[The vascular neuroeffector system (author's transl)].
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Blood Vessels↗
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The therapeutic use of cholinergic drugs acting on the vegetative nervous system. I - Direct, indirect and mixed agonists.
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Animals↗
L-tyrosine and adrenergic neuroeffector interaction in the canine saphenous vein.
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Animals↗
Structure-activity relationships of 2-aminotetralins and 2-aminoindanes: inhibitory neuroeffector mechanisms in isolated guinea-pig ilea.
The ability of 2-aminotetralins (2-ATs), 2-aminoindanes (2-AIs), morphine (M) and clonidine (CLON) to alter neuroeffector transmission was studied on field-stimulated (FS) guinea-pig ilea (GPI). The activity of these compounds to inhibit K+, histamine (H), actylcholine (ACh), nicotine (Nic) and serotonin (5-HT) induced contractions was determined using superfused GPI segments. 2-ATs, 2-AIs, M and CLON dose-dependently inhibited contractions produced by low frequency stimulation through alpha-adrenergic, opioid or unknown receptor mediated mechanisms. 2-ATs inhibited ACh, Nic, 5-HT and FS, but not K+- or H-induced contractions. 2-ATs, 2-Ais and M were more potent than hexamethonium in inhibiting Nic-induced contractures. 2-AT and 2-AI-induced inhibition was not antagonized by naloxone or phentolamine. However, the inhibitory effects of 2-ATs. 2-AIs and M on FS-GPI were antagonized by increasing the concentration of Ca2+ ion in the media. These data are consistent with the supposition that 2-ATs, 2-AIs or M alter neuroeffector transmission through competitive changes in Ca2+ disposition in cholinergic neurons of guinea-pig isolated ilea. A discussion relating other biological actions of 2-ATs or 2-AIs (e.g. alpha-adrenergic mediated antinociception) to the observed inhibitory neuroeffector responses is provided.
Acetylcholine↗
Effects of fentanyl on adrenergic function in canine coronary arteries.
The effects of fentanyl on sympathetic nerve endings in canine coronary arteries have been examined. Measurements were made of change in endogenous norepinephrine in isolated coronary artery in the presence of fentanyl, and of the effects of fentanyl on norepinephrine release and metabolism using superfused strips of coronary arteries in which transmitter stores had been prelabeled with [3H]norepinephrine. [3H]Norepinephrine and its 3H metabolites were separated from samples of superfusate (physiologic salt solution flowing continuously over the prelabeled coronary artery) by column chromatography and measured by scintillation spectrometry. The addition of fentanyl (2 x 10(-6) and 8 x 10(-6) M) caused the overflow of total radioactivity (radiolabeled norepinephrine and radiolabeled metabolites of norepinephrine entering the superfusate) to increase significantly above basal levels in both unstimulated and electrically stimulated arteries. The increased overflow could be accounted for by a small increase in norepinephrine and a sizeable increase in 3,4-dihydroxyphenylglycol, the metabolite arising from the intraneuronal metabolism of norepinephrine. Because this metabolite is without agonist activity and the increases in norepinephrine were small, fentanyl in the concentrations studied had minimal effects on adrenergic neurotransmission in this vascular bed.
Animals↗
[Ultrastructural relationships between terminal vegetative nerve fibers, ground substance and differentiations of cell surface (author's transl)].
Ultrastructural findings concerning the terminal vegetative nerve formation indicate a functional coupling via proteoglycans of the extracellular matrix with effector cells. The biological function of proteoglycans in the ground substance and in surface coats of axons and cells are discussed in connection with fusiform varicose swellings along terminal vegetative nerve fibers. These contain accumulated vesicles which probably are active in releasing transmitter substances.
Animals↗
9th International Symposium on Vascular Neuroeffector Mechanisms. Porto, Portugal, 2-5 August 1998. Abstracts.
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Animals↗
Actions of prostacyclin (PGI2) on adrenergic neuroeffector transmission in the rabbit kidney.
In the Tyrode's perfused rabbit kidney PGI2 (1.3 x 10(-8)-3.3 x 10(-7)M) dose-dependently inhibited vasoconstrictor responses to sympathetic nerve stimulation, as did PGE2. The dose-effect curve of the two compounds differed, making PGI2 the less potent in the low concentration and the more potent in the high. PGI2 also inhibited the vasoconstrictor response to exogenous noradrenaline, but it had no effect on transmitter release. The main metabolite of PGI2, 6-keto-PGF1 alpha, was ineffective both on noradrenaline release and on vascular responses to nerve stimulation or exogenous noradrenaline. It is suggested that PGI2, if a significant renal prostaglandin, may modulate renal neuroeffector transmission post-junctionally, thereby forming a complement to the prejunctional action of PGE2.
Animals↗
Electrical and mechanical properties and neuro-effector transmission in the smooth muscle layer of the guinea-pig ileocecal junction.
Electrical and mechanical properties and neuroeffector transmission were studied in circular strips of smooth muscle taken from the ileocecal junction of guinea-pigs in relation to sphincter action, using the microelectrode, and tension recording methods. The membrane potential of the smooth muscle was low (-43mV) compared with the membrane potential of circular muscle cells of the ileum or caecum (-58 mV or 62 mV). Only small populations of the muscle cells (about 5%) generated spontaneous action potentials. Field stimulation of the tissue produced an initial slight relaxation followed by a contraction, and the mechanical responses were accompanied by membrane hyperpolarization (i.j.p.) followed by repolarization with rebound spikes. Treatment with atropine increased the amplitude of i.j.p.s and decreased the amplitude of the rebound repolarization. Propranolol or phentolamine did not affect the amplitude of i.j.p., however, phentolamine slightly reduced the amplitude of the rebound repolarization. These results indicate that the ileocecal junction is predominantly controlled by non-adrenergic, non-cholinergic inhibitory nerve fibres and that the distribution of adrenergic and cholinergic excitatory nerve fibres is sparse.
Animals↗
The guinea-pig oesophagus is a versatile in vitro preparation for pharmacological studies.
1. The isolated oesophagus of the guinea-pig is a useful preparation that can be used as an alternative to the phrenic nerve-diaphragm preparations that have been used traditionally in the determination of the actions of drugs and toxins at the neuromuscular junction. The guinea-pig isolated oesophagus can also provide information about effects at ganglionic nicotinic receptors, which are not present in the diaphragm preparations. 2. The muscularis externa of the body of the oesophagus consists exclusively of striated muscle fibres. The myenteric plexus is found between the outer longitudinally arranged layer and the inner circular layer. The muscularis mucosae contains smooth muscle fibres arranged longitudinally. 3. The vagal nerves are comprised of special vagal efferents that innervate the striated muscle fibres directly and 'parasympathetic' vagal fibres that synapse in the myenteric ganglia and, subsequently, affect the smooth muscle of the muscularis mucosae. Thus, both striated and smooth muscle responses to vagal nerve stimulation can be studied. In addition, afferent neurons run in the vagus. 4. Studies using various isolated oesophageal preparations have been reviewed. These consist of the whole oesophagus (including striated muscle, myenteric plexus and smooth muscle), the isolated mucosal layer (striated muscle and the myenteric plexus both absent) and the whole oesophagus with the vagus nerve attached. Comparative studies of the effects of drugs acting directly on the muscularis mucosae and/or indirectly via the intramural plexuses can be performed using the whole oesophagus and the isolated mucosal layer. 5. The use of the guinea-pig isolated vagus nerve-oesophagus preparation allows potency determinations for both neuromuscular and ganglion blockade of various non-depolarizing muscle relaxants to be performed simultaneously under identical conditions. Furthermore, the phenomenon of fade, a waning of tetanic tension during the stimulation period, can be studied. 6. A potential application of this preparation is the simultaneous screening of the constituents of snake venoms for activity at the neuromuscular junction and/or the ganglion. It is also suggested that new calcium channel blockers could be screened in this preparation because different voltage-sensitive calcium channels are involved in neurotransmitter release from nerve terminals at the neuromuscular junction and autonomic cholinergic neuroeffector sites.
Animals↗
An electrophysiological study of presynaptic alpha-adrenoceptors in the vas deferens of the mouse.
1--Effects of clonidine and alpha-adrenoceptor antagonists were studied on sympathetic neuroeffector transmission in the mouse vas deferens. The amplitude of excitatory junction potentials (e.j.ps) was taken as a measure of transmitter release per impulse. 2--At a concentration of 0.5 microM, prazosin abolished depolarizations evoked by iontophoretically applied noradrenaline, but changed neither spontaneous nor nerve stimulation-evoked e.j.ps. 3--Yohimbine 0.1 and 1 microM, rauwolscine 1 microM and corynanthine 1 microM di not change the e.j.p. amplitudes elicited by the first 2-3 pulses in trains of 15 pulses at 3 Hz, but increased the e.j.ps elicited by the subsequent pulses. Corynanthine 1 microM was much less effective than yohimbine 1 microM or rauwolscine 1 microM, and corynanthine 0.1 microM had no effect. 4--Clonidine 0.01 microM reduced the e.j.p. amplitudes evoked by single pulses and its effect was counteracted by yohimbine 1 microM. 5--In vasa deferentia from reserpine-treated mice the e.j.p. trains were changed in much the same way as by yohimbine and rauwolscine. Yohimbine 1 microM did not further increase the e.j.p. amplitudes in these organs, whereas clonidine 0.01 microM caused a marked inhibition. 6--It is concluded that the release of the motor transmitter in the mouse vas deferens is inhibited by activation of presynaptic alpha-adrenoceptors, and that these receptors are normally activated by neurally released noradrenaline.
Animals↗
Calcium reverses the inhibitory action of morphine on neuroeffector transmission in the mouse vas deferens.
In the mouse vas deferens, the amplitude of excitatory junction potentials (e.j.p.s.) recorded intracellularly from smooth muscle cells was found to be proportional to stimulus intensity. Normorphine (0.4-2-10 microM) reduced the amplitude of these postsynaptic transients and shifted the stimulus-response curve to the right; i.e. in its presence, higher stimulus intensities were required to elicit an e.j.p. of a similar size to one generated in its absence. Naloxone (0.4 microM) reversed the inhibitory effect of normophine (2 microM). Membrane potentials were unaffected by the concentrations of normorphine employed in solutions of varying ionic compositions. Manoeuvres designed to increase intracellular free calcium, that is increasing the extracellular Ca+ ion concentration (from 2.5 to 5 or 10 mM), removing Mg2+ ions from a medium containing 5 mM Ca2+ or applying 4-aminopyridine (100 microM), enhanced the e.j.p. amplitude and reversed the inhibitory effect of normorphine. Lowering the concentration of Ca2+ ions (from 2.5 to 1 mM) or increasing the concentration of Mg2+ ions (from 1.2 to 4.8 mM) in the bathing solution reduced the amplitude of e.j.p.s. Short trains of impulses (3Hz) facilitated the amplitude of successive e.j.p.s., probably by elevating the intracellular Ca2+ ion concentration. The inhibitory effect of normorphine upon these transients was inversely proportional to the length of the train. It is concluded that the reversal of the effect of normorphine by calcium does not occur at the level of the opiate receptor, and that the opiate depresses the stimulated release of the excitatory transmitter by a reduction in the supply of Ca2+ ions to the stimulus-release coupling mechanism in the sympathetic nerve terminals.
Aminopyridines↗
Inhibition of neuroeffector transmission by morphine in the vas deferens of naive and morphine-treated mice.
1 The amplitude of excitatory junction potentials (e.j.ps) recorded intracellularly from smooth muscle cells of the mouse vas deferens varied with the strength of stimulation. Normorphine (0.4, 2 and 10 microM) shifted the stimulus-response curve to the right, without any change in slope. This shift of the curve was proportional to the concentration of the opiate in the bath. Naloxone (0.4 and 2 microM) antagonized this effect of normorphine. 2 The action of normorphine (2 and 10 microM) was studied in vasa deferentia prepared from control mice and mice that had been implanted with morphine pellets. Both groups of tissues were continuously exposed to a low concentration of normorphine (0.4 microM), to simulate the plasma concentration in the morphine-treated mice. Addition of 10 microM normorphine produced a parallel displacement of the curve in vasa deferentia from control animals, and a non-parallel displacement in tissues from morphine pellet-implanted mice. In the preparations from morphine-treated mice a pronounced degree of tolerance to normorphine was observed at a low stimulus strength. 3 Naloxone (0.4 and 2 microM) had a greater effect on vasa deferentia prepared from morphine-treated animals than on tissues from control mice, when both organs were continuously exposed to 0.4 microM normorphine. The difference in the effect of the antagonist in the two groups of preparations was absent when the incubating solution contained 2 microM normorphine. 4 It is concluded that a low intensity of stimulation the e.j.ps are more readily depressed by normorphine and also the degree of tolerance displayed is larger than at a high intensity of stimulation.
Animals↗
Sympathetic neuroeffector transmission in the rat anococcygeus muscle.
1. When intracellular recordings were made from preparations of rat anococcygeus muscle, transmural nerve stimulation evoked noradrenergic excitatory junction potentials (EJPs) made up of two distinct components. Both components were abolished by either guanethidine or alpha-adrenoceptor antagonists, indicating that they resulted from the release of transmitter from sympathetic nerves and the subsequent activation of alpha-adrenoceptors. 2. The first component was associated with a transient increase in the intracellular concentration of calcium ions ([Ca2+]i) and a contraction. Although the second component was often associated with a long lasting increase in [Ca2+]i it was not associated with a contraction unless the second component initiated an action potential. 3. The increase in [Ca2+]i associated with the first component resulted from Ca2+ release from an intracellular store and from entry of Ca2+ through voltage-dependent Ca2+ channels. The increase in [Ca2+]i associated with the second component resulted only from the entry of Ca2+ through L-type Ca2+ channels (CaL channels). The depolarization associated with the initial increase in [Ca2+]i was abolished by reducing the external concentration of chloride ions ([Cl-]o), suggesting that it involved the activation of a Cl- conductance. 4. When the relationships between changes in [Ca2+]i, membrane depolarization and contraction produced by an increasing number of sympathetic nerve stimuli were determined in control, and caffeine- and nifedipine-containing solutions, it was found that an increase in [Ca2+]i recorded in nifedipine produced a larger contraction and larger membrane depolarization than did a similar increase in [Ca2+]i recorded in either control or caffeine-containing solutions. These observations indicate that Ca2+ released from stores more readily triggers contraction and membrane depolarization than does Ca2+ entry via CaL channels.
Action Potentials↗
Effects of acetaldehyde on electrical activity during neuroeffector transmission in guinea-pig vas deferens.
The effects of acetaldehyde on electrical activity during sympathetic neuroeffector transmission were studied in the guinea-pig vas deferens. Application of 1 mM acetaldehyde produced a slow depolarization of the smooth muscle membrane. The amplitudes of facilitated excitatory junction potentials (EJPs) evoked by nerve stimulation were slightly decreased. A higher concentration of acetaldehyde (5 mM) initially hyperpolarized and later depolarized the membrane. The decrease in EJP amplitudes was more pronounced during hyperpolarization. Acetaldehyde (5 mM) increased the frequency of the spontaneous EJPs and reduced their amplitudes, whereas action potentials in postganglionic nerves were unaffected. Acetaldehyde (1-5 mM) decreased the amplitudes of EJPs in vasa pretreated with reserpine but did not alter the resting membrane potentials. The decrease in the EJP amplitudes together with the hyperpolarization of the membrane could be responsible for the early inhibitory effect of acetaldehyde on neuroeffector transmission. The slow depolarization, which is presumably mediated by endogenous noradrenaline, may cause the late facilitatory effect.
Acetaldehyde↗
Vascular neuroeffector mechanisms in hypertension.
Recent studies of the peripheral sympathetic nervous system indicate the presence of other vasoactive transmitters in addition to noradrenaline. There is now evidence suggesting ATP to be a co-transmitter of noradrenaline mediating the excitatory junction potential and the phentolamine-resistant component of the vasopressor response. In hypertension, changes in the neural regulation at both pre- and post-synaptic levels have been observed. In the spontaneously hypertensive rat (SHR), abnormal feedback regulation through presynaptic adrenoceptors and increases in release and uptake by the perivascular nerves are well characterized. Whether similar changes in the ATP release mechanism occur in the SHR and other forms of hypertension remain to be determined. A more important role for ATP in the neural regulation of the SHR tail artery has been proposed. In future studies, the possible contribution of co-transmitters to the responses should be taken into consideration.
Animals↗
Effects of reserpine pretreatment on neuroeffector transmission in the vas deferens.
1. The effects of reserpine pretreatment on neurotransmission in the guinea-pig vas deferens have been re-examined with a view to study the role of noradrenaline (NA) in mediating postjunctional electrical responses and, in particular, excitatory junction potentials (EJP). 2. Reserpine (5 mg/kg, i.p.) caused almost total depletion (below detection levels) of the NA content of the vas deferens. However, spontaneous and evoked excitatory junction potentials (SEJP, EJP) and currents (SEJC, EJC) could still be recorded in NA-depleted tissues. The amplitude distribution of SEJC in control and reserpinized tissues was similar. 3. Facilitation of EJP and EJC was markedly slowed in reserpinized tissues, EJP taking 50-60 pulses to facilitate fully. However the amplitudes of fully facilitated EJP were comparable to EJP recorded in control tissues. 4. EJPs in reserpinized vasa deferentia were unaffected by the NA synthesis inhibitor, alpha-methyl tyrosine, but were abolished in the presence of the stable ATP analogue alpha,beta-methylene ATP which desensitizes postjunctional P2-purinoceptors. 5. Local application of ATP, but not NA, mimicked the EJP. These results indicate that EJP are mediated by a non-noradrenergic neurotransmitter possibly ATP.
Adenosine Triphosphate↗
Modulation of neuroeffector transmission in guinea-pig pulmonary artery and vas deferens by exogenous nitric oxide.
Blockade of nitric oxide (NO) synthesis enhances contractile responses to transmural nerve stimulation in guinea-pig pulmonary artery, indicating neuromodulation by endogenous nitric oxide. In the present study, neuromodulatory effects of exogenous NO were examined in guinea-pig pulmonary artery and vas deferens. Application of NO as acid nitrite, to the guinea-pig pulmonary artery, inhibited the contractile response to transmural nerve stimulation as well as contractions to exogenous noradrenaline. The inhibition occurred in a dose-dependent manner. Acid nitrite did not affect stimulation-induced release of [3H]noradrenaline in guinea-pig pulmonary artery. In the guinea-pig vas deferens, contractile 'twitch' responses to brief (25 pulses) transmural nerve stimulation and stimulation-induced release of [3H]noradrenaline was unaffected by acid nitrite. However, 'twitch' responses to prolonged stimulation were inhibited by acid nitrite, and tonic 'hump' responses were either enhanced or unaffected by acid nitrite. In conclusion, exogenous nitric oxide exerted an inhibition of adrenergic neurotransmission post-junctionally in guinea-pig pulmonary artery. In guinea-pig vas deferens, exogenous nitric oxide affected adrenergic and/or non-adrenergic noncholinergic neurotransmission in a complex fashion, however without alteration in noradrenaline release. The data support a role for NO in modulation of neuroeffector transmission, especially by modulation of effector sensitivity, whereas modulation of noradrenaline release seems an unlikely role for NO in these and similar peripheral tissues.
Animals↗