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PubMed1987

Modulation of neuroeffector transmission.

Local mechanisms that regulate transmitter release at autonomic neuroeffector junctions may be classified into four main types: (a) Automodulation, involving a feedback effect of the transmitter on receptors associated with the prejunctional terminals resulting in a restraint on the facilitation of release that occurs when a train of nerve impulses invades the terminals. Changes in the composition of the transmitter, such as the presence of adrenaline as a cotransmitter together with noradrenaline, can result in increased facilitation of transmission. (b) Transneuronal modulation involving an effect of the transmitter released from terminals of one type on adjacent terminals of another type; thus, noradrenaline release may be inhibited by acetylcholine released from cholinergic nerve terminals adjacent to the noradrenergic terminals. (c) Transjunctional modulation involving a feedback effect on the prejunctional nerve terminals of one or more factors released from effector cells. Such substances include adenyl compounds (adenosine and/or ATP) and metabolites of arachidonic acid. (d) Hormonal modulation involving the action of blood-borne hormones or locally generated hormone-like substances on prejunctional terminals. Some of the substances involved in modulation may act in more than one way; thus, opioids may function as cotransmitters or as hormones, and adenyl compounds may be cotransmitters or be released from effector cells. The effects of exogenous drugs on the substances involved in the modulation of transmission and on the prejunctional receptors for these substances account for many anomalous actions of drugs used or proposed for use in therapeutics.

Acetylcholine↗
PubMed1987

Identification of pre- and postsynaptic bradykinin receptor sites in the vas deferens: evidence for different structural prerequisites.

The effect of bradykinin on the neuroeffector junction of the isolated rat vas deferens was studied in tissues stimulated transmurally at a frequency of 0.15 Hz. Bradykinin caused two distinct and independent actions: it potentiated the magnitude of the muscular response to the electrically driven twitches and, in addition, contracted the smooth muscle generating an increased muscular tone. The former action is referred to as the neurogenic or presynaptic effect, whereas the latter effect is called the musculotropic or postjunctional action. The neurogenic effect was abolished by tetrodotoxin or tissue denervation either by cold storage or chemical sympathectomy after 6-hydroxydopamine administration. However, these procedures did not significantly modify the musculotropic potency of bradykinin. Both actions of the peptide are receptor-mediated, as minor structural modifications in the amino acid sequence caused significant changes in biological potency. In addition, the peptide analog, [Thi5,8-D-Phe7]-bradykinin, behaved as an agonist at the presynaptic site but as an antagonist at the muscular site. The most potent peptide analog to produce the neurogenic effect was Met-Lys-bradykinin followed by Lys-bradykinin and [Tyr8]-bradykinin. In contrast, the potency of these peptide analogs acting at the postsynaptic site was about the same. des Arg9 bradykinin and des Arg9-[Leu8]-bradykinin were inactive at the pre- and postjunctional site. The neurogenic action of bradykinin was not mimicked by angiotensin II, neurotensin, substance P or vasopressin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Prejunctional adrenergic receptors and sympathetic neurotransmission: studies in canine skeletal muscle vasculature in situ.

The effects of sympathetic nerve stimulation were studied in blood perfused canine skeletal muscle in situ. The overflow of NA and vasoconstriction, which represent pre- and postjunctional events in this vascular bed, were frequency-dependent and closely related to each other. Measurements of endogenous NA overflow were compared with a conventional radio-labelling technique using 3H-NA. Nerve stimulation evoked overflow of total radioactivity was recovered almost exclusively as 3H-NA. The relative changes of the nerve stimulation evoked overflow of endogenous NA and 3H-NA were much the same. The reproducibility was better for endogenous NA measurements than for the other two indices of transmitter release. Thus, endogenous NA overflow seems to provide a better measure of NA release. There was a preferential overflow of the newly stored radio-labelled transmitter, in agreement with earlier observations in vitro, showing that there is more than one compartment for NA storage in sympathetic nerve endings. Inhibition of neuronal uptake enhanced the nerve stimulation evoked overflow of NA and prolonged the vasoconstrictor response without influencing its amplitude. This would be consistent with a reduced clearance of the released transmitter without major alterations of the NA concentrations at the neuroeffector junction. Inhibition of prostaglandin synthesis did not influence nerve stimulation evoked NA overflow, suggesting that prostaglandin formation is of little importance for the modulation of NA release in this vascular bed. Postjunctional alpha-adrenoceptors of both subtypes may well contribute to the neurogenic control of vascular tone. Circulating catecholamines seem to be more important with regard to activation of the postjunctional alpha 2-adrenoceptors. Postjunctional beta 2-adrenoceptors are to all appearances activated principally by blood borne catecholamines. There was no evidence in favour of physiologically important neurogenic control of these receptors. Nerve stimulation evoked NA overflow was enhanced by alpha-adrenoceptor antagonists and reduced by alpha-adrenoceptor agonists. The findings lend further support to the suggested physiological role of prejunctional alpha 2-adrenoceptor mediated feed-back inhibition of NA release. There may also be a subset of prejunctional alpha 1-adrenoceptors involved in the modulation of sympathetic neurotransmission. The existence of a prejunctional facilitatory beta 2-adrenoceptor could be demonstrated, as stimulation of beta 2-adrenoceptors enhanced nerve stimulation evoked NA overflow.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1986

Spare alpha adrenoceptors in the peripheral circulation: excitation-contraction coupling.

Postsynaptic alpha adrenoceptors in arteries and veins represent a mixed population of alpha 1 and alpha 2 adrenoceptors, with both subtypes mediating vasoconstriction. In the peripheral arterial circulation, postsynaptic vascular alpha 1 adrenoceptors are found in the adrenergic neuroeffector junction, whereas postsynaptic vascular alpha 2 adrenoceptors are located extrajunctionally. In the venous circulation, it appears that alpha 2 adrenoceptors may be predominantly junctional, whereas alpha 1 adrenoceptors may be predominantly extrajunctional. In general, alpha 1 adrenoceptors play a more important functional role in arteries than in veins, with the converse being true for postsynaptic vascular alpha 2 adrenoceptors. The relationship between alpha-adrenoceptor occupancy and vasoconstrictor response is more favorable for postsynaptic vascular alpha 1 adrenoceptors than for alpha 2 adrenoceptors in both arteries and veins, and there is evidence for a receptor reserve in alpha 1 adrenoceptors in both the arterial and venous circulation. No reserve in postsynaptic vascular alpha 2 adrenoceptors is seen in the arterial circulation, but in isolated venous preparations, a reserve in alpha 2 adrenoceptors has been observed. It has been suggested that spare alpha 2 adrenoceptors found in veins, but not arteries, may be responsible, at least in part, for the exaggerated alpha 2-adrenoceptor-mediated response of veins relative to arteries.

Animals↗
PubMed1986

Increased norepinephrine release from dog pulmonary artery caused by nitrous oxide.

The effects of nitrous oxide on the release and metabolism of norepinephrine (NE) at neuroeffector junctions in dog pulmonary artery were examined. Helical strips of artery were incubated in Krebs-Ringer solution containing L-(3H)NE and mounted for superfusion. The arterial strips were studied in the presence of 95% oxygen-5% carbon dioxide, 70% nitrogen-30% oxygen, or 70% nitrous oxide-30% oxygen. During the 60 min of each experiment, five samples of superfusion fluid were collected for analysis and the effluxes of (3H)NE and its radiolabeled metabolites were measured before and during electrical stimulation and during recovery from stimulation. (3H)Norepinephrine was separated from its metabolites in the superfusate and in extracts of artery by column chromatography and quantitated by liquid scintillation spectrometry. Nitrous oxide significantly increased the fractional loss of total radioactivity and the amount of NE in the superfusate both during resting conditions and during stimulation. Nitrous oxide had no effect on the proportions of radioactivity among metabolites of NE in the superfusate or on the profile of NE metabolites remaining in the tissue after experimentation. These findings are consistent with increased NE release as a direct effect of nitrous oxide on nerve endings.

Animals↗
PubMed1983

The effects of morphine, nalbuphine, and butorphanol on adrenergic function in canine saphenous veins.

Saphenous vein rings mounted in organ chambers containing Krebs-Ringer solution were used to determine if the venodilator effects of morphine, nalbuphine, and butorphanol are the result of interference with adrenergic neurotransmission or are caused by direct depressant actions on venous smooth muscle cells. Morphine (5 X 10(-5) M and 2 X 10(-4) M) caused a dose-dependent depression of the contractile response to transmural electrical stimulation. H1- and H2- histamine antagonists did not attenuate the inhibitory effect of morphine. Concentrations of morphine and nalbuphine lower than 5 X 10(-5) M had no effect, whereas 5 X 10(-6) M butorphanol significantly depressed the evoked tension response to electrical stimulation. The contractile responses of the veins to exogenous norepinephrine (NE) were not altered by morphine, indicating a presynaptic site of action rather than a direct action on the venous smooth muscle. Transmural electrical stimulation was used to evoke release of endogenous NE. Morphine (5 X 10(-5) M and 2 X 10(-4) M), nalbuphine (2 X 10(-4) M), and butorphanol (4 X 10(-6) M) significantly decreased release of NE. Naloxone did not alter NE release and did not attenuate the inhibition of NE release observed with the opiates, indicating that the effect of morphine on this neuroeffector junction is not mediated by a naloxone-sensitive opiate receptor. Blockade of presynaptic alpha receptors by phenoxybenzamine or phentolamine augments NE release caused by transmural electrical stimulation; morphine inhibited this augmentation. The results of these experiments indicate that high concentrations of morphine may decrease NE release, an effect that may contribute to the venodilation and hypotension observed following administration of high doses of morphine in humans. In the usual analgesic doses, the venodilatory effects of morphine cannot be explained by local action on either NE release or venous smooth muscle contractility.

Adrenergic alpha-Antagonists↗
PubMed1981

Postsynaptic alpha adrenergic receptor subtypes differentiated by yohimbine in tissues from the rat. Existence of alpha-2 adrenergic receptors in rat aorta.

The selective alpha-2 adrenergic receptor antagonist, yohimbine, was used to differentiate postsynaptic alpha-adrenergic receptors in five peripheral tissues of the rat. Three distinct postsynaptic receptor subtypes were observed based on the affinity of the receptors for yohimbine. Receptors with high affinity for yohimbine were detected in the aorta, whereas low affinity receptors were observed in the vas deferens. The affinity for yohimbine in these two tissues differed by over 50-fold. Receptors with intermediate affinity for yohimbine were found in the portal vein, spleen and bladder. The Schild plot for yohimbine in the bladder suggests that blockade of alpha receptors in this tissue is not competitive or that there exists more than one type of alpha-adrenergic receptor present. Comparison of the dissociation constant of yohimbine in the aorta with dissociation constants obtained from the literature for this compound in a variety of tissues containing alpha-1 or alpha-2 adrenergic receptors indicates that the postsynaptic alpha adrenergic receptor in the aorta is of the alpha-2 type. Conversely, the postsynaptic alpha adrenergic receptor in the portal vein appears to be alpha-1. The differences in postsynaptic alpha appears to be alpha-1. The differences in postsynaptic alpha adrenergic receptors in these two vascular tissues may reflect the marked differences in adrenergic innervation and the possible relative lack of neuroeffector junctional alpha adrenergic receptors in the rat aorta.

Animals↗
PubMed1983

Alpha adrenergic receptor subtypes in human, monkey and dog cerebral arteries.

In helical strips of human and monkey cerebral arteries, norepinephrine produced a greater contraction than that in dog cerebral arteries. In monkey cerebral arteries, phenylephrine and norepinephrine produced a similar magnitude of maximum contractions, although the ED50 value of phenylephrine was approximately 5.6 times greater than that of norepinephrine. Clonidine (up to 10(-5) M) did not produce contractions. Dog cerebral arteries responded to phenylephrine in high concentrations with a greater contraction than that induced by norepinephrine and to clonidine with significant contractions. Contractions induced by norepinephrine of human and monkey cerebral arteries were attenuated by low concentrations of prazosin but were not influenced by yohimbine in concentrations up to 10(-8) M. In contrast, norepinephrine-induced contractions of dog cerebral arteries were attenuated by yohimbine but were unaffected by prazosin. It appears that norepinephrine-induced contractions are mediated by alpha-2 adrenoceptors in dog cerebral arteries and by alpha-1 receptors in human and monkey cerebral arteries as well as monkey and dog mesenteric arteries. The relative unresponsiveness of monkey and dog cerebral arteries to adrenergic nerve stimulation may not be explained by a paucity of alpha adrenoceptors in neuroeffector junction.

Adolescent↗
PubMed1984

Accumulation, subcellular localization and release of propranolol from synaptosomes of rat cerebral cortex.

Propranolol is accumulated at several adrenergic neuroeffector junctions after chronic oral administration in the dog, and is released subsequently during sympathetic nerve stimulation. In the present study, the accumulation, subcellular localization and release of propranolol was examined in rat cortical synaptosomes. Synaptosomal propranolol accumulation was rapid and attained equilibrium within 1 min. Propranolol uptake increased in a nonlinear manner with increasing drug concentration in the medium, but could not be fully saturated over the concentration range studied (10(-7) - 10(-3) M). Uptake was unaffected by cocaine or ouabain and showed no stereoselectivity. Subsynaptosomal fractionation of propranolol-loaded synaptosomes revealed that the drug was concentrated principally in fractions enriched in synaptic plasma membranes and synaptic storage vesicles. Exposure of propranolol-loaded synaptosomes to elevated potassium evoked a concentration-dependent increase in propranolol overflow, which was not seen in mitochondrial fractions, myelin fractions or in freeze-thawed synaptosomal preparations. Veratridine was also effective in promoting propranolol overflow in a concentration-dependent manner. The increase in propranolol overflow induced by elevated potassium was significantly reduced, but not completely inhibited, in a calcium-free, ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid-supplemented medium. These results indicate that propranolol may be accumulated by neuronal tissue and stored at sites from which release may occur in response to depolarizing stimuli. The data further suggest that propranolol release in the synaptosome preparation may occur by both calcium-dependent and calcium-independent processes.

Animals↗
PubMed1978

Paralytic action of manganese in the dog.

Manganese is reported to interfere with transmitter release at a number of neuroeffector junctions. This effect is apparently related to competition between manganese and calcium for sites on the prejunctional terminals. Thus manganese can block the entry of calcium into the prejunctional terminals, an essential step in the excitation-secretion process. 5-Hydroxytryptamine, epinephrine, neostigmine, potassium chloride and calcium chloride have been investigated with respect to antagonism to partial paralysis induced with manganese chloride in canine peronealtibialis anterior, nerve-muscle preparations. Close intra-arterial injection of any of these substances manifested some degree of antagonism to manganese partial paralysis. Calcium was found to be the most effective antagonist. Post-tetanic facilitation was demonstrated during partial manganese block. Manganese was found to be seven times more effective than magnesium in producing paralysis.

Animals↗
PubMed1983

Nicotine stimulates secretion of both catecholamines and acetylcholinesterase from cultured adrenal chromaffin cells.

There is conflicting evidence from studies on sympathetic ganglia and the adrenal medulla concerning the morphological and biochemical localization and physiological role(s) of the enzyme acetylcholinesterase (AChE). Furthermore, the origin of the AChE released from the adrenal medulla (whether from chromaffin cells or splanchnic nerve, or both) has not been firmly established. We have examined the efficacy of cholinergic agonists to release endogenous AChE and catecholamines (CA) from monolayer cultures of purified bovine adrenal chromaffin cells. The nicotinic agonist (nicotine), but not the muscarinic agonist (methacholine), released both AChE and CA from the adrenal chromaffin cells. The concomitant release of CA and AChE evoked by nicotine was Ca++ dependent with a correlation coefficient r = 0.82 (p less than 0.001). The results show that adrenal chromaffin cells in vitro, a system free of splanchnic nerve elements, can still release AChE. The finding that concomitant release of AChE and catecholamines occurs on exposure of the cells to nicotinic agonists suggests that released AChE may have a physiological role at neuroeffector junctions.

Acetylcholinesterase↗
PubMedDate not supplied

The nitrergic transmitter of the anococcygeus--NO or not?

Nonadrenergic noncholinergic (NANC) relaxations of the anococcygeus muscle are reduced by inhibitors of nitric oxide synthase (NOS). Since NOS can be detected within 6-hydroxydodpamine-resistant nerve tracts running through the muscle, it seems clear that these NANC relaxations result from activation of the L-arginine/NO pathway within the prejunctional nerve terminal, an example of so-called "nitrergic" transmission. However, a number of substances (hydroquinone, superoxide anions, hydroxocobalamin) profoundly reduce relaxations to exogenous NO but do not affect those to nitrergic field stimulation; such observations have raised questions over the nature of the substance actually released from the nitrergic nerves. Several possible explanations are discussed: (1) NO is released attached to a carrier molecule, perhaps in the form of a nitrosothiol; (2) NO is released in a modified redox form; (3) NO is released as a free radical, but is protected within the neuroeffector junction by other substances which preferentially interact with scavenger molecules; and (4) NO is released as a free radical and, because of a rapid and unhindered rate of diffusion over short distances (100-200 microM), it is less susceptible than exogenous NO to scavenger molecules. As yet, there is insufficient experimental evidence to decide which, if any, of these explanations is correct.

Amino Acid Oxidoreductases↗
PubMed1993

[Neuronal control and neuroeffector transmission to regulate cardiac functions].

Major advances have been made that make it necessary to revise our thinking about the mechanisms of neuronal control to regulate cardiac functions, and that have implications for our understanding of cardiac diseases and their treatment. These advances include: function-specific pathways, co-transmitters, neuromodulators, sensory-efferent functions, changes in expression of autonomic nerves, neuroeffector junctions, and subtypes of neurotransmitter receptors. Studies of the molecular structure of the superfamily of the cation amine receptors have revealed that there might be a common ancestral G-protein coupled receptor to be derived from. Although noradrenaline effectively stimulates alpha 1- and alpha 2-adrenoceptors, they are completely different as a beta-adrenoceptors subfamily. The possible subtypes of beta 1-adrenoceptors are discussed in relation with the treatment of cardiac failure.

Autonomic Nervous System↗
PubMed1997

BIBP 3226, suramin and prazosin identify neuropeptide Y, adenosine 5'-triphosphate and noradrenaline as sympathetic cotransmitters in the rat arterial mesenteric bed.

The physiological role of neuropeptide Y (NPY) and extracellular adenosine 5'-triphosphate (ATP) in sympathetic neurotransmission is becoming increasingly clear. To assess whether NPY and ATP act as cotransmitters together with noradrenaline (NA) in the sympathetic nerves of the superior mesenteric artery, the changes in perfusion pressure of the arterial mesenteric bed caused by nerve stimulation were recorded. Depolarization of the perivascular superior mesenteric arterial nerves caused frequency- and time-dependent increases in the perfusion pressure that were abolished by guanethidine, which implied the sympathetic origin of these responses. Independent perfusion with either 500 nM BIBP 3226, an NPY Y1 antagonist; 3 microM suramin, a competitive purinoceptor antagonist; or 0.1 nM prazosin, a competitive alpha-1 adrenoceptor antagonist, evoked approximately a 30% reduction in the rise in perfusion pressure caused by the 20- to 30-Hz electrical depolarization of the perimesenteric arterial nerves. Prazosin (0.1 nM) blocked the increases in perfusion pressure caused by electrical stimulation of the perimesenteric nerves but did not significantly reduce the vasomotor effect of exogenous NA. Likewise, 5-methyl urapidil and chloroethylclonidine, alpha-1 adrenoceptor antagonists with selectivity for the alpha-1A and alpha-1B receptor subtypes, respectively, concentration-dependently decreased the increase in perfusion pressure elicited by electrical stimulation of the perimesenteric nerves at concentrations lower than that required to block the vasoconstriction elicited by exogenous NA. The combined perfusion of 3 microM suramin plus 0.1 nM prazosin did not result in a complete inhibition of the physiological response. Only upon the simultaneous application of BIBP plus suramin plus prazosin was the rise in perfusion pressure abolished. These results support the working hypothesis that the sympathetic nerves of the rat mesenteric bed release NPY, ATP and NA that act as postjunctional cotransmitters in this neuroeffector junction.

Adenosine Triphosphate↗
PubMed1992

Reduced junctional permeability at interrhombomeric boundaries.

Intercellular communication is considered to have a role during pattern specification processes in early embryonic development. This report analyzes the changing gap junctional communication properties of chick neuroepithelial cells depending on their position relative to the segmental partitions of the rhombencephalon. Intercellular electrical coupling and dye transfer were studied with microelectrode techniques. Neuroepithelial cells were electrically coupled irrespective of their location relative to interneuromeric boundaries. Iontophoretic injection of biocytin or Lucifer Yellow into single cells inside the rhombomeres was followed by transjunctional diffusion to the surrounding cells. In contrast, dye transfer was strictly limited when the diffusion zone contacted the cells forming the interneuromeric limits. Label injected into the boundary cells did not spread to other cells at all. Avian interrhombomeric boundaries are thus sites of reduced junctional permeability during early morphogenesis.

Animals↗
PubMed1972

A new example of a morphine-sensitive neuro-effector junction: adrenergic transmission in the mouse vas deferens.

The isolated mouse vas deferens possesses an adrenergic excitatory motor innervation which can be inhibited by low concentrations of morphine (ID50=0.5 muM). This effect of morphine is mediated by specific receptors which are blocked by naloxone. Activation of the morphine receptors inhibits noradrenaline release. It is concluded that adrenergic neurotransmission in the mouse vas deferens differs in some important way from that at the more common, morphine-insensitive, adrenergic junctions.

Animals↗