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PubMed1995

Effects of vitamin E deficiency on autonomic neuroeffector mechanisms in the rat caecum, vas deferens and urinary bladder.

1. Modified sucrose-gap, standard organ-bath techniques and transmitter release studies were used to examine neuromuscular transmission in the caecum, vas deferens and urinary bladder in normal rats and in rats maintained for 12 months on a diet free of vitamin E. 2. In the caecum circular muscle, non-adrenergic, non-cholinergic inhibitory junction potentials were absent from 48 and 15% of preparations from vitamin E-deficient and control animals, respectively. Cholinergic excitatory junction potentials were absent from 83 and 8% of vitamin E-deficient and control preparations, respectively. Responses to applied noradrenaline (0.1-30 microM), alpha,beta-methylene ATP (3-100 microM) and acetylcholine (0.1-30 microM) were attenuated or absent in vitamin E-deficient tissues. Responses to applied KCl were similar in both groups. Release of [3H]noradrenaline or endogenous acetylcholine could not be evoked from vitamin E-deficient tissues. 3. In contrast, in isolated preparations of the vas deferens and urinary bladder, neuromuscular transmission by adrenergic, cholinergic and purinergic components were unaffected by long-term vitamin E deficiency. 4. In conclusion, vitamin E deficiency causes dysfunction of autonomic neuroeffector mechanisms in the smooth muscle of the rat caecum, at both a pre- and postjunctional level. The lesions in autonomic transmission mechanisms brought about by long-term vitamin E deficiency were found only in the caecum; no changes in sympathetic neuromuscular transmission were observed in the vas deferens, or in parasympathetic neuromuscular transmission in the urinary bladder.

Adenosine Triphosphate↗
PubMed1992

Sympathetic innervation of renal and extra-renal arterial vessels.

The innervation of arterial vessels has been analyzed using serial thin sections examined in the electron microscope. Sympathetic postganglionic noradrenergic axons have been found to make neuromuscular junctions on the outermost cells of the media of virtually all muscular arterial vessels with diameters between 20 microns and 1 mm in rat, rabbit and guinea pig. Junctions are formed by the majority of varicosities which are not covered by Schwann cell on the side towards the artery surface. The junctions resemble those on skeletal muscle fibers, having a single layer of basal lamina in the synaptic cleft. Although post-junctional specializations have not been identified, 15 to 20% of junctions show electron dense regions of the prejunctional membrane with associated clumps of synaptic vesicles. The form of the varicose axons differs, and three distinct types have been distinguished on morphological grounds. Two of these occur in the juxtaglomerular region of the kidney, with characteristic distributions of junctions which differ between the afferent and efferent arterioles. The presence of numerous close junctions has revolutionized our thinking about how sympathetic neuroeffector transmission occurs in arterial vessels.

Animals↗
PubMed2000

Neuroeffector transmission to different layers of smooth muscle in the rat penile bulb.

1. Using intracellular recording techniques, two distinct layers of smooth muscle were identified in the rat penile bulb. The inner muscle layer (parenchyma) exhibited spontaneous action potentials, while the outer sheet (sac) was electrically quiescent. 2. In the parenchyma, transmural stimulation initiated non-adrenergic, non-cholinergic (NANC) inhibitory junction potentials (IJPs) which were abolished by Nomeganitro-L-arginine (LNA) or 1H-[1,2, 4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ). The amplitude of IJPs was reduced by ouabain, dinitrophenol or decreasing the extracellular potassium concentration ([K+]o) but not by several K+ channel blockers. 3. The parenchyma also received an excitatory innervation mediated by alpha-adrenoceptors which caused a contraction that was not associated with a membrane potential change. 4. In the sac, transmural stimulation initiated two component excitatory junction potentials (EJPs) mediated by alpha-adrenoceptors and associated action potentials. The initial component was more dramatically suppressed than the secondary component by caffeine, ryanodine or cyclopiazonic acid (CPA). Lowering of the extracellular chloride concentration ([Cl-]o) selectively inhibited the rapid component of EJPs, while niflumic acid was less potent. 5. These results suggest that IJPs in the parenchyma result from the release of NO which stimulates sodium pump activity following the activation of guanylate cyclase. In the sac, the activation of alpha-adrenoceptors initiates EJPs by releasing Ca2+ from intracellular stores which activates Ca2+-activated channels.

Animals↗
PubMed1981

Effect of moderate cooling on adrenergic neuroeffector interaction in canine cutaneous veins.

Experiments were performed to investigate the effect of moderate cooling on adrenergic neuroeffector interaction in canine cutaneous veins. Helical strips of dog's saphenous vein, untreated or first incubated with 3H-norepinephrine were mounted for superfusion and isometric tension recording; the overflow of endogenous catecholamines or 3H-norepinephrine and its metabolites, respectively, were measured in the superfusate. In other experiments the monoamine oxidase activity or the catechol-O-methyltransferase (COMT) activity of the saphenous vein wall was determined. Moderate cooling (from 37 to 24 degree C) decreased the evoked release of endogenous norepinephrine during electrical stimulation of the adrenergic nerve endings in the blood vessel wall. Moderate cooling depressed the overflow of 3H-norepinephrine and its metabolites in unstimulated preparations, during electrical stimulation during superfusion with high K+ solution and during exposure to tyramine. Moderate cooling reduced the activity of monoamine oxidase significantly more than that of COMT. The relative alterations in overflow of norepinephrine and its metabolites caused by a same degree of cooling in basal conditions and during the different forms of increased overflow of adrenergic transmitter suggest that lowering the temperature inhibits the exocytotic process, but at the same time slows down the diffusion of norepinephrine from the junctional cleft to the extracellular space to the extent that during sympathetic nerve stimulation at 24 degree C the effective junctional concentration of the transmitter may be comparable to that obtained at 37 degree C. The inhibitory effect of moderate cooling on the extraneuronal metabolism of norepinephrine appears to affect little the effective junctional concentration of the adrenergic transmitter.

Adrenergic Fibers↗
PubMed1996

The possible role of nitric oxide in relaxations and excitatory neuroeffector transmission in the cat airway.

1. To study the possible role of nitric oxide (NO free radical; NO) or NO-containing compounds in the non-adrenergic, non-cholinergic (NANC) relaxations, we observed the effects of carboxy-2-phenyl-4, 4, 5, 5-tetramethyl-imidazoline-1-oxyl-3-oxide (C-PTIO; a newly synthesized NO scavenger) on NANC relaxations in the cat airway. In addition, we also observed the effects of C-PTIO on excitatory junction potentials (EJPs), since NO has a prejunctional action on transmitter release. 2. Nitrosocystine (Cys-NO) (10(-7)-10(-3) M) dose-dependently relaxed the bronchial tissue in the presence of 5-HT, atropine and guanethidine and C-PTIO (10(-4) M) shifted the concentration-response curve of the Cys-NO to the right. 3. Electrical field stimulation (EFS) evoked biphasic NANC relaxations in the small bronchi of the cat. In general, C-PTIO suppressed non-selectively both the first and second components of the NANC relaxations to a similar extent. However, in some bronchial preparations C-PTIO (10(-4) M) selectively suppressed the first component of the NANC relaxation to approximately 50% of the initial value, enhancing the amplitude of the second component of the NANC relaxations. 4. After pretreatment of the bronchial tissues with alpha-chymotrypsin (1 unit ml-1) for 30 min in order to inhibit any response to peptides, EFS evoked monophasic NANC relaxation. C-PTIO (10(-5) - 10(-4) M) dose-dependently suppressed, and at a concentration of 10(-4) M almost halved, the amplitude of NANC relaxation. Additional application of L-NAME further reduced the C-PTIO-resistant NANC relaxation to 20-30% of the initial value. 5. C-PTIO (10(-4) M) enhanced the EJP amplitude evoked by single EFS in the trachea but not in the bronchi. However, C-PTIO enhanced the summation of the EJPs to repeated stimulation to a similar extent in the tracheal and bronchial tissues. Simultaneous application of C-PTIO and L-NAME did not further enhance the summation. 6. These results indicate that NO. and NO-containing compounds are involved in the L-NAME-sensitive NANC relaxation in the cat airway, and that only NO. has a prejunctional action which inhibits excitatory neuroeffector transmission.

Animals↗
PubMed2006

Involvement of intramuscular interstitial cells of Cajal in neuroeffector transmission in the gastrointestinal tract.

Specialized cells known as interstitial cells of Cajal (ICC) are distributed in specific locations within the tunica muscularis of the gastrointestinal (GI) tract. ICC serve as electrical pacemakers, provide pathways for the active propagation of slow waves, are mediators of enteric motor neurotransmission and play a role in afferent neural signalling. Morphological studies have provided evidence that motor neurotransmission in the GI tract does not occur through poorly defined structures between nerves and smooth muscle, but rather via specialized synapses that exist between enteric nerve terminals and intramuscular ICC or ICC-IM. ICC-IM are coupled to smooth muscle cells via gap junctions and post-junctional responses elicited in ICC-IM are conducted to neighbouring smooth muscle cells. Electrophysiological studies from the stomachs and sphincters of wild-type and mutant animals that lack ICC-IM have provided functional evidence for the importance of ICC in cholinergic excitatory and nitrergic inhibitory motor neurotransmission. Intraperitoneal injection of animals with Kit neutralizing antibody or organ culture of gastrointestinal tissues in the presence of neutralizing antibody, which blocks the development and maintenance of ICC, has provided further evidence for the role of ICC in enteric motor transmission. ICC-IM also generate an ongoing discharge of unitary potentials in the gastric fundus and antrum that contributes to the overall excitability of the stomach.

Animals↗
PubMed2003

Traditional oriental herbal medicine, Bakumondo-to, suppresses vagal neuro-effector transmission in guinea pig trachea.

OBJECTIVE: Bakumondo-to (Maimendong tang) is a traditional oriental herbal medicine that has been used as an antitussive agent. We previously demonstrated that Bakumondo-to attenuates airway hyperresponsiveness induced by ozone. However, the mechanism(s) responsible for this effect remains unclear. In the present study, we examined the mechanism whereby Bakumondo-to inhibits ozone-induced airway hyperresponsiveness. First, we examined the effect of Bakumondo-to on prostanoids production, which are key mediators to airway hyperresponsiveness after ozone exposure. Second, we studied its effects on the vagal neuroeffector transmission, because vagal nerve is likely to play an important role in airway hyperresponsiveness after ozone. METHODS: We measured the effects of Bakumondo-to on the concentrations of prostanoids in bronchoalveolar lavage fluid before and after ozone. We evaluated the effects of Bakumondo-to on the contraction of guinea pig tracheal smooth muscle evoked by electrical field stimulation (EFS) or the exogenous application of acetylcholine (ACh). Isometric tension of tracheal strips was measured in the presence of indomethacin (10(-6) M) and of guanethidine (10(-6) M). RESULTS: Ozone caused significant increase in prostaglandin E2 (PGE2) and thromboxane B2 (TXB2); however, Bakumondo-to did not affect the increase in these prostanoids. Bakumondo-to (0.01 mg/mL-1 mg/mL) significantly suppressed the contraction evoked by EFS, but did not affect the ACh-evoked contraction, indicating that Bakumondo-to suppressed tracheal smooth muscle contraction pre-junctionally. CONCLUSION: These results suggest that the mechanism by which Bakumondo-to inhibits airway hyperresponsiveness depends on inhibiting the release of acetylcholine from vagal nerve terminals.

Acetylcholine↗
PubMed1994

Electrophysiological events during neuroeffector transmission in the spleen of guinea-pigs and rats.

Intracellular recordings were made from smooth muscle cells of arterioles and the capsule of the spleen of guinea-pig and rat, and the responses to periarterial or subcapsular nerve stimulation were recorded. The innervation of the spleen was studied using fluorescence and immunohistochemical techniques. Catecholamine-containing axons were associated with smooth muscle of the splenic capsule, trabeculae, arterioles and amongst cells of the periarteriolar lymphoid sheath. Axons immunoreactive for neuropeptide Y (NPY) and tyrosine hydroxylase were distributed in an identical manner to catecholamine-containing axons, whereas axons immunoreactive for substance P or calcitonin gene-related peptide were present at a very low density in spleens from both species. In segments of arterioles, single transmural stimuli evoked excitatory junction potentials (EJPs) of 1-10 mV amplitude. EJPs facilitated during short trains of stimuli (1-10 Hz) and summated at 10 Hz, often initiating a muscle action potential. EJPs persisted in the presence of prazosin (1 microM) and idazoxan (1 microM), but were abolished by the P2x-purinoceptor antagonist suramin (1 mM). Spontaneous depolarizations were observed in smooth muscle cells of arterioles and capsule. Some events in arterioles were observed in the presence of suramin and so may originate postjunctionally independently of transmitter release. As single transmural stimuli failed to evoke a depolarization in capsular smooth muscle, spontaneous depolarizations in this tissue probably also arise postjunctionally. Short trains of high frequency stimuli (10-35 Hz) evoked biphasic depolarizations of capsular smooth muscle cells. The initial component peaked 2.5 s following the onset of stimulation; the second component peaked 15 s following the onset and decayed exponentially with a time constant of 15 s. By fitting a product of exponentials to the second component, it was possible to define the initial component, which decayed with a time constant of around 1.5 s. Neurally evoked depolarizations of capsular smooth muscle were abolished by 1 microM TTX. Blockade of alpha 1-adrenoceptors with prazosin reduced the initial component of the depolarization, whereas alpha 2-adrenoceptor blockade with idazoxan virtually abolished the second component. In some cells a small, faster depolarization persisted after alpha-adrenoceptor blockade. The slow alpha 2-adrenoceptor-mediated depolarization was identical to that recorded in the rat tail artery and in the guinea-pig mesenteric vein. The data indicate that sympathetic neuroeffector transmission from noradrenergic axons containing NPY to splenic arterial and capsular smooth muscle occur by different mechanisms.

Adrenergic alpha-Antagonists↗
PubMed1985

Characterization of pre- and post-junctional adenosine receptors in guinea-pig ileum.

The receptors involved in adenosine-induced modulation of cholinergic neuroeffector transmission in guinea-pig ileum were explored by means of the non-selective stable analogue, 2-chloroadenosine and analogues with preference for AI receptors, L-N6-phenylisopropyladenosine (L-PIA), and A2 receptors, 5'-N-ethylcarboxamideadenosine (NECA) and D-N6-phenylisopropyladenosine (D-PIA). 2-chloroadenosine, L-PIA and NECA were equipotent in inhibiting contractile responses to nerve stimulation, whereas D-PIA exerted a similar activity only in high concentrations. The release of acetylcholine induced by nerve stimulation was inhibited to a similar degree by NECA, L-PIA and D-PIA. The phosphodiesterase inhibitor, ZK 62.7II, and the activator of adenylate cyclase, forskolin, enhanced the inhibitory effect of NECA, but not that of L-PIA, on contractile responses to nerve stimulation. Only NECA inhibited contractions induced by direct muscle stimulation and ZK 62.7II enhanced this inhibition. It is concluded that adenosine inhibits the neuroeffector transmission in guinea-pig ileum mainly by a prejunctional, cAMP-independent, mechanism, involving AI receptors and a supplementary activation of post-junctional A2 receptors. In addition there may be a prejunctional inhibitory effect of high agonist concentrations, exerted via A2 receptors and influenced by the prevailing levels of cAMP.

2-Chloroadenosine↗
PubMed1987

Identification of the neuroeffector transmitter in jejunal branches of the rabbit mesenteric artery.

Vasoconstriction or excitatory junction potentials (e.j.ps) evoked by nerve stimulation (15 field pulses at 2 Hz every 3 min) were recorded in rabbit isolated jejunal arteries. The resting diameter of the arteries and its decrease in response to stimulation was measured by a photoelectric method. Vasoconstriction was insensitive to prazosin 0.1 or 1 mumol/l. Yohimbine 1 mumol/l considerably enhanced, whereas alpha,beta-methylene ATP (alpha,beta-meATP) 1 mumol/l abolished the contractile response. In order to test the effect of exogenously applied transmitter candidates, noradrenaline (0.1-1 mumol/l) and ATP (10-30 mumol/l) were added in concentrations which evoked a vasoconstriction comparable to that induced by electrical stimulation. The action of noradrenaline was prevented by prazosin 0.1 mumol/l, but was unaffected by both yohimbine 1 mumol/l and alpha,beta-meATP 1 mumol/l. Alpha,beta-meATP 1 mumol/l depressed the effect of ATP. The e.j.ps evoked by a train of 15 pulses showed facilitation up to the third response and thereafter depression; a partial summation was also observed. Prazosin 0.1 mumol/l did not change the e.j.p. amplitudes. By contrast, when yohimbine 0.1 or 1 mumol/l was added to the prazosin-containing medium, both the late e.j.ps in the train and the summation were enhanced in a concentration-dependent manner. Alpha,beta-meATP 1 mumol/l almost abolished the e.j.ps. In conclusion, in rabbit jejunal arteries, stimulation of postganglionic sympathetic nerves may release noradrenaline together with ATP which is probably the sole neuroeffector transmitter under our conditions. Transmitter release seems to be modulated by the activation of presynaptic alpha 2-adrenoceptors. Under the stimulation conditions of the present experiments the released transmitter does not activate postsynaptic alpha 1-adrenoceptors.

Adenosine Triphosphate↗
PubMed1986

Autonomic neuromuscular junctions: current developments and future directions.

(1) The autonomic neuromuscular junction has been defined, with emphasis on the role of muscle effector bundles and en passage release of transmitter from extensive terminal nerve varicosities to diffuse to muscle across variable and often wide junctional clefts. (2) A multiplicity of neurotransmitters is described in the autonomic nervous system, including purines, peptides, amino acids and monoamines. The ultrastructural identification, projections, roles and interactions of the different nerve types have been discussed. (3) It has been suggested that the part played by peripheral neuroeffector control mechanisms has been underestimated and includes cotransmission, pre- and post-junctional neuromodulation, and the participation of locally released agents. (4) A time-lapse film was shown of the formation of autonomic neuromuscular junctions in culture, introducing questions relating to long-term 'trophic' influences in the autonomic nervous system.

Animals↗
PubMed1994

Effects of epithelial cell supernatant on membrane potential and contraction of dog airway smooth muscles.

We investigated the effects of cultured epithelial cells and supernatants on resting membrane potential and excitatory neuroeffector transmission in smooth muscle cells of dog trachea and bronchioles. The mean resting membrane potential of the mucosa-free tracheal smooth muscle cells was -59.5 +/- 1.5 mV (+/- SD). Application of cultured epithelial cells (> 2.5 x 10(5) cells/ml) hyperpolarized the membrane, resulting in a potential of -64.5 +/- 1.7 mV. The supernatant of the cultured epithelial cells also increased the resting membrane potential of the mucosa-free tracheal smooth muscle cells by 4 to 9 mV. These hyperpolarizing actions were not modified by indomethacin (10(-5) M), l-NG-nitroarginine (10(-5) M), or oxyhemoglobin (10(-5) M), but were inhibited by glibenclamide (10(-6) M). The supernatants of the cultured epithelial cells completely or partially suppressed the contractile response of epithelium-denuded bronchioles to electrical field stimulations and suppressed the amplitude of excitatory junction potentials of the trachealis evoked by electrical field stimulations. Indomethacin prevented the inhibitory effect of supernatants on the amplitude of twitch contractions and excitatory junction potentials and markedly suppressed supernatant-associated inhibition of the excitatory neuroeffector transmission. Furthermore, indomethacin with AA861, a lipoxygenase inhibitor, completely suppressed this effect. Our findings suggest that cultured airway epithelial cells spontaneously release at least two factors. One factor selectively modulates the resting membrane potential, and the other inhibits the excitatory neuroeffector transmission.

Animals↗
PubMed1986

Differential effect of stimulation strength in mouse vas deferens on inhibition of neuroeffector transmission by receptor type selective opioids.

In the mouse isolated vas deferens the amplitude of excitatory junction potentials (e.j.p.s) recorded intracellularly from smooth muscle cells varied with the strength of stimulation. Receptor type selective opioids were tested in this preparation. The mu-agonist normorphine (2,000 nmol/l) reduced the amplitude of e.j.p.s and shifted the stimulus-response curve in a parallel way to the right. By contrast, the kappa-agonist U-50488 (1,000 nmol/l) and the delta-agonist [D-Ala2,D-Leu5]-enkephalin (2 nmol/l) caused a non-parallel shift of the curve. In addition, opioids having a lower selectivity for one type of receptor were also used. The preferential kappa-agonists ethylketocyclazocine (40 nmol/l) and dynorphin A1-13 (100 nmol/l) produced parallel and non-parallel shifts, respectively. Thus, normorphine and ethylketocyclazocine were more effective in depressing e.j.p.s evoked by low intensities of stimulation than those evoked by high intensities of stimulation. U-50488, dynorphin A1-13 and [D-Ala2,D-Leu5]-enkephalin caused an equal depression of e.j.p.s evoked by either intensity of stimulation. The preferential mu- and delta-antagonists naloxone (1,000 nmol/l) and ICI 154129 (10,000 nmol/l), reversed the action of the respective agonists normorphine and [D-Ala2, D-Leu5]-enkephalin. In addition, ICI 154129 (10,000 nmol/l) reversed the action of dynorphin A1-13, as well. The preferential kappa-antagonist MR-2266 (1,000 nmol/l) prevented the effect of both ethylketocyclazocine and U-50488. It is concluded that under the conditions of these experiments normorphine and ethylketocyclazocine acted at mu-, U-50488 at kappa-, and dynorphin A1-13 and [D-Ala2,D-Leu5]-enkephalin at delta-receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed2000

Effects of agents that modulate intracellular cAMP levels on excitatory junction potentials recorded in the guinea-pig vas deferens in vitro.

This study used intracellular recording of excitatory junction potentials (EJPs) and focal extracellular recording of excitatory junction currents (EJCs) to investigate the effects of agents that modulate intracellular cAMP levels on sympathetic neuroeffector transmission in the guinea-pig vas deferens. In this tissue, postjunctional electrical activity is produced by neurally released ATP. The adenylate cyclase activator, forskolin (0.5-5 microM) increased the amplitude of all EJPs evoked by trains of 20 stimuli at I Hz. Forskolin (5 microM) also increased the probability of recording EJCs without changing the amplitude distributions of spontaneous EJP and EJCs, indicating that this agent does not change the postjunctional sensitivity to spontaneously released quanta of ATP. EJP amplitudes were also increased by 8-bromo-cyclic AMP (10 microM), 8-bromo-cyclic GMP (10 microM), the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (100 and 1,000 microM) and the beta-adrenoceptor agonist, isoprenaline (1 microM). The selective protein kinase A inhibitors, H-89 (10 microM) and the Rp isomer of adenosine-3',5'-cyclic monophosphorothioate (Rp-cAMPS, 100 microM), and the broad spectrum protein kinase inhibitors, [1-(5-isoquinolinesulphonyl)-3-methylpiperazine-diHCl (H-7, 100 microM) and staurosporine (1 microM), did not block the facilitatory effects of forskolin on EJP amplitude. In addition, the effects of forskolin were not blocked by the cyclic nucleotide-gated ion channel blocker, spermine (50 microM). These results suggest that elevating intracellular cAMP levels increases ATP release in the guinea-pig vas deferens by a mechanism which does not involve activation of protein kinases A or G.

Adenosine Triphosphate↗
PubMed1989

Inhibition of transmitter release from sympathetic nerve endings by omega-conotoxin.

1. The effects of the calcium channel blocker, omega-conotoxin, on sympathetic neuroeffector function in the guinea-pig vas deferens have been investigated using a combination of mechanical and electrophysiological recording techniques. 2. Biphasic contractions evoked by electrical field stimulation were irreversibly abolished by omega-conotoxin (10-100 nmol/L). 3. Electrically evoked excitatory junction potentials and currents were irreversibly blocked by omega-conotoxin (10-100 nmol/L). Spontaneous excitatory junction potentials and currents were unaffected by this treatment. 4. omega-Conotoxin did not block impulse propagation in the nerve terminals. However, in three of four experiments omega-conotoxin caused a decrease in the size of the nerve terminal impulse. 5. These findings support the suggestion the omega-conotoxin acts prejunctionally to inhibit sympathetic neuroeffector by interfering with depolarization-secretion coupling.

Animals↗
PubMed1998

Neuroeffector transmission in arterioles of the guinea-pig choroid.

1. Using conventional microelectrode techniques, membrane potentials were recorded from smooth muscle cells of guinea-pig choroidal arterioles. 2. Transmural stimulation initiated excitatory junction potentials (EJPs) which were abolished by either guanethidine or alpha,beta-methylene-ATP but not by phentolamine, indicating that they resulted from activation of purinoceptors. 3. Trains of stimuli evoked EJPs which were followed by a slow depolarization, an inhibitory junction potential (IJP) or a biphasic membrane potential change which consisted of an IJP and a subsequent slow depolarization. 4. Slow depolarizations were abolished by either phentolamine or guanethidine, indicating that they resulted from activation of alpha-adrenoceptors. 5. IJPs were abolished by atropine but not by guanethidine, and were reduced by 50 % by apamin with the residual response being abolished by charybdotoxin, indicating that they resulted from the activation of muscarinic receptors which open two sets of Ca2+-activated K+ channels. 6. Most responses were followed by slow hyperpolarizations. These were almost abolished by L-nitroarginine, an effect which was partly overcome by L-arginine, and were abolished by glibenclamide, indicating that they resulted from the release of NO and activation of ATP-sensitive K+ channels. 7. Immunohistochemical analysis showed that arterioles were densely innervated by adrenergic nerve fibres. A population of fibres, likely to be cholinergic, was also identified. Furthermore, populations of nerve fibres immunoreactive to antibodies against either nitric oxide synthase (NOS) or substance P (SP) were also identified. 8. These findings indicate that choroidal arterioles of the guinea-pig are innervated by at least three different populations of nerves, adrenergic nerves which evoke excitatory responses, cholinergic nerves which evoke inhibitory responses and a population of nerves which cause the release of NO.

Animals↗
PubMed1975

Pre- and post-junctional receptor-mediated cholinergic interactions with adrenergic transmission in guinea-pig vas deferens.

Isolated, superfused, field stimulated guinea-pig vas deferens, in which the noradrenaline stores had been labelled by preincubation with tritiated (-)-noradrenaline, was used to study the interaction between exogenous and endogenous acetylcholine and adrenergic neuroeffector function. Exogenous acetylcholine was found to exert a dual muscarinic effect on the preparation, consisting of depression of the secretion of tracer noradrenaline from the sympathetic nerves, as well as enhancement of the nerve stimulation-induced contraction of the preparation. The results indicate that endogenous acetylcholine may play an analogous role, since eserine enhanced the nerve stimulation-induced contraction, without markedly affecting the secretion of labelled noradrenaline (the effect was abolished by atropine), while higher concentrations of atropine depressed the contraction and actually enhanced the secretion of labelled noradrenaline. The findings support the concept that guinea-pig vas deferens has a dual, cholinergic as well as adrenergic, innervation, and that the cholinergic nerves exert a dual modulatory effect on sympathetic neuro-effector function in this tissue: Firstly they appear to restrict the secretion of sympathetic neurotransmitter (via pre-junctional muscarinic receptors, on the adrenergic nerve terminals), and secondly they seem to enhance the excitability of the smooth muscle to sympathetic neurotransmitter (via post-junctional muscarinic receptors, on the smooth muscle cells).

Acetylcholine↗