Disease relevance of Neuroeffector Junction

• This study tested the hypothesis that interactions of endogenous angiotensin II (AII) with the noradrenergic neuroeffector junction are important in renin-dependent hypertension [1].

High impact information on Neuroeffector Junction

• SCL increased linearly with the frequency of simulated vagal stimulation, as it does in animal experiments, because the concentration of ACh in the neuroeffector junction [( ACh]) saturated as the frequency of stimulation was increased and because SCL increased geometrically in response to increases in [ACh] [2].
• We performed experiments to determine the effects of acetylstrophanthidin (ACS) and ouabain on the adrenergic neuroeffector junction in dog saphenous veins [3].
• 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 [4].
• Thus, endothelin can interact with the neuroeffector junction in addition to having a vasoconstricting effect in peripheral vessels [5].
• The excess available norepinephrine failed to increase myocardial contractility, suggesting a dysfunction at the cardiac adrenergic neuroeffector junction [6].

Biological context of Neuroeffector Junction

• Acetylcholine (ACh) kinetics in neuroeffector junctions (NEJ) of the sinus node plays a key role in vagal control of heart rate [7].

Anatomical context of Neuroeffector Junction

• The effects of thiopental sodium on the adrenergic neuroeffector junction were studied in isolated rabbit pulmonary arteries [8].
• 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 [9].
• We conclude that in human atrial and ventricular myocardium a sensitization to catecholamines is induced by halothane, the mechanism of which is likely to be located at the postsynaptic level of the sympathetic neuroeffector junction [10].
• Acetylcholine release at motor endplates and autonomic neuroeffector junctions: a comparison [11].
• 1. Acetylcholine, the principal neurotransmitter of the parasympathetic nervous system, is released at both ganglionic synapses and postganglionic neuroeffector junctions and acts by activation of nicotinic and muscarinic cholinoceptors [12].

Associations of Neuroeffector Junction with chemical compounds

• They are innervated, and there is convincing evidence that dopamine is a neurotransmitter at the neuroeffector junction controlling fluid secretion [13].
• Histamine mediation of nicotine effects on postganglionic sympathetic neuroeffector junctions [14].
• These results demonstrate that, in addition to being a direct vasodilatator, NO can also alter vascular reactivity at the sympathetic neuroeffector junction in the rat mesenteric bed by deactivating the vasoconstrictor norepinephrine [15].
• 4 This study indicates that bradykinin reduces the renal vascular reactivity to adrenergic stimuli and suggests that part of the action of the kinin at the vascular adrenergic neuroeffector junction in the rabbit kidney depends upon the biosynthesis of renal prostaglandins [16].
• An electrophysiological study of the actions of angiotensin II at the sympathetic neuroeffector junction in the guinea-pig vas deferens [17].

Gene context of Neuroeffector Junction

• 5. The presynaptic NPY receptor in hippocampal CA1 therefore shares an identical agonist profile with the presynaptic Y2 receptor at the peripheral sympathetic neuroeffector junction [18].
• NPY and PYY appear to exert three principally different effects at the level of the sympathetic neuroeffector junction [19].
• In conclusion, ET interacts with two different receptor types, ETA and non-ETA receptors (probably ETB) which exist post- and presynaptically at cholinergic neuroeffector junctions of the rat iris preparation [20].
• Effects of neuropeptide Y (NPY) at the sympathetic neuroeffector junction. Can pre- and postjunctional receptors be distinguished [21]?
• 5. The immunoblockade of exogenous and endogenous CGRP described here, together with complementary evidence from other studies, strongly suggest that CGRP has a major neurotransmitter role at the neuroeffector junction of the rat vas deferens [22].

Analytical, diagnostic and therapeutic context of Neuroeffector Junction

• Dopamine receptor protein immunohistochemistry confirmed the localization of dopamine D1 and D5 receptors in the tunica media of systemic arteries and of prejunctional dopamine D2-D4 receptors closely associated with sympathetic neuroeffector junctions [23].

References