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PubMed2003

Neuroeffector mechanisms involved in the regulation of dog splenic arterial tone.

It has been recognized that sympathetic neurons release several transmitters but mainly adenosine 5'-triphosphate (ATP), noradrenaline, and neuropeptide Y (NPY). Recently, we reported that periarterial nerve electrical stimulation (PNS) produced biphasic vasoconstrictions consisting of an initial transient, predominantly P2X-purinoceptor-mediated constriction followed by a prolonged, alpha(1)-adrenoceptor-mediated one in canine isolated splenic arteries. In this article, we tried to analyze the effects of several selective key drugs that influence the PNS-induced responses, and we functionally showed sympathetic transmitter releasing mechanisms by pharmacological analysis using purinergic, adrenergic, and NPYergic agonists and antagonists.

Animals↗
PubMed1986

Low-sodium resistant non-adrenergic inhibitory neurotransmission in the guinea-pig duodenum.

The evoked inhibitory potentials (i.p.s) in the longitudinal smooth muscle cells of the guinea-pig duodenum were recorded intracellularly. The i.p.s were not blocked by adrenergic blocking agents, guanethidine (10(-6) g/ml), propranolol (10(-6) g/ml) and phentolamine (10(-6) g/ml), and atropine (10(-6) g/ml). Tetrodotoxin (10(-7)-10(-6) g/ml) abolished the non-adrenergic non-cholinergic i.p.s evoked by single or repeated stimulation without changes in the resting membrane potential of the longitudinal smooth muscle. In the presence of atropine (10(-6) g/ml), acetylcholine (5 X 10(-9)-7 X 10(-7) g/ml) had no effect on the amplitude of the i.p.s d-tubocurarine (2 X 10(-5) g/ml) reduced the amplitude of the i.p.s and produced a small depolarization in the muscle membrane. The longitudinal muscle membrane was slightly depolarized by Li-solution and the i.p.s could be evoked in the Li-solution for a long period, accompanying with the slight decrease in the amplitude of the i.p.s. In the choline-solution, the depolarization of the muscle membrane and the slight increase in the amplitude of the i.p.s were obtained. The i.p.s were abolished in the Ca2+-free choline-solution. In the sucrose-solution, the decrease of the resting membrane potential of the longitudinal smooth muscle was observed and the amplitude of the i.p.s was gradually reduced during the perfusion of the sucrose-solution. Chloride deficiency had no considerable effect on the amplitude of i.p.s. The results obtained suggest that the non-adrenergic non-cholinergic inhibitory neurotransmission is low-sodium resistant and the excitation-secretion coupling in the non-adrenergic non-cholinergic inhibitory nerves is mainly dependent on the external calcium ions but not sodium ions.

Acetylcholine↗
PubMed1992

Axo-somatic contacts in the postnatal developing white rat spiral ganglion.

Development of the spiral ganglion in white rats was followed during the first 2 weeks after birth and morphological characteristics of the two neuronal types (I and II) were examined. In some neurons different stages of partial degeneration leading to formation of residual bodies were found without observation of degenerated cell, supporting the idea that differentiation at this time is not associated with cell death. Contacts between cell body of type II neurons and neuronal endings is reported for the first time. Such axo-somatic contacts previously observed only in monkey and man, also exists in lower mammals.

Animals↗
PubMed1980

Physiology of the urinary bladder and urethra.

Activation of the parasympathetic pathways to the detrusor muscle and inhibition of somatic input to the external urethral sphincter are the essential neuronal events initiating release of urine. The former occurs via a spinobulbospinal pathway, whereas the latter is produced by inhibitory mechanisms in the sacral spinal cord. The sympathetic outflow to the urinary tract promotes urine storage by increasing urethral resistance and depressing detrusor contractions. Sympathetic activity is generated at least in part by a spinal vesicosympathetic reflex pathway. Evidence indicates that the integration of sympathetic and parasympathetic inputs to the bladder can occur at the level of the peripheral autonomic ganglion as well as at levels of the effector organ. The existence of facilitatory and adrenergic inhibitory mechanisms in ganglia and the identification of spontaneously active ganglion cells raise the possibility that vesical ganglia may have a role in modulating or "filtering" the efferent neural input to the bladder.

Animals↗
PubMed2001

Effects of cannabinoids on sympathetic and parasympathetic neuroeffector transmission in the rabbit heart.

Cannabinoids elicit marked cardiovascular responses. It is not clear how peripheral effects on the autonomic nervous system contribute to these responses. The aim of the present study was to characterize the peripheral actions of cannabinoids on the autonomic innervation of the heart. Experiments were carried out on pithed rabbits. In the first series of experiments, postganglionic sympathetic cardioaccelerator fibers were stimulated electrically. The synthetic cannabinoid receptor agonists WIN55212-2 (0.005, 0.05, 0.5, and 1.5 mg kg(-1) i.v.) and CP55940 (0.003, 0.03, 0.3, and 1 mg kg(-1) i.v.) dose dependently inhibited the electrically evoked cardioacceleration. The inhibition by WIN55212-2 (0.5 mg kg(-1) i.v.) was prevented by the CB(1) cannabinoid receptor antagonist SR141716A (0.5 mg kg(-1) i.v.). WIN55212-2 (0.5 mg kg(-1) i.v.) did not change the increase in heart rate evoked by injection of isoprenaline. In the second series of experiments, preganglionic vagal fibers were stimulated electrically. WIN55212-2 (0.005, 0.05, and 0.5 mg kg(-1) i.v.) and CP55940 (0.003, 0.03, and 0.3 mg kg(-1) i.v.) dose dependently inhibited the stimulation-evoked decrease in heart rate. The inhibition produced by WIN55212-2 (0.005, 0.05, and 0.5 mg kg(-1) i.v.) was antagonized by SR141716A (0.5 mg kg(-1) i.v.). The results indicate that cannabinoids, by activating CB(1) cannabinoid receptors, inhibit sympathetic and vagal neuroeffector transmission in the heart. The mechanism of the sympathoinhibition is probably presynaptic inhibition of noradrenaline release from postganglionic sympathetic neurons. The mechanism of the inhibition of vagal activity was not clarified: cannabinoids may have an inhibitory action on both pre- and postganglionic vagal neurons.

Adrenergic beta-Agonists↗
PubMed2001

Beta2-adrenoceptor-mediated prejunctional facilitation and postjunctional inhibition of sympathetic neuroeffector transmission in the guinea pig vas deferens.

This study examines the role of prejunctional and postjunctional beta-adrenoceptors in the modulation of sympathetic cotransmission in the guinea pig vas deferens. The prejunctional involvement of beta-adrenoceptors was evaluated by testing the effects of several agonists and antagonists on the nerve stimulation-evoked overflow of ATP and norepinephrine (NE) from the "in vitro" vas deferens. The nonsubtype-selective beta-adrenoceptor agonist isoproterenol and the beta2-subtype-selective agonist clenbuterol increased, to a similar degree, the overflow of ATP and NE, while the beta1-subtype-selective agonist xamoterol and the beta3-subtype-selective agonist BRL 37 344 had no effect. Pretreatment with ICI 118, 551, a beta2-subtype-selective antagonist, abolished the facilitation of cotransmitter release by isoproterenol and clenbuterol, while the beta1-subtype-selective antagonist atenolol had no effect. Activation of beta-adrenoceptors by either isoproterenol or clenbuterol, but not by xamoterol and BRL 37 344, reduced the amplitude of contractions evoked by exogenously applied ATP. Pretreatment with propranolol or ICI 118, 551, but not atenolol, prevented these inhibitory effects. Isoproterenol in lower concentrations produced dose-dependent reduction of the purinergic but not the adrenergic phase of nerve stimulation-induced contraction of the guinea pig vas deferens. When applied in concentrations greater than 1 microM, isoproterenol, but not clenbuterol, actually produced a concentration-dependent facilitation of contractions evoked by both nerve stimulation and exogenously applied ATP. Antagonists of alpha-adrenoceptors blocked these facilitatory effects. Together, these results demonstrate that beta2-adrenoceptors can influence sympathetic neuroeffector transmission both prejunctionally, where they facilitate equally well the release of sympathetic cotransmitters and postjunctionally, where they inhibit smooth muscle contractions evoked by ATP.

Adenosine Triphosphate↗
PubMed1992

Effects of xylamine on vascular neuroeffector transmission.

The effect of xylamine on sympathetic neuroeffector transmission in rabbit isolated blood vessels was examined. Xylamine (10(-8) to 10(-6) M) caused a slowly progressing inhibition of the contractions of pulmonary artery evoked by electrical field stimulation. The inhibition was irreversible. Cocaine (3 x 10(-5) M) prevented the inhibitory action of xylamine (10(-7) M), but it did not reverse the inhibition caused by xylamine (10(-6) M). Xylamine (10(-7) to 3 x 10(-5) M) reduced the accumulation of [3H]norepinephrine (NE) (10(-8) M). In the presence of desipramine (10(-6) M), xylamine (10(-7) to 3 x 10(-5) M) and corticosterone (10(-6) to 10(-4)) reduced the 3H-accumulation. Xylamine (10(-7) to 10(-5) M) reduced the tissue NE content by up to 50%. Xylamine (10(-7) to 10(-6) M) antagonized in a noncompetitive manner the contractions of aorta evoked by NE (10(-9) to 3 x 10(-5) M), histamine (10(-6) to 3 x 10(-4) M) and 5-hydroxytryptamine (10(-8) to 3 x 10(-4) M). In the case of NE, the antagonism was more marked in the presence of either cocaine (3 x 10(-5) M) plus corticosterone (4 x 10(-5) M) or corticosterone (4 x 10(-5) M). In the presence of xylamine (10(-7) to 10(-6) M), cumulative addition of near maximally effective concentrations of NE, 5-hydroxytryptamine and histamine caused a progressive and complete relaxation of aorta. Xylamine (10(-7) to 10(-5) M) did not alter the contractions of aorta evoked by potassium (17-55 mM). The results support the contention that xylamine is an inhibitor of neuronal and extraneuronal uptake, an adrenergic neurone blocking agent and a noncompetitive antagonist of alpha-1 adrenoceptors, histamine and 5-hydroxytryptamine2 receptors. Xylamine is not a direct acting vasodilator on smooth muscle.

Animals↗
PubMed1991

Neuroeffector functions of sensory nerve fibers in the cerebral circulation after global cerebral ischemia.

The importance of trigeminal neuroeffector mechanisms in the regulation of postischemic cerebral blood flow (CBF) was evaluated in cats subjected to chronic unilateral denervation of cortical sensory nerve fibers by trigeminal ganglionectomy or by the topical application of capsaicin to a cortical branch of the middle cerebral artery. CBF was determined using isotopically labeled microspheres before and at intervals after reperfusion following 10 min of global cerebral ischemia induced by four vessel occlusion combined with systemic hypotension. Postocclusive hyperemia 30 min after reperfusion in cortical gray matter ipsilateral to the side of denervation was attenuated by up to 58% (176 vs. 91 ml/100 g per min; p less than 0.05), but resting CBF, the duration of hyperemia, and the cerebrovascular response to hypercapnia were unaffected. These data underline the influence of neurogenic mechanisms in the regulation of postischemic CBF. Blockade of this axon reflex-like mechanism may reduce the morbidity associated with several hyperperfusion syndromes.

Administration, Topical↗
PubMed1979

Diet, central nervous system, and aging.

A variety of morphological, structural, and chemical changes have been described in the central nervous systems of aging humans and animals. Brain size and volume decline during senescence, and the brain atrophy is accompanied by changes in the number, size, and ultrastructural characteristics of nerve and glial cells. Moreover, recent evidence suggests that the ability of central nervous system cells to communicate with one another via the release of neurotransmitter compounds might be impaired in the elderly. Nutritional factors may play important roles in the aging process of the central nervous system by influencing brain neurotransmission, or by accelerating or retarding geriatric changes in central nervous system structure.

Aged↗