Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ganglionic Blockers”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources
PubMed1985

Entero-pancreatic reflexes revealed by duodenal anesthesia in the dog.

This study was designed to improve our understanding of duodeno-pancreatic reflexes, the existence of which was suggested by the previous observation of a reduction in secretin-stimulated pancreatic secretion during local anesthesia of the duodenal mucosa. The effects on this reduction in secretin-stimulated secretion of cholinergic or adrenergic blocking agents (alone or in combination) and of truncal vagotomy, were studied in conscious dog with gastric and pancreatic fistulae. For each agent and for secretin alone in normal and vagotomized dogs, a comparison was made of pancreatic secretion with and without lignocaine anesthesia of the duodenal mucosa. Lignocaine reduced pancreatic secretion with secretin alone, and stimulated it during infusion of atropine. The changes in both protein bicarbonate secretion were blocked by pentolinium and by phenoxybenzamine whereas propranolol mainly blocked the effects on bicarbonate output. The effect of truncal vagotomy resembled that of atropine. These results suggest the existence of two enteropancreatic reflex mechanisms; an excitory cholinergic vagal reflex and an inhibitory, atropine-resistant non-vagal reflex. Both are blocked by pentolinium (a ganglion blocker) and by phenoxy-benzamine, suggesting the involvement of alpha-adrenergic receptors probably also at the level of the ganglion cell. Beta-adrenergic receptors are also involved in the regulation of bicarbonate and fluid secretion.

Anesthesia↗
PubMed2005

Tachycardia caused by A2A adenosine receptor agonists is mediated by direct sympathoexcitation in awake rats.

Adenosine-induced tachycardia is suggested to be mediated via A(2A) receptors; however, the exact mechanism for this effect remains to be understood. The present study was carried out using regadenoson, a selective A(2A) adenosine receptor agonist, to determine the role of the A(2A) receptor subtype in adenosine-induced tachycardia. Regadenoson (0.3-50 microg/kg) given as a rapid i.v. bolus to awake rats caused a dose-dependent increase in heart rate (HR). Mean arterial pressure (MAP) increased at lower doses, whereas at higher doses, there was a decrease in MAP. The increase in HR was evident at the lowest dose (0.3 microg/kg) of regadenoson at which there was no appreciable decrease in MAP. Pretreatment with 30 microg/kg ZM 241385 [4-(2-[7-amino-2-(2-furyl)-[1,2,4]-triazolo-[2,3-a]-[1,3,5]-triazin-5-ylamino]ethyl)phenol], an A(2A) receptor antagonist, attenuated the decrease in MAP and the increase in HR caused by regadenoson. Pretreatment with metoprolol (1 mg/kg), a beta-blocker, attenuated the increase in HR but had no effect on the hypotension caused by regadenoson. In the presence of hexamethonium (10 mg/kg), a ganglionic blocker, the tachycardia was completely prevented even though MAP was further reduced. Regadenoson treatment (10 microg/kg) significantly (p < 0.05) increased plasma norepinephrine levels almost 2-fold above baseline. The dissociation of HR and MAP effects by dose, time, and pharmacological interventions provides evidence that tachycardia caused by regadenoson is independent of the decrease in MAP and may not entirely be baroreflex-mediated, suggesting that regadenoson may cause a direct stimulation of the sympathetic nervous system via activation of A(2A) adenosine receptors.

Adenosine A2 Receptor Agonists↗
PubMed1986

Cholinergic influence on duodenal bicarbonate response to hydrochloric acid perfusion in the conscious rat.

Present information suggests that endogenous prostaglandins, hormonal factors, and neuropeptides participate in the regulation of duodenal bicarbonate secretion in response to luminal hydrochloric acid. The purpose of this study was to examine the effects of cholinergic antagonists and agonists on basal and acid-stimulated bicarbonate secretion in the proximal duodenum of the conscious rat. The basal bicarbonate secretion, 9 mumol X cm-1 X h-1, increased to 21 +/- 3 mumol X cm-1 X h-1 after 5 min of exposure to 150 mM HCl and remained significantly elevated for more than 3.5 h. The muscarinic blocker atropine, 0.5 mg X kg-1, reduced the acid-stimulated bicarbonate response by a third, and higher doses did not increase the inhibition. The ganglionic blocker hexamethonium, 10-20 mg X kg-1, suppressed in a dose-related manner the alkaline response by maximally one half. The opioid inhibitor naloxone was also an effective inhibitor. Hexamethonium, but not atropine, inhibited the basal duodenal bicarbonate secretion, which was unaffected by graded doses of the cholinergic agonists bethanechol and carbachol. We conclude that cholinergic nicotinic activity participates in maintaining basal duodenal bicarbonate secretion in the conscious rat. The bicarbonate response to luminal 150 mM HCl is partially dependent on cholinergic sites, but activation of such sites is not a single final step, since cholinergic agonists failed to elevate bicarbonate secretion from basal.

Animals↗
PubMed1997

Cholinergic modulation of electrogenic ion transport in different regions of the rat small intestine.

Acetylcholine acting via muscarinic receptors located in the intestinal mucosa controls ion and fluid transport. This study examined the pathway(s) by which cholinergic receptors mediate secretion in rat isolated duodenum, jejunum and ileum using the short-circuit current (Isc) as an index of electrogenic CL- secretion. Carbachol and bethanechol induced electrogenic CL- transport which was insensitive to the neural blocker tetrodotoxin, indicating their direct action on the enterocytes. Functional characterization of electrogenic secretion activated via muscarinic receptors on jejunal and ileal enterocytes was achieved by use of selective muscarinic antagonists in the presence of tetrodotoxin. In both regions the rank order of potency of these compounds (atropine > 4-diphenylacetoxy-N-piperidine methiodide (4-DAMP) > hexahydro-sila-difenidol (HHSiD) > pirenzepine > methoctramine) indicated the M3 receptor subtype. Secretion activated by the muscarinic agonist 4-[[(3-chlorophenyl)amino]carbonyl]-N,N, N-trimethyl-2-butyn-1-ammonium chloride (McN-A-343) was sensitive to tetrodotoxin and pirenzepine but not to the ganglionic blocker, hexamethonium, indicating the M1 receptor subtype on post ganglionic neurons. Regional differences for bethanechol-activated secretion showed an increasing gradient in secretory capacity (Isc max) in a proximal-to-distal direction along the small intestine. Responses to McN-A-343 also showed regional differences but these were unlike those of bethanechol. These results show that cholinomimetic-induced electrogenic CL- secretion in rat isolated small intestine appears to be mediated by two dissimilar populations of muscarinic receptor: M3 muscarinic receptors positioned on enterocytes and M1 muscarinic receptors sited on submucosal neurons.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMedDate not supplied

Role of cholinergic, vagal reflexes on the bronchoconstrictor responses to histamine during carbon dioxide inhalation in conscious guinea-pigs.

Histamine-induced bronchoconstriction in conscious guinea-pigs involves a cholinergic, bronchoconstrictor reflex, but the role of this reflex during elevated levels of inspired carbon dioxide is unknown. In this study we examined the role of cholinergic, vagal reflexes on the bronchoconstrictor responses to histamine during CO2 inhalation. Guinea-pigs were placed inside a whole body plethysmograph for measurement of tidal volume (VT), respiratory rate (f) and minute volume (V) and a head chamber was used to deliver a hypercapnic gas mixture (10% CO2, 21% O2, 69% N2) and for inhalation of aerosolized drugs. Inhalation of CO2 caused an increase in VT, f and V and these effects were reduced by exposure to aerosolized histamine (0.01-0.05% for 30 s). The histamine-induced reduction of VT was significantly (P less than 0.05) attenuated following a 60 s exposure to inhaled atropine (0.03 and 0.1%) as was the reduction of VT due to inhaled methacholine. Intravenous atropine (1 mg/kg) also blocked the VT reduction due to aerosolized histamine. Intravenous administration of the ganglionic blockers hexamethonium (1 mg/kg) and mecamylamine (10 mg/kg) did not inhibit the histamine-induced reduction of VT at doses of these drugs that revealed systemic evidence of ganglionic blockade, i.e. inhibition of vagally stimulated bronchoconstriction and bradycardia. The results demonstrate that the bronchoconstrictor responses to histamine during CO2 inhalation in guinea-pigs involves stimulation of airway cholinergic receptors, but this response does not involve ganglionic neurotransmission. It is speculated that histamine's bronchoconstrictor effects during CO2 breathing involves stimulation of postganglionic, parasympathetic nerves innervating airway smooth muscle.

Aerosols↗
PubMedDate not supplied

Differential cardiovascular effects of pharmacological agents in chickens selected for high and low body weight.

This study was conducted to investigate whether there are differences in the autonomic nervous system function of chickens from lines selected for high (HWS) or low body weight (LWS). The cardiovascular response to various pharmacological agents was used as an indicator of autonomic nervous system response. Ten individuals from each line and sex were used in the study. Catheters were introduced into the left brachial artery and vein and connected to a MP100-BIOPAC system to record blood pressure and heart rate (HR). Chickens were injected with phenylephrine, atropine, propranolol, and tetraethylammonium chloride (TEAC). The LWS birds exhibited a greater increase in mean arterial blood pressure (MABP) and a lesser increase in HR than the HWS birds following atropine. The response to atropine showed a line and sex interaction in which male birds had a greater increase in HR than females and LWS females had a lower increase in HR than the HWS females. Injection of phenylephrine following pretreatment with atropine caused a baroreceptor reflex in which males showed a greater decrease in HR than females. In response to the beta-adrenergic receptor blocker propranolol, females displayed a greater decrease in MABP than males and LWS birds had a greater decrease in HR than HWS birds. In response to the autonomic ganglionic blocker TEAC, MABP and HR decreased equally in both lines. The percentage of adrenal and sympathetic impact on regulation of HR showed that LWS females required greater adrenal activity than those from the other subclasses. Although changes in HR and MABP ratios in response to phenylephrine were different between lines, these responses were not different when phenylephrine was given following atropine. This pattern of response suggested that HWS birds had greater parasympathetic nervous system activity in order to maintain cardiovascular function. These results demonstrate that selection for HWS or LWS has resulted in greater parasympathetic and sympathetic nervous system tone in birds from the HWS and LWS birds, respectively, and suggest that differences between the lines could be at the level of the chromaffin tissue in the adrenal gland.

Animals↗
PubMed1991

Cholinoceptor blockers protect against ethanol-induced gastric mucosal damage in rats.

The role of the cholinergic nervous system in ethanol-induced gastric mucosal damage has been examined in rats. Oral administration of 50 or 80% ethanol produced haemorrhagic lesions which were reduced by atropine pretreatment (0.65, 2.5, 5 or 10 mg/kg injected i.p.); there was lesser protection against the higher dose of ethanol. Pirenzepine (a specific M1 receptor antagonist) pretreatment (0.1, 0.2, 1 or 2 mg/kg, injected s.c.) also protected against ethanol-induced gastric injury to a similar extent; it also increased the amount of adherent mucus on the glandular mucosa. This action may, therefore, account for the protective action of the ganglion blocker. It is concluded that ethanol may stimulate the stomach wall ganglionic nicotinic receptors to activate the postganglionic fibres and subsequently the muscarinic receptors which would then trigger off some of the ulcerogenic mechanisms in the stomach. However, ethanol could also produce gastric damage via the non-cholinergic mechanisms; this action becomes more prominent in gastric injury produced by high doses of ethanol.

Administration, Oral↗
PubMed1987

Role of sympathetic nervous system in hypotensive action of taurine in DOCA-salt rats.

We tested the hypothesis that the antihypertensive effects of dietary taurine supplementation in deoxycorticosterone acetate (DOCA)-salt rats may be attributed to the suppression of sympathetic nervous system activity. In uninephrectomized rats treated with DOCA while receiving 1% NaCl solution for 2 weeks, systolic blood pressure was significantly increased as compared with that in control rats treated with vehicle suspension and tap water. Sympathetic nervous system activity was assessed by tissue norepinephrine turnover, which was determined from the rate of decline of tissue norepinephrine concentration after the administration of alpha-methyl-p-tyrosine, a potent inhibitor of the rate-limiting step of catecholamine synthesis. Cardiac and splenic norepinephrine turnover during either normal conditions or cold exposure (4 degrees C, 8 hours) were markedly increased in DOCA-salt rats as compared with control rats. Also, DOCA-salt rats had increased depressor response to hexamethonium bromide, a ganglion blocker. In contrast, supplementation of 1% taurine in DOCA-salt rats attenuated the development of the hypertension associated with the normalization of both the increased depressor response to ganglionic blockade and the accelerated cardiac and splenic norepinephrine turnover during either normal conditions or cold exposure. Taurine supplementation in control rats, however, had no effect on blood pressure or norepinephrine turnover during cold exposure. These results suggest that taurine supplementation suppresses sympathetic overactivity in DOCA-salt rats, thus leading to inhibition of the development of hypertension.

Animals↗
PubMed1979

Neurogenic activity--angiotensin II interaction during the development and maintenance of renal hypertension in the rat.

1. Pentolinium tartrate (a ganglionic blocker) was injected in conscious rats during the early and late phases of two-kidney renal hypertension produced by aortic ligation. 2. In the early phase ( 5 days after aortic ligation), ganglionic blockade resulted in a decrease in blood pressure equal to that obtained in normotensive rats. Later, at days 12 and 40, for equally severe hypertension, ganglion blockade resulted in a greater decrease in blood pressure. 3. A 30 min infusion of [Sar1, Ala8]angiotensin II during the pentolinium-induced nadir in blood pressure resulted in a further decrease in blood pressure at day 5. Later, at days 12 and 40, this effect was smaller. 4. A 300 min infusion of [Sar1, Ala8]angiotensin II normalized the blood pressure in hypertensive rats at day 40. This delay response may be secondary to a central effect of the antagonist, reducing neurogenic tone or peripheral antagonism of locally generated angiotensin II in the blood vessel walls. 5. At day 40, removal of the small left kidney resulted in a greater decrease in blood pressure. This suggests the presence of a renal factor other than renin in the chronic phase of this hypertension.

Angiotensin II↗
PubMed1985

The effect of inhaled hexamethonium bromide and atropine sulphate on airway responsiveness to histamine.

The degree of protection against inhaled histamine achieved by inhalation of the ganglion blocker hexamethonium bromide plus placebo, hexamethonium plus atropine sulphate, and placebo plus placebo was examined in six atopic subjects, four of whom had current asthma. Hexamethonium was administered until there was systemic evidence of ganglionic blockade with a postural drop in blood pressure of 31 +/- 7.5 mm Hg (mean +/- SD) (p = 0.01) and an increase in heart rate of 30 +/- 3.1 bpm (mean +/- SD) (p = 0.01). Atropine was inhaled in a dose (18 mg nebulized during tidal breathing) known to produce systemic inhibition of cardiac and salivary cholinergic (muscarinic) receptors. The airway effects were measured by FEV1. Hexamethonium caused bronchoconstriction in all four subjects with asthma, which was reversed by atropine. The mean provocation concentration of histamine to provoke a 20% fall in FEV1 was 2.97 mg/ml after premedication with placebo, it was not different at 2.84 mg/ml after hexamethonium alone, and it increased slightly to 5.31 mg/ml after both hexamethonium and atropine (p = 0.06). The results suggest that the main effect of inhaled histamine is not by reflex bronchoconstriction but rather through stimulation of H1-receptors on airway smooth muscle. Therefore, histamine hyperresponsiveness in asthma is not primarily caused by a defect in the parasympathetic nervous supply to the airway.

Adult↗
PubMed1982

Cholinergic therapy of abnormal open-field behavior in thiamin-deficient rats.

Although thiamin deficiency is associated with impaired acetylcholine metabolism, the functional significance of the cholinergic lesion is controversial. Therefore, we tested the effect of cholinergic drugs on abnormal open-field behaviors in rats that were treated with a thiamin-deficient diet and thiamin antagonist. After only 1 day of treatment, staring increased significantly in rats given pyrithiamin, a centrally acting thiamine antagonist, but not in rats given oxythiamin, which acts only peripherally. Sniffing, resting and grooming were not altered by either treatment. The acetylcholinesterase inhibitor physostigmine was as effective as thiamin in decreasing staring in pyrithiamin-treated rats, but its peripherally acting analogue neostigmine had no effect. The central muscarinic blocker, atropine, blocked the effect of physostigmine. Methatropine, which acts only peripherally, did not. Arecoline, a direct muscarinic agonist, was as effective as physostigmine in decreasing staring. Nicotine had no effect, and the nicotinic ganglionic blocker mecamylamine did not block the effect of physostigmine. Increased staring behavior in pyrithiamin-treated rats appears to reflect an early central cholinergic muscarinic deficit.

Animals↗
PubMed1994

Organ-localized hypothalamic-stimulated vasculature changes in the cat.

Stimulation of specific lateral hypothalamic targets in a cat model induces vascular and/or cardiac changes. Evidence is presented that these may consist of discretely localized sympathetically mediated changes taking place in just one or two organs. Moreover, following stimulation of either one of two adjacent lateral hypothalamus sites, pressor effects are induced that superficially look similar, but prove to be mediated by different pathways. To investigate possible synapsing at sympathetic ganglia, e.g. in superior cervical or stellate ganglia, 50 micrograms atropine methyl nitrate, a ganglionic blocker, was applied directly to the ganglia. This was shown to potentiate the pressor effects, in some cases when applied to the superior cervical ganglia, in others to stellate ganglia, presumably by blockade of a ganglionic attenuating mechanism. The contributions made by different sympathetic nerves to the lateral hypothalamus-induced pressor effect were analysed. Stimulation of one of the lateral hypothalamus sites (TAR.I) in eight cats induced a pressor effect that was abolished by severing a nerve branch, from the superior cervical ganglia laterally, shown to innervate neck muscle vasculature. In another group of nine cats stimulation of TAR.II induced a pressor effect abolished by cutting a branch from the superior cervical ganglia medially, shown to be destined to the vasculature of pharyngeal muscles and possibly lower respiratory tract. The hypothesis that central control via the sympathetic nervous system is responsible for differential organ specific regulation of blood flow to individual organs is discussed.

Animals↗
PubMedDate not supplied

Hemodynamic, neural, and humoral mechanisms of aortic coarctation hypertension in the rat.

The present study was designed: (a) to examine the contribution of the renin-angiotensin system (RAS) to elevated regional vascular resistance during the onset of aortic coarctation hypertension, and (b) to determine the role of angiotensin II (Ang II)-neural interactions during the maintenance of high arterial pressure (AP). In the first study, rats were instrumented chronically with miniaturized pulsed Doppler flow probes on the right renal and superior mesenteric arteries 3 days prior to complete aortic ligation. After ligation, AP and renal and mesenteric vascular resistances increased significantly. In sham-ligated rats, small increases in AP and decreases in regional vascular resistances were observed. Captopril, administered 6 h postligation, reduced AP and regional vascular resistance in ligated rats to preligation levels, indicating that the RAS was responsible for these acute increases. In the second study, Ang II-neural interactions were examined by treating 12- to 14-day postligation hypertensive rats with captopril or with hexamethonium, a ganglionic blocker, followed by captopril. Depressor responses to captopril were also examined in aortic-ligated rats pretreated with hydralazine. Captopril alone and captopril after hydralazine caused similar reductions in AP (-26 +/- 2% and -27 +/- 1%, respectively). After ganglionic blockade, the depressor responses to captopril were attenuated (-13 +/- 2%). The marked differences in the efficacy of captopril to lower AP in the ganglionic-blocked group of rats suggested that the pressor actions of Ang II were mediated, in part, through indirect actions on the sympathetic nervous system.

Animals↗
PubMed1993

Nicotinic cholinergic influences in pancreatic secretion induced by intraduodenal alkaline and acid solutions in the rabbit.

1. The effect of hexamethonium on the exocrine pancreatic response to intraduodenal acidification and alkalinization, and the secretin and VIP release after these stimuli, was studied. 2. The hydroelectrolyte secretion after hydrochloric acid and sodium carbonate perfusion was reduced by hexamethonium treated (322 +/- 44% of maximum response in flow rate to sodium carbonate perfusion in untreated animals vs 140 +/- 12% in pretreated animals, and 252 +/- 19% of maximum response in flow rate to HCl in untreated animals vs 166 +/- 11% in pretreated animals). 3. However, hexamethonium has no effect on secretin plasma levels after either intraduodenal acidification or alkalinization. 4. On the contrary, the ganglion blocker significantly (P < 0.01) reduced plasma VIP levels in response to intraduodenal HCl (maximum response 320 +/- 74% in untreated vs 184 +/- 44% in hexamethonium-treated animals). 5. Plasma VIP levels showed a similar increase in both untreated (maximum response: 151 +/- 12%) and ganglion blocked animals (170 +/- 26%) in response to sodium carbonate. 6. These data suggest the existence of complex neural mechanisms in the exocrine pancreatic response to intraduodenal stimuli, these mechanisms being different depending on the intraduodenal stimulus.

Acids↗
PubMed1983

Mediation of nicotine-induced convulsions by central nicotinic receptors of the 'C6' type.

The nature of the central receptors mediating the convulsant actions of nicotine has been investigated. Clonic tonic convulsions were seen in mice following intracerebroventricular (i.c.v.) injection of nicotinic agonists. (-)Nicotine was the most potent agonist tested, with a CD50 of 7.9 X 10(-9) mol. (+)Nicotine, cytisine, DMPP and lobeline were 10-100 times less potent than (-)nicotine. Nicotine induced convulsions were antagonized by ganglion blocking drugs administered intraventricularly. Pentolinium was the most potent antagonist, with an ED50 of 4 X 10(-11) mol. The ganglion-blockers also produced convulsions in their own right at doses 80-1000 times the anti-nicotine ED50 dose. 'C10' blockers, such as d-tubocurarine, did not antagonize nicotine-convulsions, but produced convulsions in their own right. alpha-Bungarotoxin had neither convulsant nor anticonvulsant activity at the doses tested. It is concluded that the central receptors mediating this nicotinic effect resemble ganglionic ('C6') receptors, rather than neuromuscular ('C10') receptors.

Animals↗
PubMed1989

Effects of vasodilator drugs on venous tone in conscious rats.

The dose-response effects of vasodilator drugs, nitroglycerin, sodium nitroprusside and hydralazine, on mean arterial pressure (MAP) and mean circulatory filling pressure (MCFP), an index of body venous tone, were investigated in conscious, unrestrained, intact rats as well as in rats treated with the ganglionic blocker, hexamethonium. The effects of these drugs were compared with those of the vehicle, normal saline, in control rats. In intact rats, i.v. infusion of nitroglycerin did not alter MAP while i.v. infusions of nitroprusside or hydralazine caused dose-dependent decreases in MAP. After ganglionic blockade, all three drugs decreased MAP. In intact rats, nitroglycerin and sodium nitroprusside did not affect MCFP but hydralazine increased MCFP. After treatment with hexamethonium, all three drugs decreased MCFP. The decreases in MCFP caused by nitroglycerin and nitroprusside, but not that by hydralazine, were significantly greater than the corresponding changes in control rats. Thus, in intact rats, the direct venodilator actions of nitroprusside and nitroglycerin were masked by endogenous sympathetic tone. When sympathetic nerve activity was attenuated, both nitroprusside and nitroglycerin have venodilator effects. Hydralazine, on the other hand, had insignificant venodilator effect both in the presence and absence of sympathetic reflexes.

Animals↗
PubMed1987

Effect of ganglion blockade on cerebrospinal fluid norepinephrine.

The source of norepinephrine (NE) in CSF has been unclear. It has been suggested that CSF NE indicates central neural noradrenergic tone and is determined differently from plasma NE. If CSF NE depended specifically on NE release in the CNS, then interference with ganglionic neurotransmission would be expected to decrease plasma NE but not CSF NE. Hypotension caused by ganglionic blockade might be expected to increase CSF NE reflexively. We infused the ganglion blocker, trimethaphan, intravenously into anesthetized dogs and measured the effects on mean arterial blood pressure (MAP) and on cisterna magna CSF levels of NE. The results were compared with those obtained on administration of saline, clonidine (2 micrograms/kg), yohimbine (0.25 mg/kg), or nitroprusside and with those obtained when hypotension during ganglion blockade was prevented by concurrent treatment with phenylephrine. Trimethaphan decreased MAP by 40%, arterial NE by 64%, and CSF NE by 61%. Nitroprusside administered intravenously to produce the same 40% depressor response increased arterial NE by 612% and CSF NE by 155%. Prevention of ganglion blockade-induced hypotension using phenylephrine did not prevent the decrease in CSF NE caused by trimethaphan, and when phenylephrine was discontinued, the resulting hypotension was not associated with increases in CSF NE. The similar decreases in plasma NE and CSF NE during ganglionic blockade, and the abolition of reflexive increases in CSF NE during hypotension in ganglion-blocked subjects, cast doubt on the hypothesis that CSF NE indicates central noradrenergic tone and are consistent instead with at least partial derivation of CSF NE from postganglionic sympathetic nerve endings.

Animals↗
PubMed1986

Capsaicin stimulates mucociliary activity by releasing substance P and acetylcholine.

Intraarterial injection of the neuropeptide substance P (SP) accelerates mucociliary (MC) activity. The physiological significance of this finding was investigated using capsaicin, which is known to release SP from unmyelinated C-fibers in sensory nerves. Capsaicin (3.0-150.0 micrograms/kg) stimulated MC activity in the rabbit maxillary sinus in vivo, recorded with a photoelectric technique. This effect was resistant to pretreatment with the adrenergic blocker guanethidine, and to a combination of propranolol and phentolamine. Pretreatment with an SP antagonist (D-Pro2, D-Trp7,9)SP totally inhibited the effect of capsaicin. The muscarinic antagonist atropine suppressed the initial phase of the response to capsaicin, whereas the response was uniformly suppressed by the ganglionic blocker hexamethonium. These results suggest that capsaicin activates a reflex, via afferent C-fibers containing SP and efferent parasympathetic cholinergic neurons. The final response of the MC system reflects the local release of both SP and acetylcholine.

Acetylcholine↗