Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neuroeffector Junction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed2004

Critical role for the alpha-1B adrenergic receptor at the sympathetic neuroeffector junction.

The alpha-1 adrenergic receptors (alpha(1)ARs) are critical in sympathetically mediated vasoconstriction. The specific role of each alpha(1)AR subtype in regulating vasoconstriction remains highly controversial. Limited pharmacological studies suggest that differential alpha(1)AR responses may be the result of differential activation of junctional versus extrajunctional receptors. We tested the hypothesis that the alpha(1B)AR subtype is critical in mediating sympathetic junctional neurotransmission. We measured in vivo integrated cardiovascular responses to a hypotensive stimulus (induced via transient bilateral carotid occlusion [TBCO]) in alpha(1B)AR knockout (KO) mice and their wild-type (WT) littermates. In WT mice, after dissection of the carotid arteries and denervation of aortic baroreceptor buffering nerves, TBCO produced significant pressor and positive inotropic effects. Both responses were markedly attenuated in alpha(1B)AR KO mice (change systolic blood pressure 46+/-8 versus 11+/-2 mm Hg; percentage change in the end-systolic pressure-volume relationship [ESPVR] 36+/-7% versus 12+/-2%; WT versus KO; P<0.003). In vitro alpha(1)AR mesenteric microvascular contractile responses to endogenous norepinephrine (NE; elicited by electrical field stimulation 10 Hz) was markedly depressed in alpha(1B)AR KO mice compared with WT (12.4+/-1.7% versus 21.5+/-1.2%; P<0.001). In contrast, responses to exogenous NE were similar in alpha(1B)AR KO and WT mice (22.4+/-7.3% versus 33.4+/-4.3%; NS). Collectively, these results demonstrate a critical role for the alpha(1B)AR in baroreceptor-mediated adrenergic signaling at the vascular neuroeffector junction. Moreover, alpha(1B)ARs modulate inotropic responses to baroreceptor activation. The critical role for alpha(1B)AR in neuroeffector regulation of vascular tone and myocardial contractility has profound clinical implications for designing therapies for orthostatic intolerance.

Animals↗
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↗
PubMed1995

Neuropeptide-Y-ATP interactions at the vascular sympathetic neuroeffector junction.

Neuropeptide Y (NPY) and ATP are considered cotransmitters with norepinephrine (NE) in sympathetic neurons innervating some blood vessels, including those of the mesentery. A prominent action of NPY is to potentiate the postjunctional contractile effect of NE as well as that of other vasoactive agents. We wished to investigate whether NPY also potentiates the contractile effect of ATP and, if so, to determine which receptor subtype mediates such an effect. The effect of NPY, the NPY-Y1-selective agent Leu31Pro34 NPY, and the NPY-Y2-selective fragment NPY 14-36 on the increase in perfusion pressure produced by ATP was examined in rat perfused mesenteric arterial bed. Results demonstrated that both NPY and Leu31Pro34 NPY but not NPY 14-36 potentiated the increase in perfusion pressure produced by ATP. These results suggest that NPY acts on Y1 receptors to enhance the postjunctional response of ATP. The putative NPY antagonist PYX2, but not the putative antagonists benextramine or PYX1, attenuated the effect of NPY, indicating that PYX2 acts as an NPY antagonist in this system. A major action of NPY is to enhance the postjunctional response of both cotransmitters, ATP and NE at the vascular sympathetic neuroeffector junction in the mesenteric arterial bed, and this may be mediated by NPY-Y1 receptors.

Adenosine Triphosphate↗
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↗
PubMed1985

The parasympathetic neuroeffector junction of the heart.

This review has directed attention to the anatomical, biochemical, physiological, and pharmacological features of cardiac parasympathetic neuroeffector transmission. The relationships among these properties have permitted a synthesis of the operation of the parasympathetic nervous system at the subcellular, cellular, tissue, and organ level in the heart. However, the attempt to obtain a comprehensive model of parasympathetic neuroeffector transmission in the heart has not only unmasked many features of junctional activity that are poorly understood, but also indicated significant gaps between in vitro and in vivo experimental situations.

Acetylcholine↗
PubMed1991

An electrophysiological study of the actions of angiotensin II at the sympathetic neuroeffector junction in the guinea-pig vas deferens.

1. The effects of angiotensin II on sympathetic neuroeffector transmission in the guinea-pig vas deferens have been investigated by the use of intracellular and focal extracellular recording techniques to measure indirectly, the release of adenosine 5'-triphosphate (ATP). 2. Angiotensin II (10-100 nM) did not alter the amplitude of the first excitatory junction potential (e.j.p.) in a train but increased the amplitude of subsequent e.j.ps. There was a corresponding increase in the probability of occurrence of extracellularly recorded evoked excitatory junction currents (e.j.cs). Spontaneous quantal transmitter release was unaffected by angiotensin II. 3. The enhancement of transmitter release produced by angiotensin II was prevented by the angiotensin receptor antagonist, saralasin. 4. The increase in transmitter release produced by angiotensin II was due to an increase in the probability of transmitter release from individual varicosities and not due to any detectable change in the configuration of the nerve terminal impulse or to the induction of repetitive firing. 5. There was no overall enhancement of e.j.ps or e.j.cs by angiotensin II in reserpinized tissues. Surprisingly, the predominant effect of angiotensin II in reserpinized vasa deferentia was to inhibit evoked transmitter release, an effect reversed by indomethacin (3 microM). 6. The results show that angiotensin II increases the release of sympathetic transmitter by activating prejunctional angiotensin II receptors. However, when the co-transmitter noradrenaline was depleted, angiotensin II now inhibited transmitter release indirectly, presumably by stimulating prostaglandin formation in the smooth muscle cells which then inhibited release transjunctionally.

Angiotensin II↗
PubMed1988

Time course of transmitter action at the sympathetic neuroeffector junction in rodent vascular and non-vascular smooth muscle.

1. Transmitter release from sympathetic postganglionic nerve terminals innervating the guinea-pig and mouse vas deferens and the rat tail artery has been studied in vitro by focal extracellular recording with particular emphasis on the time course of transmitter action underlying the intracellular potential changes. 2. In the absence of stimulation, spontaneous excitatory junction currents (SEJCs) were recorded with amplitudes up to 500 microV and durations between 40 and 100 ms. SEJCs were unaffected by the competitive alpha-adrenoceptor antagonist prazosin but blocked by alpha, beta-methylene ATP which desensitizes P2-purinoceptors. 3. During trains of supramaximal stimuli at 0.1-4 Hz stimulus locked excitatory junction currents (EJCs) were evoked intermittently from the population of varicosities located under the suction electrode. 4. SEJCs were similar in amplitude and time course to EJCs evoked by low-frequency stimulation in the same attachment in all three tissues. 5. SEJCs recorded using either a conventional AC amplifier or a patch clamp amplifier had the same time course. 6. These studies show that the time course of the current underlying the excitatory junction potential is brief and essentially the same in three different tissues. The prolonged time course of the excitatory junction potential in different tissues can be accounted for by the passive membrane properties.

Action Potentials↗