.

Medullary sites inducing gastric acid secretion in response to microinjection of the stable analogue of thyrotropin-releasing hormone (TRH; RX 77368, pGlu-His-[3,3'-dimethyl]-Pro-NH2) were investigated in urethan-anesthetized rats. Gastric acid output was recorded every 2 min through a double gastric cannula constantly perfused with 0.9% saline solution maintained at pH 5.5 using an automatic titrator. Unilateral microinjection of RX 77368 (10-100 ng in 50-nl volume) into the dorsal vagal complex (DVC), the dorsal vagal nucleus and nucleus tractus solitarius, induced a significant dose-dependent stimulation of gastric acid secretion. The peak response occurred within 50 min and lasted over 1 h. Other medullary sites, including the lateral, dorsal, and parvocellular reticular nuclei; the medial longitudinal fasciculus; and the medial cuneate nucleus injected with RX 77368 (10-100 ng), were inactive. The TRH metabolites, TRH-OH and His-Pro diketopiperazine (100 ng), injected into the DVC did not influence gastric acid secretion. The stimulation of gastric acid secretion induced by DVC injection of TRH was abolished by vagotomy. These results demonstrate that 1) the DVC is an important site of action for TRH-induced stimulation of gastric acid secretion, 2) TRH action in the DVC is not secondary to the formation of TRH metabolites, and 3) the effect is expressed by vagal efferent pathways. These findings added to the high concentration of TRH-immunoreactivity and receptors in the DVC suggest a role for endogenous TRH in the regulation of vagal outflow to the stomach.

Animals↗
PubMed1994

Mechanisms coordinating gastric and small intestinal MMC: role of extrinsic innervation rather than motilin.

We have investigated the role of vagal and efferent adrenergic innervation coordinating the gastric and small intestinal migrating motor complexes (MMCs) after removal of the pylorus, duodenum, and upper jejunum in three dogs. The cervical vagus nerves were previously isolated in bilateral skin loops to permit reversible cooling blockade of the vagi. Pharmacological alpha- and beta-receptor blockade was accomplished by bolus intravenous injection of phentolamine and propranolol followed by intravenous infusion of the combined drugs. Gastric and upper jejunal MMC-like activity was initially absent after bowel resection but reappeared after 1-4 mo with the gastric and jejunal MMC-like activities coordinated as if the jejunum were the duodenum. Motilin peaks were absent. All gastric contractions were abolished by vagal blockade. Pharmacological adrenergic blockade immediately induced an intense burst of contractile and electrical activity in the stomach, which propagated to the distal ileum. This phase III-like burst was followed by ongoing intermittent bursts of contractile and electrical activity in the stomach and small intestine, lasting throughout the blockade, without further MMC-like activity. Vagal cooling blockade in combination with adrenergic blockade did not restore gastric MMC-like activity but abolished or decreased the number of gastric contractions, with the reappearance of the small intestinal MMC. Atropine boluses abolished all control and adrenergic blockade-induced stomach and small intestinal contractile and electrical activity. In conclusion, after duodenectomy, the gastric MMC-like activity that is reestablished and is coordinated with the small intestinal MMC is vagally dependent and cholinergic, but its cyclical nature requires adrenergic efferent pathways. Under these circumstances, coordination of the gastric and jejunal MMCs appears to require extrinsic innervation.

Animals↗
PubMed1978

Reflex circulatory changes due to the afferent stimulation of cat pericoronary nerve.

Two different types of circulatory reflexes evoked by electrical stimulation of afferent fibers in the left pericoronary nerves were studied in anesthetized cats. A depressor response (-32.5 mmHg) with bradycardia (-48.7 beats/min) in 21 of 31 cats was mediated by the C fibers in the right vagal cardiac nerve trunk. The efferent pathway for the bradycardia was in caudal cardiac branches of the right vagus. Neither sympathetic denervation to the heart nor atropine attenuated the hypotensive response significantly, suggesting that the depressor response results from reflex inhibition of peripheral sympathetic activity. A pressor reflex without heart rate change was observed either when the vagi were blocked or when the distribution of vagal afferents in the pericoronary nerve was considered to be small. The pressor reflex was mainly mediated by the afferent C fibers within the left cardiac sympathetic nerves. The depressor response was enhanced by sympathectomy, suggesting the sympathetic counteraction on the inhibitory vagal afferents, Similarly, an enhancement of the pressor reflex by vagal blockade was observed, indicating tonic vagal restraint on excitatory sympathetic reflexes.

Afferent Pathways↗
PubMed1979

Neural mechanism underlying tachycardia induced by nonhypotensive a-v shunt.

The mechanism underlying tachycardia resulting from nonhypotensive arteriovenous shunt (shunt open plus infusion of blood to compensate for the fall in mean arterial pressure resulting from opening of a shunt) was investigated in anesthetized, artificially ventilated dogs. In dogs with intact autonomic innervation, dogs with beta-adrenergic blockage (BB), and dogs with BB plus spinal section at C7 (BBSS), opening of the shunt resulted in tachycardia (P less than 0.01 for all comparisons), which was, however, not significantly different on comparison among groups (P greater than 0.40 for all comparisons). This shows that afferent and efferent sympathetic-mediated reflexes do not play a significant role in this tachycardia response. Additionally, the tachycardia response was significant in dogs with BBSS plus right or left vagotomy, but it was completely abolished in dogs with BBSS plus bilateral vagotomy. This suggests that in dogs with blockade of sympathetic afferent and efferent pathways, tachycardia resulting from nonhypotensive arteriovenous shunt may be due to a cardioacceleratory reflex with its ascending and its descending pathways in each vagus nerve.

Animals↗
PubMed1995

Participation of hypothalamic paraventricular nucleus in locus ceruleus-induced baroreflex suppression in rats.

We evaluated the potential role of the paraventricular nucleus (PVN) of the hypothalamus in the suppression of baroreceptor reflex (BRR) response by locus ceruleus (LC), using adult male Sprague-Dawley rats anesthetized with pentobarbital sodium. Electrical stimulation of histologically verified sites in the LC elicited significant reduction in the BRR response. This suppressive effect of LC on BRR response was appreciably antagonized by bilateral electrolytic lesions of the PVN and reversibly blocked by bilateral microinjection of 2% lidocaine into similar hypothalamic loci. Local administration of the alpha 1-adrenoceptor antagonist, prazosin (50 pmol), or an antiserum directed against neuropeptide Y (NPY) (1:20) into the bilateral PVN also significantly attenuated the suppression elicited by LC on BRR response. In contrast, treatments with the alpha 2-adrenoceptor blocker, yohimbine (50 pmol), heat-inactivated NPY antiserum (1:20), artificial cerebrospinal fluid, or normal rabbit serum (1:20) produced no discernible effect. These results suggest that the PVN may constitute part of the efferent pathways through which LC elicits its inhibition on the BRR response. Furthermore, LC may activate this pathway via alpha 1-adrenoceptors and NPY receptors in the PVN.

Adrenergic alpha-Antagonists↗
PubMed1997

Frequency-response characteristics of autonomic nervous system function in conscious rats.

To characterize the efferent pathway from the hypothalamic paraventricular nucleus (PVN) to peripheral autonomic neurons and finally to selected effector organs, we stimulated the PVN in 10 conscious rats at frequencies ranging from 0.05 to 2.0 Hz. Simultaneously, blood pressure, heart rate, splanchnic sympathetic nerve activity, and mesenteric artery blood flow were measured. The sinus node of the heart responded to PVN stimulation via the parasympathetic pathway (during beta 1-adrenergic blockade) up to a stimulation frequency of 2.0 Hz, whereas the sympathetically mediated response (during muscarinic blockade) was limited to stimulation frequencies < 0.5 Hz. The splanchnic nerve responded to PVN stimulation with synchronous discharges up to stimulation frequencies of 2.0 Hz, whereas the oscillatory component of the vasoconstrictor response of the mesenteric artery was negligible beyond stimulation frequencies of 1.0 Hz. We conclude that sympathetic transmission to the heart is at least four times slower than parasympathetic transmission. In addition, the time-limiting step in sympathetic transmission from the hypothalamus to vascular smooth muscle contraction and pacemaker activity of the sinus node may be located at the site of synaptic transmission to the adrenergic receptors.

Animals↗
PubMed1975

Neuropharmacological characterization of insulin-sensitive CNS glucoregulator.

Regional insulinization of the central nervous system (CNS) through the carotid artery causes an immediate decrease of the systemic blood sugar level in rats under light barbiturate anesthesia. Cervical vagotomy or intraperitoneal or intravenous atropine pretreatment results in partial inhibition of the systemic hypoglycemic response that follows intracarotid insulin injection. Intraperitoneal, intravenous, or intracarotid pretreatment with phentolamine or propranolol or intracarotid pretreatment with epinephrine had no effect on this centrally induced hypoglycemia. Intracarotid atropine injection immediately prior to intracarotid insulin injection completely abolished the systemic hypoglycemic response. Pretreatment with neostigmine administered intravenously prevented the inhibitory effect of intracarotid atropine on the hypoglycemic response that followed intracarotid insulin injection. It is consluded that the insulin-sensitive glucoregulator center of the CNS is under cholinergic influence, or its efferent pathways have a centrally located cholinergic synapsis.

Animals↗
PubMed2003

Attenuated defense response and low basal blood pressure in orexin knockout mice.

The perifornical area of the hypothalamus has been known as the center for the defense response, or "fight or flight" response, which is characterized by a concomitant rise in arterial blood pressure (AP), heart rate (HR), and respiratory frequency (Rf). We examined whether orexin, a recently identified hypothalamic neuropeptide, contributes to the defense response and basal cardiovascular regulation using orexin knockout mice. Microinjection of a GABA-A receptor antagonist, bicuculline methiodide (0.1-1 mM in 20 nl), to the perifornical area in urethane-anesthetized wild-type mice elicited dose-dependent increases in AP, HR, and Rf. Although similar changes were observed in orexin knockout mice, intensities were smaller and duration was shorter than those in wild-type mice. Moreover, in an awake and freely moving condition, telemeter-indwelling orexin knockout mice showed diminished cardiovascular and behavioral responses to emotional stress in the resident-intruder test. We also found that basal AP in orexin knockout mice was significantly lower in both anesthetized (117 +/- 8 mmHg in wild type and 92 +/- 3 in knockout) and conscious (125 +/- 6 mmHg in wild type and 109 +/- 2 in knockout) conditions. alpha-Adrenergic blockade with prazosin or ganglion blockade with hexamethonium canceled the difference in basal AP. HR and cardiac contractile parameters by echocardiography did not differ between the two strains of mice. These results indicate lower sympathetic vasoconstrictor tone in knockout mice. The present study suggests that orexin-containing neurons in the perifornical area play a role as one of the efferent pathways of defense response and also operate as a regulator of AP at basal condition by activating sympathetic outflow.

Animals↗
PubMed2006

Orexin neuron-mediated skeletal muscle vasodilation and shift of baroreflex during defense response in mice.

We have previously shown that some features of the defense response, such as increases in arterial blood pressure (AP), heart rate (HR), and ventilation were attenuated in prepro-orexin knockout (ORX-KO) mice. Here, we examined whether the same was true in orexin neuron-ablated [orexin/ataxin-3 transgenic mice (ORX/ATX-Tg)] mice. In addition, we examined other features of the defense response: skeletal muscular vasodilation and shift of baroreceptor reflex. In both anesthetized and conscious conditions, basal AP in ORX/ATX-Tg mice was significantly lower by approximately 20 mmHg than in wild-type (WT) controls, as was the case in ORX-KO mice. The difference in AP disappeared after treatment with an alpha-blocker but not with a beta-blocker, indicating lower sympathetic vasoconstrictor outflow. Stimulation of the perifornical area (PFA) in urethane-anesthetized ORX/ATX-Tg mice elicited smaller and shorter-lasting increases in AP, HR, and ventilation, and skeletal muscle vasodilation than in WT controls. In addition, air jet stress-induced elevations of AP and HR were attenuated in conscious ORX/ATX-Tg mice. After pretreatment with a beta-blocker, atenolol, stimulation of PFA suppressed phenylephrine (50 microg/kg iv)-induced bradycardia (DeltaHR=-360+/-29 beats/min without PFA stimulation vs. -166+/-26 during stimulation) in WT. This demonstrated the resetting of the baroreflex. In ORX/ATX-Tg mice, however, no significant suppression was observed (-355+/-16 without stimulation vs. -300+/-30 during stimulation). The present study provided further support for our hypothesis that orexin-containing neurons in PFA play a role as a master switch to activate multiple efferent pathways of the defense response and also operate as a regulator of basal AP.

Adrenergic alpha-Antagonists↗
PubMed1985

Mechanism of inhibition of renin secretion by increased left atrial pressure.

Experiments were designed to elucidate the mechanism of the failure of systemic hypotension to stimulate renin release in the presence of elevated left heart pressure. We conducted a series of graded ascending aortic and suprarenal cuff inflations in dogs with bilateral renal denervation (n = 5). The renal perfusion pressure (RPP) was reduced by 10, 20, and 30% of control by inflation of either cuff. Comparison of the renin response with inflation of the ascending aortic to the suprarenal cuff revealed a clear increase in the threshold required to elicit a renin response to graded reduction of RPP after inflation of the ascending aortic cuff. These results may be explained by differential effects of the two maneuvers on left heart pressure. Left atrial pressure increased during inflation of the ascending aortic cuff but did not change during inflation of the suprarenal cuff. Since the kidneys were denervated, the shift in threshold must be caused by a humoral substance(s). In conclusion, our findings suggest that the efferent pathway of potent inhibition of renin release from the left heart is mediated, at least partially, by a humoral substance.

Angiotensin I↗