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At least 19 recordsLinked to original sources
PubMed1989

Simulation of the diffusion of acetylcholine in the neuroeffector junctions of the sinus node.

Traditionally, the diffusion of acetylcholine (ACh) from a neuron to cardiac muscle in a neuroeffector junction has been modeled as radial diffusion from a nerve ending into a spherical homogeneous medium. Various microscopic structures in the heart may or may not influence the spatial distribution of ACh within neuroeffector junctions. To determine the effect of microscopic anatomy on the diffusion of ACh in neuroeffector junctions, we simulated the diffusion of ACh in a two-dimensional inhomogeneous geometry that was based on micrographs of neuroeffector junctions in the sinus node. ACh was released at sites adjacent to a neuron. Simulations showed that the times of peak concentration after release and the peak concentrations per se were distributed symmetrically above and below and to the right and left of the neuron, but not radially about the neuron. We conclude that the diffusion of ACh in the neuroeffector junctions of the sinus node cannot be predicted well by a mathematical model that assumes radial diffusion in a spherical and homogeneous medium.

Acetylcholine↗
PubMed1984

Estimation of intrasynaptic norepinephrine concentrations at vascular neuroeffector junctions in vivo.

We estimated vascular neuroeffector junctional norepinephrine concentrations and their relation to pressor responses by measuring plasma norepinephrine levels and blood pressure during sympathetic stimulation or norepinephrine infusion in pithed, vagotomized, alpha 2-adrenoceptor blocked, adrenal-demedullated rats with and without uptake1 blockade by desipramine. For an increment in mean arterial pressure of 50 mm Hg, the estimated mean junctional norepinephrine concentration ( ES50m ) was about 7 nmol/l. Norepinephrine concentration gradients between the site of norepinephrine release and plasma appeared to be equal and reciprocal for sympathetic stimulation and for norepinephrine infusion. These gradients were reduced equally (by about two-thirds) after desipramine treatment, indicating that removal of both released and infused norepinephrine is mainly by neuronal uptake.

Animals↗
PubMed1990

Effects of endothelin on neuroeffector junction in mesenteric arteries of hypertensive rats.

The effect of endothelin, a novel vasoconstrictor peptide, on the adrenergic neuroeffector junction was investigated in isolated perfused mesenteric arteries of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. The vasoconstrictor responses to periarterial sympathetic nerve stimulation and exogenous norepinephrine were determined. Infusion of endothelin-1 increased the baseline perfusion pressure dose dependently to similar extents in the two strains. A subpressor dose of endothelin-1 (10(-10) M) enhanced the pressor response to norepinephrine; its effect was greater in WKY rats than in SHR. Endothelin-1 (10(-12) to 10(-10) M) attenuated the pressor response to sympathetic nerve stimulation, and the degree of inhibition tended to be less in SHR than in WKY rats. Higher doses (3 x 10(-10) and 10(-9) M) of endothelin-1 enhanced the pressor response to nerve stimulation in both WKY rats and SHR. Endothelin-1 inhibited norepinephrine release from rat mesenteric arteries; the inhibition was significantly less in SHR than in WKY rats. These results suggest that endothelin enhances the responsiveness of alpha-adrenergic receptors to catecholamines, whereas it inhibits presynaptic adrenergic neurotransmission. Thus, endothelin can interact with the neuroeffector junction in addition to having a vasoconstricting effect in peripheral vessels. The difference in the mode of modulation by endothelin at the vascular neuroeffector junction in SHR from that in WKY rats might explain the maintenance of hypertension.

Animals↗
PubMed1989

Actions of endothelin on adrenergic neuroeffector junction.

The effect of endothelin, a novel vasoconstrictor peptide, on the adrenergic neuroeffector junction was investigated in isolated perfused rat mesenteric arteries. The vasoconstrictor responses to periarterial nerve stimulation and exogenous noradrenaline were determined. Infusion of endothelin-1 (10(-14) to 10(-8) mol/l) increased the baseline perfusion pressure dose dependently. Subpressor doses of endothelin-1 (10(-11) and 10(-10) mol/l) enhanced the pressor response to noradrenaline, and 10(-12) to 10(-10) mol/l endothelin-1 attenuated the pressor response to periarterial nerve stimulation. Endothelin-1 also caused a dose-dependent inhibition of [3H]-noradrenaline release during the periarterial nerve stimulation. However, higher doses of endothelin-1 (3 x 10(-10) to 10(-8) mol/l) enhanced the pressor response to stimulation. These results suggest that endothelin potentiates adrenergic vasoconstriction postjunctionally while it inhibits adrenergic neurotransmission. Thus endothelin may have actions on the neuroeffector junction in addition to its direct vasoconstricting effect.

Animals↗
PubMed1977

Autonomic neuroeffector junctions--reflex vasodilatation of the skin.

A general model of the autonomic neuroeffector junction is proposed. In this model, emphasis is placed on the muscle effector bundle with electrotonic coupling between individual cells via gap junctions (or nexuses) and en passage release of transmitter from autonomic nerve varicosities. This release results in transmission to effector cells across junctional clefts ranging from about 20 nm in the vas deferens and iris to as much as 2000 nm in some large arteries. The ultrastructural identification of different autonomic nerve types is described. Current theories on the synthesis, storage, release, and inactivation of transmitter during cholinergic, adrenergic, and purinergic transmission are summarized. Some speculations are made about the possible involvement of purinergic nerves in the innervation of vessels and mast cells in the skin, and whether this involvement results in a functional link between ATP, histamine, bradykinin, and prostaglandin in cutaneous vasodilatation. Another possibility considered as the basis for this reflex is the release of substance P from sensory (pain) nerve collaterals in the skin.

Acetylcholinesterase↗
PubMed1982

Effects of Mepivacaine on adrenergic neuroeffector junction of the isolated rabbit aorta.

The effect of mepivacaine on adrenergic neuroeffector junction was studied in the isolated rabbit aorta. Mepivacaine, 5 X 10(-5) to 5 X 10(-4) M, attenuated the contractile response to transmural neural stimulation, the attenuation being greater in the response at high frequency stimulations. The attenuation of the responses by mepivacaine was not prevented by prior application of cocaine. The concentration-response curve for norepinephrine was shifted to the right by mepivacaine, 5 X 10(-5) to 2 X 10(-3) M. The attenuation of the response to transmural stimulation was greater than that of the response to an equipotent concentration of exogenous norepinephrine. Pretreatment with mepivacaine, 5 X 10(-5) to 2 X 10(-3) M, protected alpha-adrenoceptors from persistent blockade by phenoxybenzamine in a dose-dependent manner. The contractile response to histamine was not significantly altered by mepivacaine in concentrations up to 5 X 10(-4) M. Mepivacaine, 5 X 10(-4) and 2 X 10(-3) M, decreased the response to high concentrations of KCl. Ca2+-induced contractions in aortic strips previously exposed to Ca2+-free media and depolarized by excess K+ were significantly inhibited by mepivacaine, 5 X 10(-4) and 2 X 10(-3) M. It may be concluded that mepivacaine causes vasodilation through an alpha-adrenoceptor antagonism in addition to a sympathetic nerve conduction blockade. High concentrations of mepivacaine appear to interfere with the transmembrane influx of calcium in the vascular smooth muscle.

Animals↗
PubMed1987

Alterations in the release of norepinephrine at the vascular neuroeffector junction in hypertension.

The field stimulation induced release of 3H-norepinephrine (NE) from the isolated portal vein and endogenous NE from the isolated caudal artery and perfused mesenteric arterial bed of spontaneously hypertensive rats (SHR) and age-matched normotensive rats (Wistar-Kyoto or Sprague-Dawley) was studied. There was a significantly greater release of NE from all three preparations obtained from 10- to 12-week-old SHR compared to normotensive animals. In addition, there was a greater release of NE from the caudal artery of 5- to 6-week-old SHR compared to controls. No differences were seen in the evoked release of NE from portal vein or caudal artery obtained from renal or DOCA salt hypertensives compared to vessels obtained from sham controls. Neuropeptide Y (NPY) produced a concentration-dependent decrease in the field stimulation induced release of NE from the perfused mesenteric artery. Low concentrations of NPY decreased while higher concentrations potentiated the increase in perfusion pressure. The NPY induced inhibition of evoked NE release was not altered by alpha 1- or alpha 2-adrenoceptor antagonists while the alpha 1-adrenoceptor antagonist, prazosin, prevented the postjunctional response. These results are consistent with there being an alteration of NE release at the vascular neuroeffector junction in SHR which may contribute to the development or maintenance of hypertension. NPY exerts a modulatory role in noradrenergic transmission at the vascular neuroeffector junction.

Animals↗
PubMed1981

In vitro studies on 6-fluoronoradrenaline at several peripheral sympathetic neuroeffector junctions.

A comparison of the effects of noradrenaline and 6-fluoronoradrenaline has been made at several peripheral sympathetic neuroeffector junctions. In the rat vas deferens preparation in the presence of 1 microM cocaine, 6-fluoronoradrenaline was found to be about 9 times more potent than noradrenaline as an agonist at presynaptic inhibitory alpha 2- adrenoceptors. In the rabbit aorta, 6-fluoronoradrenaline had approximately one tenth of the potency of noradrenaline in stimulating the postsynaptic alpha 1-adrenoceptors. Furthermore 6-fluoronoradrenaline, in contrast to previous reports, appears to be a substrate for the neuronal uptake process since exposure to cocaine potentiated the inhibition of the twitch response of the vas deferens by 6-fluoronoradrenaline. In addition, 6-fluoronoradrenaline increased the spontaneous outflow of radioactivity from rabbit pulmonary artery strips prelabelled with 3H-noradrenaline and this increase was blocked by cocaine (30 microM). These results demonstrate that 6-fluoronoradrenaline is a preferential alpha 2-adrenoceptor agonist which is a substrate for the neuronal uptake process in peripheral sympathetically innervated smooth muscle preparations.

Animals↗
PubMed1988

Fade responses at neuroeffector junction to vagal stimulation in the isolated, blood-perfused dog atrium.

Effects of physostigmine and of beating rate on the negative chronotropic and inotropic responses to tonic intramural parasympathetic nerve stimulation at a frequency of 5 Hz for 2 min were investigated, using the isolated, blood-perfused dog atrium which was pretreated with propranolol. The responses to stimulation reached a maximum, and then "faded" back toward the control levels during stimulation. Before physostigmine, the fade of the inotropic response was consistently observed but the fade of the chronotropic response was minimal. Both the maximum effect and the fade of the chronotropic response were augmented dose-dependently by physostigmine in spontaneously beating atria. Physostigmine increased the maximum chronotropic response to infusion of acetylcholine (ACh) but did not potentiate the fade response. These results suggest that the potentiation of the fade of the chronotropic response to stimulation after physostigmine is due to decreases in the amount of ACh at the neuroeffector junction. The maximum negative inotropic responses were dose-dependently potentiated similarly by physostigmine in isolated spontaneously beating or paced atria. The fade of the inotropic response in spontaneously beating atria was decreased along with reduction of the rate by physostigmine, whereas the fades in paced atria at 2 and 3 Hz were not changed, showing that decreases in rate during stimulation influenced the reduction of the fade. Increases in contractile force induced by infusion of CaCl2 did not alter the maximum and fade responses to stimulation in 2 Hz paced atria. The blood flow into an isolated atrium was not changed detectably during stimulation. These results suggest that the fade of the inotropic response to parasympathetic nerve stimulation is related subsidiarily to acetylcholinesterase or washout of ACh at the neuroeffector junction in isolated perfused atria.

Acetylcholine↗
PubMed1984

Facilitation at single release sites of a sympathetic neuroeffector junction in the mouse.

Electrophysiological techniques were used to observe the release of transmitter from one or a few release sites of the sympathetic neuroeffector junction of the mouse vas deferens. Release produces transient accelerations of the depolarizing phase of the excitatory junction potential, known as 'discrete events'. Discrete events associate into families at a constant latency and peak time, but vary in amplitude between a few preferred values. As facilitation develops there is a decrease in the frequency of small members of families and an increase in the frequency of large members, a change in apparent 'quantal content'. A similar change in amplitude distribution occurs when the [Ca]o is raised. The alpha-adrenoceptor antagonist yohimbine increases quantal content when facilitation has developed, but has no significant effect on unfacilitated discrete event amplitude unless the [Ca]o is below 2.0 mM. The alpha-adrenoceptor agonist clonidine reduces facilitated and unfacilitated quantal content under all conditions examined.

Action Potentials↗
PubMed1984

Effects of age on the adrenergic cardiac neuroeffector junction.

Although it is clear that adrenergic nervous system control of cardiac function decreases with age and that the effector organ fails to adjust to this decreased control, it is not completely evident which of the many mechanisms operant at the adrenergic-cardiac neuroeffector junction contribute to this state. Prejunctionally, it appears that norepinephrine content decreases with age and that adrenergic axonal degeneration occurs. Also, evidence is available to suggest that modulation by prejunctional alpha adrenergic receptors of norepinephrine release is altered with increasing age, as is neuronal uptake of norepinephrine. Postjunctionally, it appears that beta-adrenergic receptor sensitivity to agonists undergoes age-related alterations, and possibly post receptor mechanisms involved in receptor-response coupling. Other mechanisms, such as those involved in transmitter uptake into extraneuronal sites, adrenergic neuronal responsiveness to stimulation, transmitter release and turnover, calcium and prejunctional receptor modulation of transmitter release, postjunctional receptor development of supersensitivity or subsensitivity, need further elucidation in order to have an understanding of the factors that contribute to the breakdown of homeostatic mechanisms that regulate the heart.

Aging↗
PubMed1984

Intimacy of the neuroeffector junction and resistance to alpha-adrenoceptor-blockade of the neurogenic contractile response in vasa deferentia from guinea pig and rat.

The effect of phentolamine on the neurogenic contractile response in vasa deferentia from rat and guinea pig was studied during Wallerian degeneration. This response was also investigated after partial denervation (surgery or chemical sympathectomy by guanethidine treatment) in vasa deferentia from guinea pig. During Wallerian degeneration the response showed a gradual increase in sensitivity to phentolamine and was abolished in the late stages. The neurogenic contractile response of the partially denervated vas deferens was blocked by low concentrations of phentolamine. It is concluded that decreased intimacy of the neuroeffector junctions leads to increased susceptibility to alpha-adrenoceptor blockade of the contractile response to nerve stimulation. It is further concluded that the motor transmission in the vas deferens is essentially adrenergic. The resistance to alpha-adrenoceptor blockade of the initial phase of the contractile response to nerve stimulation of intact vasa deferentia from guinea pig and rat might well be explained by the "proximity theory" of Dale & Gaddum although participation of supplementary mediators cannot be excluded.

Adrenergic alpha-Antagonists↗
PubMed1986

Pre- and postjunctional alpha-adrenoceptors at sympathetic neuroeffector junction in bovine mesenteric lymphatics.

We studied isolated bovine mesenteric lymphatics to elucidate the pharmacological characteristics of pre- and postjunctional alpha-adrenoceptors at the sympathetic neuroeffector junction. Cylindrical strips were incubated with [3H]-noradrenaline and mounted for superfusion. Electrical stimulation (2 Hz, 0.5 msec, 50 V) augmented the fractional release of labeled noradrenaline. Exogenous noradrenaline and clonidine caused a depression of the evoked tracer release. Phenoxybenzamine and yohimbine markedly enhanced the evoked overflow of adrenergic transmitter. Rings of lymphatic vessels were mounted for isometric tension recording in organ chambers filled with Krebs-Ringer bicarbonate solution. The vessels contracted when exposed to phenylephrine and clonidine. The ED50 of clonidine was significantly lower than that of phenylephrine. Prazosin caused a parallel shift to the right of the dose-response curve to phenylephrine. The antagonist, however, suppressed the magnitude of the maximum response to clonidine. Yohimbine caused parallel shift to the right of the dose-response curves to phenylephrine and clonidine, respectively. The Schild plots for yohimbine demonstrated that the drug was a competitive antagonist to phenylephrine and clonidine. The pA2 value of yohimbine to clonidine (7.6 +/- 0.4) was larger than that to phenylephrine (6.2 +/- 0.4). The pA2 value of prazosin to phenylephrine was 7.2 +/- 0.3. These results suggest that prejunctional alpha-adrenoceptors are involved in the negative feedback mechanism for autoregulation of noradrenaline release during postganglionic sympathetic nerve stimulation, and that both alpha 1- and alpha 2-like adrenoceptors do exist on lymphatic smooth muscle cells.

Adrenergic Fibers↗
PubMed1992

Distribution of sympathetic neuroeffector junctions in the juxtaglomerular region of the rabbit kidney.

Two structurally distinct types of sympathetic axon (Type I and Type II) have recently been identified in the renal cortex of the rat and the rabbit. This study describes the distribution and density of the neuroeffector junctions made by these two types of axon on the different tissues from the juxtaglomerular region of the rabbit renal cortex. Immunohistochemical studies showed that tyrosine hydroxylase-positive axons were located only in regions adjacent to the arteries and arterioles in the renal cortex. Ultrastructural studies of the juxtaglomerular region indicated that both types of axon formed junctions on vascular smooth muscle cells, epithelial cells of proximal tubules and renin-secreting granular epithelioid cells. The density of neuromuscular junctions (18 x 10(3)/mm2 of vessel surface) was more than twice as high on the afferent arteriole as on the efferent arteriole or proximal tubules immediately adjacent to the glomerular arterioles (both about 6 x 10(3)/mm2). The junction density on granular epithelioid cells was much lower (about 2 x 10(3)/mm2) and were rarely observed on the distal tubule. Afferent arterioles preferentially received junctions from Type I axons at a relatively high density (14.2 x 10(3)/mm2) whereas junctions formed by Type II axons were less selectively distributed and occurred at lower densities on all other tissues (range, 1-6.3 x 10(3)/mm2). Presynaptic membrane specialisations were identified only at junctions on arterioles and granular epithelioid cells and occurred more frequently at Type I than at Type II junctions. The data suggest that the predominant effect of the sympathetic innervation in the juxtaglomerular region of the renal cortex is on the afferent arteriole and that the two axon types within the kidney may have different functions.

Animals↗
PubMed1986

Effects of neuropeptide Y (NPY) at the sympathetic neuroeffector junction. Can pre- and postjunctional receptors be distinguished?

Neuropeptide Y (NPY) is widely distributed in central and peripheral neurons. In sympathetic postganglionic neurons, NPY coexists with noradrenaline. NPY and its structural relative peptide YY (PYY) appear to exert three principally different effects at the sympathetic neuroeffector junction. Firstly, NPY has a direct postjunctional effect; this effect is manifested as a vasoconstriction when studied on the guinea pig iliac vein. Secondly, NPY has an indirect postjunctional effect in that it potentiates the response to various vasoconstrictors; this was studied on the rabbit femoral artery and vein, using noradrenaline and histamine, respectively, as vasoconstrictors. Thirdly, NPY acts prejunctionally in that it suppresses the release of noradrenaline from sympathetic nerve terminals; this was studied in the rat vas deferens. The aim of the investigation was to examine whether the three effects of NPY were mediated by the same type of receptor. For this purpose, we examined the effects of a series of NPY-related peptides, namely NPY, PYY, desamido-NPY, and five C-terminal fragments (NPY 19-36, NPY 24-36, PYY 13-36, PYY 24-36 and PYY 27-36). NPY and PYY were active in all three assay systems. The C-terminal amide appears to be crucial for maintaining the biological activity, since desamido-NPY was inactive in the three test systems. Interestingly, PYY 13-36 was almost as active as NPY and PYY in suppressing the electrically evoked contractions of the vas deferens; PYY 13-36 was inactive in the two other test systems. None of the shorter fragments had any biological activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Fibers↗
PubMed1992

Transmission at autonomic neuroeffector junctions.

For organs innervated by the autonomic nervous system, it is generally held that neuroeffector transmission is achieved by varicosities releasing transmitters some distance from the membranes of target cells. Transmitters are thought to diffuse through the extracellular space and interact with post-junctional receptors that are widely distributed over the cell membranes. This article presents an alternative view, suggesting that transmission can occur at organized neuroeffector contacts, that transmitters interact with restricted pools of specialized junctional receptors, and that many receptors on target cells are not involved in neuroeffector transmission.

Animals↗