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PubMedDate not supplied

Attenuation by captopril of pressor responses to peripheral sympathetic nerve stimulation in rats is abolished after bilateral nephrectomy and during mineralocorticoid hypertension.

Intravenous administration of captopril (0.1-0.3 mg/kg) to normotensive pithed rats, with or without unilateral nephrectomy, was followed by a sustained fall in arterial blood pressure. Concomitantly pressor responses to electrical stimulation of the spinal sympathetic outflow (T11-L3), ganglion stimulation with McNeil-A-343 (4-(m-chlorophenylcarbamoyloxy)-2-butynyl-trimethylammonium chloride) or intravenous injection of noradrenaline were reduced. Attenuation by captopril (1 mg/kg) of pressor responses to McNeil-A-343 persisted after intravenous propranolol (1 mg/kg). Tachycardia caused by electrical stimulation of the spinal sympathetic nerves (C7-T2) was unchanged after 3.0 mg/kg captopril. After procedures reducing the activity of the renin angiotensin system, bilateral nephrectomy or induction of mineralocorticoid hypertension by unilateral nephrectomy and administration of desoxycorticosterone acetate, pressor responses to McNeil-A-343 or noradrenaline were unchanged after 1 mg/kg captopril. It is concluded that in the pithed rat, basal arterial blood pressure and the height of pressor responses to either postganglionic sympathetic nerve activation or intravenous noradrenaline depend on converting enzyme activity maintaining circulating angiotensin II levels.

Animals↗
PubMed1980

Left stellate stimulation: regional myocardial flows and ischemic injury in dogs.

The effects of left stellate ganglion stimulation (LSGS) on regional myocardial blood flow (RMBF) and epicardial S-T segment were investigated in the normal and ischemic myocardium of anesthetized dogs. In nonischemic myocardium LSGS decreased calculated coronary resistance, increased RMBF, and reduced the endocardial-to-epicardial (endo-to-epi) ratio. These effects were reversed after atenolol (1 mg/kg) and abolished after combined atenolol and phenoxybenzamine (3 mg/kg) treatments. In ischemic myocardium LSGS did not change RMBF but increased S-T segment. However, after atenolol, LSGS increased ischemic RMBF and the ischemic-to-nonischemic areas flow ratio (reverse coronary steal phenomenon), these effects being abolished by phenoxybenzamine. We conclude that 1) LSGS increases RMBF and decreases endo-to-epi ratio in nonischemic areas by beta 1-adrenergic stimulation through metabolic autoregulation, 2)beta 1-adrenergic blockade in nonischemic areas unmasks alpha-adrenergic vasoconstriction inducing a redistribution of flow towards ischemic areas, and 3) further elevation of S-T segment by LSGS is due to oxygen requirements enhancement by beta 1-adrenoceptors stimulation.

Animals↗
PubMed1985

Permissive role of spinal alpha 1-adrenoceptors in sudomotor efferents.

The electrodermal potential (EDP) recorded in the forepaws of anaesthetized cats in response to stimulation of the cholinergic-sympathetic nervous system at different levels was taken as a measure for sudomotor activity. Electrical stimulation of the hypothalamus with square wave pulses (1 ms duration, 0.5-64 Hz, 2 s train length) at intervals of 1 min induced rate-dependent EDPs which were inhibited at all rates of stimulation by intravenous (i.v.) injection of doses less than 40 micrograms/kg of the alpha 1-adrenoceptor blocking drug prazosin. However, prazosin (50-500 micrograms/kg i.v.) did not impair EDPs induced by preganglionic stimulation (0.5-64 Hz) or by injection of the nicotinic ganglion stimulant DMPP (50 micrograms/kg i.v.). Prazosin (50 micrograms/kg i.v.) inhibited EDPs induced by unilateral electrical stimulation (square wave pulses, 1 ms duration, 16 Hz, 2 s train length, 1 min intervals) of the spinal cord at C 1 in cats with an axotomy at the level of the medulla oblongata, thus indicating a spinal site of prazosin action and suggesting a permissive role of spinal catecholamines by activation of alpha 1-adrenoceptors. In spinal preparations pretreated with 250 micrograms/kg yohimbine i.v. to block inhibition by alpha 2-adrenoceptors of catecholamine reuptake, cocaine 2.5 mg/kg i.v. potentiated EDPs induced by spinal stimulation with 8 Hz. This effect could be antagonized by 50 micrograms/kg prazosin or 1000 micrograms/kg corynanthine i.v. In spinal preparations pretreatment with 5 mg/kg reserpine i.p. for depletion of catecholamines and 250 micrograms/kg yohimbine i.v., EDPs (16 Hz) were smaller than in undepleted preparations. Under these conditions injection of 100 micrograms/kg clonidine i.v. caused amplification of EDPs. This effect was antagonized by 50 micrograms/kg prazosin i.v. After i.v. pretreatment with 250 micrograms/kg yohimbine the i.v. injection of 2.5 mg/kg cocaine also potentiated EDPs which were induced by hypothalamic stimulation in intact cats. The results indicate that catecholaminergic neurons influence sudomotor activity by interaction with efferents of the cholinergic-sympathetic nervous system at the level of the spinal cord. Catecholamines seem to facilitate impulse transmission in non-catecholaminergic synapses by activation of alpha 1-adrenoceptors.

Animals↗
PubMed1996

Neuropeptide Y Y2 receptor-mediated attenuation of neurogenic plasma extravasation acting through pertussis toxin-sensitive mechanisms.

1. The effects of neuropeptide Y (NPY) receptor agonists (administered intravenously) were examined on plasma protein ([125I]-bovine serum albumin) leakage within dura mater evoked by unilateral trigeminal ganglion stimulation (0.6 mA, 5 ms, 5 Hz, 5 min), capsaicin (1 mumol kg-1, i.v.) or substance P (1 nmol kg-1, i.v.) in anaesthetized Sprague-Dawley rats. 2. NPY (EC50: 5.6 nmol kg-1) and NPY fragment 13-36 [NPY (13-36)] (ED50: 4.3 nmol kg-1), an NPY Y2 receptor agonist, dose-dependently attenuated [125I]-bovine serum albumin extravasation from meningeal vessels when administered 10 min prior to electrical stimulation. [Leu31, Pro34]-NPY, an NPY Y1 and Y3 receptor agonist, inhibited the response at a higher dose only (23 nmol kg-1) (P < 0.05). 3. NPY also significantly decreased plasma protein extravasation induced by capsaicin (1 mumol kg-1) but not by substance P (1 nmol kg-1). 4. Pertussis toxin (20 micrograms kg-1, administered intracisternally 48 h prior to stimulation) blocked completely the inhibitory effect of NPY and NPY (13-36) but did not inhibit extravasation alone. 5. We conclude that NPY inhibits neurogenically-mediated plasma protein extravasation acting through presynaptic pertussis toxin-sensitive NPY Y2 receptors, possibly by inhibition of neuropeptide release from perivascular trigeminovascular afferents.

Animals↗
PubMed1983

Physiological and pharmacological response of canine bronchial smooth muscle in situ.

We studied the isometric response of bronchial smooth muscle in a single third-order bronchus of 24 dogs in situ. Length-tension studies were performed in six dogs by repeated injection of 10(-5) mol acetylcholine (ACh) into the right bronchoesophageal artery, and the resting tension (30.6 +/- 6.9 g/cm) and length (0.76 +/- 0.14 cm) permitting maximal contraction were determined. In eight other dogs, dose-related bronchial contraction was obtained with 10(-10) to 10(-5) mol intra-arterial (ia) ACh. Supramaximal electrical stimulation of the right cervical vagus nerve and bronchial parasympathetic ganglion stimulation with ia 1-1-dimethyl-4-phenylpiperazinium (DMPP) also caused bronchial contraction. The maximal response to ia ACh (28.5 +/- 1.7 g/cm), supramaximal electrical stimulation (15.2 +/- 1.1 g/cm), and ia DMPP (10.5 +/- 3.0 g/cm) was blocked by an ia dose of atropine (1-5 micrograms/kg) that did not alter the sympathetic relaxation response in the trachea. In four dogs, the bronchial response to sympathetic activation was studied by intravenous (iv) bolus injection of DMPP after cholinergic blockade with atropine. DMPP (25 micrograms/kg iv) caused 9.5 +/- 2.2 g/cm bronchial relaxation, which was blocked completely by 2-4 mg/kg iv propranolol. In six other dogs, hypoxia induced by ventilation with pure nitrogen caused bronchial contraction, which was blocked by vagotomy, atropine, and hexamethonium. We report a sensitive method for selective measurement of bronchial smooth muscle response in a single resistance bronchus. This preparation preserves regional innervation and circulation and permits selective physiological stimulation in situ.

Acetylcholine↗
PubMed1997

[Control of blood flow in nasal mucosa by electro-stimulation of sphenopalatine ganglion].

The effects of control of blood flow on cat nasal mucosa by stimulating sphenopalatine ganglion (SPG) were studied using laser Doppler flowmetry in order to investigate the role of SPG. The study showed that the stimulation on one side of SPG could induce vasodilation, with increased blood flow, as well as protective reflexes on both sides. The reactivity depended on the stimulation intensity, frequency and duration. The stimulation on one side of postganglionic parasympathetic nerves, in which the stellate ganglion was resected, caused vasodilation only ipsilaterally. The results indicated that the vasodilation induced by stimulating SPG might be mediated via central reflex arc. The "reverse blood regulation" phenomenon was observed during stimulation of SPG as well. The mechanisms of "reverse blood regulation" induced by stimulating SPG need further investigation.

Animals↗
PubMed1988

Reflex effects evoked by stimulation of hypoglossal afferent fibers.

In pentobarbitone-anesthetized cats, electrical stimulation of the central ends of the main trunks of transected hypoglossal nerves evoked vascular (pressor or depressor) reactions, mydriasis, slow and deep breathing, and reflex activation of laryngeal and facial muscles. Stimulation of the central end of the transected ramus descendens hypoglossi also provoked reflex contraction of cricothyroideus. These reflexes may be elicited also after intracranial section of hypoglossal nerve roots, but not after intracranial section of ipsilateral vagal roots. The above reflexes were abolished by acute section of the ipsilateral hypoglossonodosal branch, but they may be reproduced by electrical stimulation of the central end of this anastomotic branch between hypoglossal nerve and nodose ganglion. Stimulation of the central end of one transected hypoglossus evoked reflex efferent discharges in contralateral hypoglossus and contraction of contralateral tongue muscles. Stimulation of the central end of one transected hypoglossal end-branch inhibited efferent discharges in another end-branch. The crossed hypoglossohypoglossal reflex and the ipsilateral reflex inhibition were abolished by section of the hypoglossonodosal branch or vagal roots at the stimulated side. We conclude that reflexes evoked by stimulation of peripheral hypoglossal nerve in cats are mediated by afferent fibers directed to the nodose ganglion and entering the brain stem via vagal roots.

Afferent Pathways↗
PubMed1979

Altered adrenergic activity in coronary arterial spasm: insight into mechanism based on study of coronary hemodynamics and the electrocardiogram.

To elucidate the pathophysiologic mechanism of coronary arterial spasm, the hypothesis was examined that underlying alterations in sympathetic activity may account for this syndrome in some patients. Observations were directed to alterations in coronary arterial hemodynamics and the electrocardiogram. Spasm of the left anterior descending coronary artery produced a mean increase in coronary vascular resistance of 107 percent (P less than 0.05) in four patients in whom coronary sinus blood flow was measured with the thermodilution technique. The alpha adrenergic blocking agent phentolamine, given intravenously, acutely reversed coronary spasm and its clinical manifestations in eight patients and reduced coronary resistance. In four patients, administration of the long-acting oral alpha blocking agent phenoxybenzamine (20 to 80 mg/day) caused disappearance of symptoms during a follow-up period of 3 to 12 months. Transient prolongation of the corrected Q-T interval preceded spontaneous or ergonovine maleate-provoked coronary spasm in 11 patients with variant angina pectoris, whereas no significant change in the Q-T interval followed ergonovine administration in 27 control patients with atypical chest pain who did not have coronary spasm. T wave inversions in the resting electrocardiogram were normalized by isoproterenol infusion in one patient and by long-term phenoxybenzamine treatment in four patients with variant angina pectoris. These Q-T and T wave changes are analogous to those described with unilateral or asymmetric stellate ganglion stimulation in animals. These observations suggest that alterations in the sympathetic nervous system that are consistent with asymmetric stellate ganglion activity and transient alpha adrenergic receptor stimulation can presage the development of coronary arterial spasm in some patients with variant angina pectoris.

Adult↗
PubMed1983

Differential role of M-1 and M-2 receptors in sympathetic ganglia of the pithed normotensive rat in alpha adrenoceptor-mediated vasoconstriction.

In the pithed normotensive rat the adrenoceptors involved in the hypertensive and tachycardic effects of the muscarinic ganglionic stimulants 1,1-dimethyl-4-carboxypiperidine methylester (DMCPM) and (4-m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium (McN-A-343) were analyzed. The selective alpha-1 adrenoceptor antagonist prazosin, the selective alpha-2 adrenoceptor antagonist rauwolscine, the selective beta-1 adrenoceptor antagonist atenolol and the selective beta-2 adrenoceptor antagonist ICI 118,551 were used as tools for the identification of the adrenoceptors. DMCPM elicited a release of catecholamines which activated vascular alpha-1, alpha-2 and cardiac beta-1 adrenoceptors. McN-A-343, however, was induced by a release of neurotransmitter stimulation of predominantly vascular alpha-1 and cardiac beta-1 adrenoceptors. Both DMCPM and McN-A-343 were characterized with respect to their ability to stimulate muscarinic-1 (M-1) and/or muscarinic-2 (M-2) receptors. To demonstrate the M-1 component the selective M-1 receptor antagonist pirenzepine was used. M-2 receptor activation was identified by means of the muscarinic receptor-induced bradycardia after pretreatment with a high dose of atenolol. DMCPM proved to be a mixed M-1/M-2 agonist, in contrast to McN-A-343 which behaved as a rather selective M-1 agonist. The data led us to formulate the hypothesis that the activation of ganglionic M-1 receptors elicits the stimulation of predominantly alpha-1 adrenoceptors in the vascular wall. Activation of ganglionic M-2 receptors may induce an additional stimulation of vascular alpha-2 adrenoceptors. The increase in heart rate seems to be mediated by beta-1 adrenoceptors only.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1979

Autonomic block, cardiovascular depression and histamine release produced by polymyxin B in the cat.

The present study quantifies the autonomic block, the cardiovascular depression and the histamine releasing effects of polymyxin B in nine anaesthetized cats. The dose requirements for 50 per cent depression of the mean arterial blood pressure, the bradycardiac response to vagal stimulation, and the contraction of the nictitating membrane elicited by pre-ganglionic and post-ganglionic stimulation of the cervical sympathetic trunk have a narrow range of scatter, being of the order of 6--12 mg.kg-1 of the polymycin B base. The neuromuscular blocking dose (ED50), previously determined and hereby confired, also falls in the same range. Bradycardia and possibly histamine release are also observable. The relatively unremarkable effect of polymyxin B on the heart rate can be attributed to the balance between the vagal, sympathetic and ganglionic blocks, as well as the possible histamine release. All effects are long-lasting. Thus lack of tissue specificity makes it implausible to explain the neuromuscular and the cardiovascular effects of polymyxin B solely by the cholinergic mechanism of action. Ganglionic block and histamine release do not completely explain hypotension induced by polymyxin B. We propose that all biological effects of polymyxin B derive from a common mechanism of action, which may be its antimembrane antibacterial action. We would like to alert anaesthetists to the possiblity that polymyxin B may cause severe multiple organ system depression, in addition to neuromuscular block.

Animals↗
PubMed1963

THE EFFECTS OF NEOSTIGMINE UPON GANGLION RESPONSES AFTER ADMINISTRATION OF BLOCKING DRUGS.

The effects of block of autonomic ganglia by chlorisondamine and by hexamethonium, the administration of neostigmine and of atropine upon blood pressure, nervous transmission through the superior cervical ganglion, stimulation of autonomic ganglia by dimethylphenylpiperazinium, and the carotid occlusion reflex, have been studied in the dog anaesthetized with sodium pentobarbitone. The results of these studies have shown: (1) A ganglion blocking agent blocks synaptic transmission in the superior cervical ganglion at the same time as it lowers blood pressure. Neostigmine administered after ganglion-block raises the blood pressure without much change in the response to stimulation of the preganglionic cervical sympathetic nerve. (2) If the effects of preganglionic nerve stimulation are recorded as a contraction of the nictitating membrane, a ganglion-blocking agent also abolishes this response at the same time as it blocks the reflex rise in blood pressure produced by occlusion of both common carotid arteries. Neostigmine administered under these conditions does not affect the responses of the nictitating membrane, but restores the carotid occlusion reflex. This restoration of reflex activity is sensitive to atropine, as is the blood pressure rise. (3) At the same time that neostigmine restores the carotid occlusion reflex, there is no restoration of sensitivity of autonomic ganglia to chemical stimulation by dimethylphenylpiperazinium. In these animals atropine not only blocked the restored carotid occlusion reflex, but produced a further inhibition of the pressor response to dimethylphenylpiperazinium. It is concluded that neostigmine may raise blood pressure by partially restoring autonomic ganglionic transmission, but that total ganglionic function is not restored.

Animals↗
PubMed1984

Cardiac vagolytic action of some neuromuscular blockers.

Cardiac vagolytic effect of four commonly used neuromuscular blockers, (viz. D-tubocurarine, decamethonium, pancuronium and gallamine) was compared in midcollicular decerebrate rats. The intravenous doses of neuromuscular blockers used (d-tubocurarine: 0.1 mg/kg; decamethonium: 2 mg/kg; pancuronium: 0.1 mg/kg; gallamine: 20 mg/kg) were sufficient to produce the paralysis of respiratory muscles. Bradycardia was induced by electrical stimulation of the vagus or by injecting dimethyl-phenyl-piperazinium (DMPP; a ganglionic stimulant). It was observed that d-tubocurarine and decamethonium were devoid of cardiac vagolytic action. On the other hand, pancuronium and gallamine inhibited significantly the bradycardia induced by electrical stimulation of the vagus or injection of DMPP; gallamine was found to have greater vagolytic action. The pressor responses to DMPP were not attenuated by pancuronium and gallamine indicating that in the dose administered, these agents did not block the ganglia. Bradycardia induced by the administration of acetylcholine in the left atrium was also attenuated by pancuronium and gallamine suggesting that the drugs produce cardiac vagolytic action by acting on the post-synaptic cholinergic receptors of the heart.

Acetylcholine↗
PubMed1983

Attenuation by captopril of pressor responses to sympathetic stimuli: effects of procedures reducing activity of the renin-angiotensin system.

Low doses (0.1-1.0 mg/kg) of the converting enzyme inhibitor captopril given intravenously to pithed rats were followed by long lasting falls in systolic and diastolic arterial blood pressures. Concomitantly pressor responses were reduced to either electrical stimulation of the thoraco-lumbar sympathetic outflow or intravenous injection of the ganglion stimulant McNeil-A-343. Positive chronotropic responses of the heart to cardiac nerve stimulation were unchanged after relatively large doses of the drug (3.0 mg/kg). The reductions in arterial blood pressure and pressor responses to McNeil-A-343 caused by captopril persisted following beta-adrenoreceptor blockade, renal sympathectomy or unilateral nephrectomy, but did not occur after acute bilateral nephrectomy nor during sodium and water retention due to unilateral nephrectomy plus subacute administration of desoxycorticosterone and saline. Pressor responses to noradrenaline were reduced after 1.0 mg/kg captopril i.v. whereas those to methoxamine or vasopressin were unaltered after 5.0 mg/kg. It is concluded that in the rat, after elimination of sympathetic tone by pithing, the level of the arterial blood pressure and the magnitude of pressor responses to peripheral sympathetic nerve activation depend on the basal activity of the renin-angiotensin system. This maintains sufficient angiotensin II production to ensure retention of some tone in resistance vessels together with presynaptic augmentation of noradrenaline output at a sympathetic postganglionic nerve endings. The latter effects are abolished after converting enzyme inhibition with captopril, consequent to reduced tissue levels of angiotensin II and perhaps potentiation of the actions of bradykinin.

Animals↗
PubMed1977

Relaxations mediated by adrenergic and non-adrenergic nerves in human isolated taenia coli.

In human taenia coli electrical field stimulation after cholinergic blockade excited mainly non-adrenergic inhibitory nerves. Adrenergic relaxations during stimulation were demonstrated only with short electrical pulses at high frequencies or with ganglion stimulants. Reduction by tetrodotoxin of relaxations to indirectly acting sympathomimetics supports the histochemical finding that colonic adrenergic nerves are mainly preganglionic, and possibly synapse with non-adrenergic inhibitory nerves. When the latter undergo direct maximal stimulation, responses to adrenergic nerve excitation are masked.

Adenosine Triphosphate↗
PubMed1973

The spinal origin of the motor and inhibitory innervation of the rat anococcygeus muscles.

1. A preparation is described whereby the responses of the two anococcygeus muscles can be recorded in vivo in the pithed rat and the autonomic outflows to the muscle selectively stimulated in the spinal canal.2. Motor responses are obtained from stimulation at two levels; an upper extending from T 11 to L 3 and a lower from L 6 to S 2. Stimulation between these levels, i.e. between L 3 and L 6, produces no response. The response to stimulation at both upper and lower levels is abolished by phentolamine. The response to stimulation in the upper region is abolished by hexamethonium and is, therefore, presumably preganglionic; the response to stimulation at the lower level is resistant to hexamethonium and presumably post-ganglionic. Stimulation at levels above T 11 causes contraction after a delay, by liberating catecholamines from the adrenal medulla. This effect is blocked by both phentolamine and hexamethonium.3. If the adrenergic motor nerves are blocked and the muscle tone raised by a combination of guanethidine and tyramine, stimulation between L 5 and S 2 produces inhibition. The inhibitory outflow, therefore, overlaps the motor outflow but extends one segment more rostral (L 5). Stimulation restricted to this L 5 segment even in the presence of a normal unblocked motor innervation causes inhibition. The inhibitory response is blocked by hexamethonium or mecamylamine but desensitization and ;escape' occurs. This desensitization is less than that observed in the vas deferens when its motor nerves are similarly stimulated in the spinal cord.4. It is concluded that inhibitory fibres to the anococcygeus arise in the spinal cord and are organized in the pattern of the autonomic nervous system with a peripheral synapse. The site of origin of these inhibitory fibres is different from the motor adrenergic fibres to the muscle.

Anal Canal↗
PubMedDate not supplied

Immunocytes modulate ganglionic nitric oxide release which later affects their activity level.

Pedal ganglia excised and maintained in culture for up to 2 h, release NO at low levels. The range can vary between 0 to 1.1 nM. Non-stimulated immunocytes do not significantly stimulate ganglionic NO release when incubated with pedal ganglia. However, ganglia exposed to immunocytes that had been previously activated by a 30 min incubation with interleukin 1 beta, release NO significantly above basal levels. In these experiments, 91 +/- 2.5% of the non-stimulated immunocytes exhibited form factors in the 0.72 to 0.89 range (sampled prior to ganglionic addition), whereas 62 +/- 10.3% of the interleukin 1 beta stimulated immunocytes had form factors in the 0.39 to 0.49 range, demonstrating activation. Addition of the nitric oxide synthase inhibitor, L-NAME (10(-4) M), inhibited basal ganglionic NO release as well as that initiated by exposing the ganglia to activated immunocytes. Interestingly, non activated immunocytes, following ganglionic exposure, exhibited activity levels in the 13% range, representing a non significant increase. Cells exposed to interleukin 1 beta had a 65% activity level at the beginning of the experiment, followed by a drop of activity to 19 +/- 3.2% after ganglionic exposure. Repeating this last observation in the presence of L-NAME (10(-4) M), brought the activity level of the immunocytes back to the pre-ganglionic exposure level of activity, demonstrating that ganglionic NO was involved in down regulating immunocyte activity.

Animals↗
PubMed1978

Sensitization by caerulein of guinea-pig ileum to contractions by acetylcholine, histamine, 5-hydroxytryptamine and nicotine.

Low concentrations (0.63 and 1.25 ng/ml) of caerulein increase the submaximal contractions of the guinea-pig isolated ileum induced by several agonists and electrical stimulation. These effects of the polypeptide are due partly to neuronal pathways (i.e., a ganglionic stimulation) and partly to a non specific muscular sensitization. At higher concentrations of caerulein the effects of all the agonists were decreased. This seems related to the contractile effect of the peptide itself on the longitudinal muscle which interfers non specifically with the development of contractions induced by any other agonist.

Acetylcholine↗