The Experts below are selected from a list of 225 Experts worldwide ranked by ideXlab platform
Allen C. Myers - One of the best experts on this subject based on the ideXlab platform.
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A novel role for tachykinin neurokinin-3 receptors in regulation of human bronchial ganglia neurons
American Journal of Respiratory and Critical Care Medicine, 2004Co-Authors: Allen C. Myers, Roy G. Goldie, Douglas W. P. HayAbstract:The neuropeptide tachykinins and their receptors have been implicated in the pathogenesis of lung disease, although the role of the tachykinin neurokinin-3 receptor has not been elucidated. Using confocal microscopy, we identified tachykinin neurokinin-3 receptors on human bronchial Parasympathetic Ganglion neurons. Electrophysiologic recordings demonstrated that activation of sensory nerve fibers, either by antidromic stimulation or capsaicin, depolarized these neurons. This response was mimicked by exogenously applied tachykinin neurokinin-3 receptor–selective agonist, senktide analogue, but not significantly by tachykinin neurokinin-1 or neurokinin-2 receptor–selective agonists. Responses to endogenous tachykinins or exogenous selective tachykinin neurokinin-3 receptor activation with senktide analogue were inhibited by the selective tachykinin neurokinin-3 receptor antagonists, SB 223412 or SB 235375. We provide the first evidence that tachykinin neurokinin-3 receptors regulate human bronchial parasym...
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Role of cyclooxygenase activation and prostaglandins in antigen-induced excitability changes of bronchial Parasympathetic ganglia neurons.
American journal of physiology. Lung cellular and molecular physiology, 2003Co-Authors: Radhika Kajekar, Bradley J. Undem, Allen C. MyersAbstract:In vitro antigen challenge has multiple effects on the excitability of guinea pig bronchial Parasympathetic Ganglion neurons, including depolarization, causing phasic neurons to fire with a repetit...
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Effect of bradykinin on membrane properties of guinea pig bronchial Parasympathetic Ganglion neurons
American journal of physiology. Lung cellular and molecular physiology, 2000Co-Authors: Radhika Kajekar, Allen C. MyersAbstract:The effect of bradykinin on membrane properties of Parasympathetic Ganglion neurons in isolated guinea pig bronchial tissue was studied using intracellular recording techniques. Bradykinin (1–100 n...
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Anatomical and electrophysiological comparison of the sensory innervation of bronchial and tracheal Parasympathetic Ganglion neurons.
Journal of the autonomic nervous system, 1996Co-Authors: Allen C. Myers, Bradley J. Undem, Wolfgang KummerAbstract:Anatomical and electrophysiological techniques were used to examine differences in the level of sensory nerve terminals localized in Parasympathetic ganglia in guinea pig trachea and bronchus. We quantified substance-P-immunoreactive nerve terminal profiles within the ganglia and the amplitude of capsaicin-sensitive depolarization (slow excitatory postsynaptic potential or sEPSP) evoked by vagus (bronchial) or recurrent (tracheal) nerve-stimulation. Substance-P-immunoreactive axon profiles per intrinsic tracheal neuron were fewer in number than per bronchial Ganglion neuron. The average amplitude and duration of the capsaicin-sensitive sEPSPs were similar in tracheal and bronchial Ganglion neurons. Furthermore, capsaicin evoked a nearly equal depolarization of bronchial and tracheal Ganglion neurons. The sEPSPs were reduced in both areas by a selective neurokinin-3 receptor antagonist, SR142801. These results demonstrate that although the number of sensory nerve fibers in tracheal ganglia are significantly less than those in the bronchus, this did not translate to an obvious physiological difference in sEPSP amplitude.
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Antigen depolarizes guinea pig bronchial Parasympathetic Ganglion neurons by activation of histamine H1 receptors.
American Journal of Physiology-Lung Cellular and Molecular Physiology, 1995Co-Authors: Allen C. Myers, Bradley J. UndemAbstract:Myers, Allen C., and Bradley J. Undem. Antigen depolarizes guinea pig bronchial Parasympathetic Ganglion neurons by activation of histamine H 1 receptors. Am. J. Physiol. 268 (Lung Cell. Mol. Physiol. 12) : L879-L884, 1995.-Studies were carried out to evaluate the mechanism by which neurotransmission through airway Parasympathetic ganglia may be modulated during immediate hypersensitivity reactions. Guinea pigs were passively sensitized by injection of guinea pig serum containing high-titer anti-ovalbumin antibodies. Intracellular recordings were obtained from intrinsic Parasympathetic Ganglion neurons from the right mainstem bronchus in vitro. Ovalbumin (10 μg/ml) elicited a membrane potential depolarization and changes in membrane resistance in bronchial Ganglion neurons from passively sensitized guinea pigs. Histamine mimicked the depolarizing effect of ovalbumin in a concentration-dependent manner (0.1-10 μM) and caused a transient increase and decrease in membrane resistance. Pyrilamine, a histamine H 1 -receptor antagonist, inhibited the histamine-induced membrane depolarization and decrease in resistance. By contrast, blocking histamine H 2 and H 3 receptors did not inhibit histamine-induced depolarization. Pyrilamine also reduced the antigen-induced depolarization of Ganglion neurons, demonstrating a role for histamine H 1 receptors in this response. The data provide evidence that the antigen-induced depolarization of airway Ganglion neurons is secondary to an antigen-antibody interaction on intrinsic mast cells and the consequential effect of histamine on H 1 receptors. These studies demonstrate that histamine released during an immediate hypersensitivity reaction has direct effects on airway Parasympathetic nerves.
Janet R. Keast - One of the best experts on this subject based on the ideXlab platform.
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Structural effects and potential changes in growth factor signalling in penis-projecting autonomic neurons after axotomy
BMC neuroscience, 2006Co-Authors: Catalina A Palma, Janet R. KeastAbstract:Background The responses of adult Parasympathetic Ganglion neurons to injury and the neurotrophic mechanisms underlying their axonal regeneration are poorly understood. This is especially relevant to penis-projecting Parasympathetic neurons, which are vulnerable to injury during pelvic surgery such as prostatectomy. We investigated the changes in pelvic ganglia of adult male rats in the first week after unilateral cavernous (penile) nerve axotomy (cut or crush lesions). In some experiments FluoroGold was injected into the penis seven days prior to injury to allow later identification of penis-projecting neurons. Neurturin and glial cell line-derived neurotrophic factor (GDNF) are neurotrophic factors for penile Parasympathetic neurons, so we also examined expression of relevant receptors, GFRα1 and GFRα2, in injured pelvic Ganglion neurons.
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Neurturin has multiple neurotrophic effects on adult rat sacral Parasympathetic Ganglion neurons.
The European journal of neuroscience, 2005Co-Authors: Yewlan Wanigasekara, Janet R. KeastAbstract:Neurturin (NTN) is an important neurotrophic factor for Parasympathetic neurons; however, no studies to date have investigated the signalling mechanisms downstream of GFRα2 and Ret activation underlying this neurotrophic support. This is particularly important for pelvic Parasympathetic neurons, which are prone to injury during surgical procedures such as prostatectomy, and where there are no current therapies for axonal regeneration. To address this issue we have cultured dissociated adult rat pelvic Ganglion neurons and also examined the structural changes in pelvic Ganglion neurons after axotomy. Axotomised penile neurons deprived of target-derived support had smaller somata than intact neurons. Studies of cultured adult pelvic Ganglion neurons also demonstrated that NTN stimulated soma growth. Further experiments showed that NTN reduced the up-regulation of tyrosine hydroxylase expression in cultured pelvic Parasympathetic neurons. NTN stimulated the extension of neurites in cultured Parasympathetic, but not sympathetic, pelvic Ganglion neurons. Inhibition of phosphatidylinositol 3-kinase prevented initiation of neurite outgrowth, whereas inhibition of the mitogen-activated protein kinase and the Src family kinase pathways disrupted NTN-stimulated microtubule assembly. Surprisingly, NTN did not activate the transcription factor cAMP-response element binding protein (CREB), which is typically involved in neurotrophic signalling in sympathetic neurons. This is the first study to identify signalling pathways activated by NTN in adult Parasympathetic neurons. Our results may lead to a better understanding of regenerative mechanisms in Parasympathetic neurons, especially for those innervating urogenital organs. Our results also indicate that neurotrophic signalling in Parasympathetic neurons is different from that in other types of peripheral neurons.
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neurturin signalling via gfrα2 is essential for innervation of glandular but not muscle targets of sacral Parasympathetic Ganglion neurons
Molecular and Cellular Neuroscience, 2004Co-Authors: Y Wanigasekara, Matti S Airaksinen, Robert O Heuckeroth, Jeffrey Milbrandt, Janet R. KeastAbstract:Neurturin, a member of the glial cell-derived neurotrophic factor familys of ligands, is important for development of many cranial Parasympathetic Ganglion neurons. We have investigated the sacral component of the Parasympathetic nervous system in mice with gene deletions for neurturin or its preferred receptor, GFRα2. Disruption of neurturin signalling decreased cholinergic VIP innervation to the mucosa of the reproductive organs, but not to the smooth muscle layers of these organs or to the urinary bladder. Thus, neurturin and its receptor are involved in Parasympathetic innervation of a select group of pelvic visceral tissues. In contrast, noradrenergic innervation was not affected by the gene ablations. The epithelium of reproductive organs from knockout animals was atrophied, indicating that cholinergic innervation may be important for the maintenance of normal structure. Cholinergic neurons express GFRα2 on their terminals and somata, indicating they can respond to neurotrophic support, and their somata are smaller when neurturin signalling is disrupted. Colocalisation studies showed that many peripheral glia express GFRα2 although its role in these cells is yet to be determined. Our results indicate that neurturin, acting through GFRα2, is essential for Parasympathetic innervation of the mucosae of reproductive organs, as well as for maintenance of a broader group of sacral Parasympathetic neurons.
Bradley J. Undem - One of the best experts on this subject based on the ideXlab platform.
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Role of cyclooxygenase activation and prostaglandins in antigen-induced excitability changes of bronchial Parasympathetic ganglia neurons.
American journal of physiology. Lung cellular and molecular physiology, 2003Co-Authors: Radhika Kajekar, Bradley J. Undem, Allen C. MyersAbstract:In vitro antigen challenge has multiple effects on the excitability of guinea pig bronchial Parasympathetic Ganglion neurons, including depolarization, causing phasic neurons to fire with a repetit...
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Anatomical and electrophysiological comparison of the sensory innervation of bronchial and tracheal Parasympathetic Ganglion neurons.
Journal of the autonomic nervous system, 1996Co-Authors: Allen C. Myers, Bradley J. Undem, Wolfgang KummerAbstract:Anatomical and electrophysiological techniques were used to examine differences in the level of sensory nerve terminals localized in Parasympathetic ganglia in guinea pig trachea and bronchus. We quantified substance-P-immunoreactive nerve terminal profiles within the ganglia and the amplitude of capsaicin-sensitive depolarization (slow excitatory postsynaptic potential or sEPSP) evoked by vagus (bronchial) or recurrent (tracheal) nerve-stimulation. Substance-P-immunoreactive axon profiles per intrinsic tracheal neuron were fewer in number than per bronchial Ganglion neuron. The average amplitude and duration of the capsaicin-sensitive sEPSPs were similar in tracheal and bronchial Ganglion neurons. Furthermore, capsaicin evoked a nearly equal depolarization of bronchial and tracheal Ganglion neurons. The sEPSPs were reduced in both areas by a selective neurokinin-3 receptor antagonist, SR142801. These results demonstrate that although the number of sensory nerve fibers in tracheal ganglia are significantly less than those in the bronchus, this did not translate to an obvious physiological difference in sEPSP amplitude.
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Antigen depolarizes guinea pig bronchial Parasympathetic Ganglion neurons by activation of histamine H1 receptors.
American Journal of Physiology-Lung Cellular and Molecular Physiology, 1995Co-Authors: Allen C. Myers, Bradley J. UndemAbstract:Myers, Allen C., and Bradley J. Undem. Antigen depolarizes guinea pig bronchial Parasympathetic Ganglion neurons by activation of histamine H 1 receptors. Am. J. Physiol. 268 (Lung Cell. Mol. Physiol. 12) : L879-L884, 1995.-Studies were carried out to evaluate the mechanism by which neurotransmission through airway Parasympathetic ganglia may be modulated during immediate hypersensitivity reactions. Guinea pigs were passively sensitized by injection of guinea pig serum containing high-titer anti-ovalbumin antibodies. Intracellular recordings were obtained from intrinsic Parasympathetic Ganglion neurons from the right mainstem bronchus in vitro. Ovalbumin (10 μg/ml) elicited a membrane potential depolarization and changes in membrane resistance in bronchial Ganglion neurons from passively sensitized guinea pigs. Histamine mimicked the depolarizing effect of ovalbumin in a concentration-dependent manner (0.1-10 μM) and caused a transient increase and decrease in membrane resistance. Pyrilamine, a histamine H 1 -receptor antagonist, inhibited the histamine-induced membrane depolarization and decrease in resistance. By contrast, blocking histamine H 2 and H 3 receptors did not inhibit histamine-induced depolarization. Pyrilamine also reduced the antigen-induced depolarization of Ganglion neurons, demonstrating a role for histamine H 1 receptors in this response. The data provide evidence that the antigen-induced depolarization of airway Ganglion neurons is secondary to an antigen-antibody interaction on intrinsic mast cells and the consequential effect of histamine on H 1 receptors. These studies demonstrate that histamine released during an immediate hypersensitivity reaction has direct effects on airway Parasympathetic nerves.
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Antigen depolarizes guinea pig bronchial Parasympathetic Ganglion neurons by activation of histamine H1 receptors.
The American journal of physiology, 1995Co-Authors: A C Myers, Bradley J. UndemAbstract:Studies were carried out to evaluate the mechanism by which neurotransmission through airway Parasympathetic ganglia may be modulated during immediate hypersensitivity reactions. Guinea pigs were passively sensitized by injection of guinea pig serum containing high-titer anti-ovalbumin antibodies. Intracellular recordings were obtained from intrinsic Parasympathetic Ganglion neurons from the right mainstem bronchus in vitro. Ovalbumin (10 micrograms/ml) elicited a membrane potential depolarization and changes in membrane resistance in bronchial Ganglion neurons from passively sensitized guinea pigs. Histamine mimicked the depolarizing effect of ovalbumin in a concentration-dependent manner (0.1-10 microM) and caused a transient increase and decrease in membrane resistance. Pyrilamine, a histamine H1-receptor antagonist, inhibited the histamine-induced membrane depolarization and decrease in resistance. By contrast, blocking histamine H2 and H3 receptors did not inhibit histamine-induced depolarization. Pyrilamine also reduced the antigen-induced depolarization of Ganglion neurons, demonstrating a role for histamine H1 receptors in this response. The data provide evidence that the antigen-induced depolarization of airway Ganglion neurons is secondary to an antigen-antibody interaction on intrinsic mast cells and the consequential effect of histamine on H1 receptors. These studies demonstrate that histamine released during an immediate hypersensitivity reaction has direct effects on airway Parasympathetic nerves.
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Neurophysiology of Mast Cell-Nerve Interactions in the Airways
International archives of allergy and immunology, 1995Co-Authors: Bradley J. Undem, Margerita M. Riccio, Daniel Weinreich, James L. Ellis, Allen C. MyersAbstract:The sensitized guinea pig was employed as a model to study the effect of immunological activation of resident mast cells on neuronal activity in the airways. The trachea was isolated with the vagus nerves and vagal sensory ganglia intact. Using conventional electrophysiological recording techniques, we noted that antigenic stimulation led to an increase in the sensitivity of sensory nerve endings located in the airway wall. Moreover, previous work has revealed that antigen challenge potentiates action-potential-driven tachykinin release from afferent fibers in the guinea pig isolated airway. Anatomical and electrophysiological studies indicate that tachykinin-containing sensory fibers directly innervate the local Parasympathetic Ganglion neurons in the airway. Therefore, antigen-induced increases in the excitability of sensory fibers in the airways can increase Parasympathetic tone in the airway by increasing central and peripheral reflex arcs. In addition, we have found that antigen stimulation has direct effects on the excitability of the Parasympathetic Ganglion neurons. Considered together, the data demonstrate that increased vagal sensory and Parasympathetic activity may be a consequence of the allergic reaction in the airways.
Toshiko Kuchiiwa - One of the best experts on this subject based on the ideXlab platform.
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Morphological distinction between vasodilator and secretomotor neurons in the pterygopalatine Ganglion of the cat
Neuroscience letters, 2000Co-Authors: Satoshi Kuchiiwa, Shi-bin Cheng, Toshiko KuchiiwaAbstract:We investigated whether vasodilator and secretomotor Ganglion neurons are morphologically distinguishable from each other in the Parasympathetic Ganglion of the cat. When Cholera toxin B subunit, a retrograde tracer, was injected into the palatine gland, both large and small Ganglion neurons were retrogradely labeled in the pterygopalatine Ganglion. On the other hand, when the tracer was injected into gland-free areas (the upper gingiva or epidural space), all neurons labeled in the Ganglion were small in size. Thus, it was assumed that small and large neurons labeled in the Ganglion represented, respectively, vasomotor and secretomotor and neurons [corrected].
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morphological distinction between vasodilator and secretomotor neurons in the pterygopalatine Ganglion of the cat
Neuroscience Letters, 2000Co-Authors: Satoshi Kuchiiwa, Shi-bin Cheng, Toshiko KuchiiwaAbstract:We investigated whether vasodilator and secretomotor Ganglion neurons are morphologically distinguishable from each other in the Parasympathetic Ganglion of the cat. When Cholera toxin B subunit, a retrograde tracer, was injected into the palatine gland, both large and small Ganglion neurons were retrogradely labeled in the pterygopalatine Ganglion. On the other hand, when the tracer was injected into gland-free areas (the upper gingiva or epidural space), all neurons labeled in the Ganglion were small in size. Thus, it was assumed that small and large neurons labeled in the Ganglion represented, respectively, secretomotor and vasomotor neurons.
Torill Berg - One of the best experts on this subject based on the ideXlab platform.
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M-CURRENTS (Kv7.2-7.3/KCNQ2-KCNQ3) ARE RESPONSIBLE FOR DYSFUNCTIONAL AUTONOMIC CONTROL IN HYPERTENSIVE RATS
Frontiers Media S.A., 2016Co-Authors: Torill BergAbstract:Autonomic dysfunctions play important roles in hypertension, heart failure and arrhythmia, often with a detrimental and fatal effect. The present study analysed if these dysfunctions involved M-channels (members of the Kv7/KNCQ family) spontaneously hypertensive rats (SHR). Cardiac output and heart rate (HR) were recorded by a flow probe on the ascending aorta in anesthetized SHR and normotensive rats (WKY), and blood pressure (BP) by a femoral artery catheter. Total peripheral vascular resistance (TPR) was calculated. XE-991 (Kv7.1-7.4-inhibitor) reduced resting HR in WKY but only after reserpine in SHR. XE-991 increased TPR and BP baseline in both strains. Retigabine (Kv7.2-7.5-opener) reduced HR, TPR and BP, also after reserpine. Depolarization induced by 3,4-diaminopyridine (3,4-DAP), a voltage-sensitive K+ channel (Kv) inhibitor, activated release of both acetylcholine and norepinephrine, thus activating an initial, cholinergic bradycardia in SHR, followed by sustained, norepinephrine-dependant tachycardia in both strains. XE-991 augmented the initial 3,4-DAP-induced bradycardia and eliminated the late tachycardia in SHR, but not in WKY. The increased bradycardia was eliminated by hexamethonium and methoctramine (M2muscarinic receptor antagonist) but not reserpine. Retigabine eliminated the increased bradycardia observed in reserpinized SHR. XE-991 also increased 3,4-DAP-stimulated catecholamine release, but not after hexamethonium or reserpine. Conclusions: M-currents hampered Parasympathetic Ganglion excitation and, through that, vagal control of HR, in SHR but not WKY. M-currents also opposed catecholamine release in SHR but not in WKY. M-currents represented a vasodilatory component in resting TPR-control, with no strain-related difference detected. Excessive M-currents may represent the underlying cause of autonomic dysfunctions in hypertension
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Voltage-Sensitive K(+) Channels Inhibit Parasympathetic Ganglion Transmission and Vagal Control of Heart Rate in Hypertensive Rats.
Frontiers in neurology, 2015Co-Authors: Torill BergAbstract:Parasympathetic withdrawal plays an important role in the autonomic dysfunctions in hypertension. Since hyperpolarizing, voltage-sensitive K(+) channels (K V) hamper transmitter release, elevated K V-activity may explain the disturbed vagal control of heart rate (HR) in hypertension. Here, the K V inhibitor 3,4-diaminopyridine was used to demonstrate the impact of K V on autonomic HR control. Cardiac output and HR were recorded by a flow probe on the ascending aorta in anesthetized, normotensive (WKY), and spontaneously hypertensive rats (SHR), and blood pressure by a femoral artery catheter. 3,4-diaminopyridine induced an initial bradycardia, which was greater in SHR than in WKY, followed by sustained tachycardia in both strains. The initial bradycardia was eliminated by acetylcholine synthesis inhibitor (hemicholinium-3) and nicotinic receptor antagonist/Ganglion blocker (hexamethonium), and reversed to tachycardia by muscarinic receptor (mAchR) antagonist (atropine). The latter was abolished by sympatho-inhibition (reserpine). Reserpine also eliminated the late, 3,4-diaminopyridine-induced tachycardia in WKY, but induced a sustained atropine-sensitive bradycardia in SHR. Inhibition of the Parasympathetic component with hemicholinium-3, hexamethonium, or atropine enhanced the late tachycardia in SHR, whereas hexamethonium reduced the tachycardia in WKY. In conclusion, 3,4-diaminopyridine-induced acetylcholine release, and thus enhanced Parasympathetic Ganglion transmission, with subsequent mAchR activation and bradycardia. 3,4-diaminopyridine also activated tachycardia, initially by enhancing sympathetic Ganglion transmission, subsequently by activation of norepinephrine release from sympathetic nerve terminals. The 3,4-diaminopyridine-induced Parasympathetic activation was stronger and more sustained in SHR, demonstrating an enhanced inhibitory control of K V on Parasympathetic Ganglion transmission. This enhanced K V activity may explain the dysfunctional vagal HR control in SHR.
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voltage sensitive k channels inhibit Parasympathetic Ganglion transmission and vagal control of heart rate in hypertensive rats
Frontiers in Neurology, 2015Co-Authors: Torill BergAbstract:Parasympathetic withdrawal plays an important role in the autonomic dysfunctions in hypertension. Since hyperpolarizing, voltage-sensitive K(+) channels (K V) hamper transmitter release, elevated K V-activity may explain the disturbed vagal control of heart rate (HR) in hypertension. Here, the K V inhibitor 3,4-diaminopyridine was used to demonstrate the impact of K V on autonomic HR control. Cardiac output and HR were recorded by a flow probe on the ascending aorta in anesthetized, normotensive (WKY), and spontaneously hypertensive rats (SHR), and blood pressure by a femoral artery catheter. 3,4-diaminopyridine induced an initial bradycardia, which was greater in SHR than in WKY, followed by sustained tachycardia in both strains. The initial bradycardia was eliminated by acetylcholine synthesis inhibitor (hemicholinium-3) and nicotinic receptor antagonist/Ganglion blocker (hexamethonium), and reversed to tachycardia by muscarinic receptor (mAchR) antagonist (atropine). The latter was abolished by sympatho-inhibition (reserpine). Reserpine also eliminated the late, 3,4-diaminopyridine-induced tachycardia in WKY, but induced a sustained atropine-sensitive bradycardia in SHR. Inhibition of the Parasympathetic component with hemicholinium-3, hexamethonium, or atropine enhanced the late tachycardia in SHR, whereas hexamethonium reduced the tachycardia in WKY. In conclusion, 3,4-diaminopyridine-induced acetylcholine release, and thus enhanced Parasympathetic Ganglion transmission, with subsequent mAchR activation and bradycardia. 3,4-diaminopyridine also activated tachycardia, initially by enhancing sympathetic Ganglion transmission, subsequently by activation of norepinephrine release from sympathetic nerve terminals. The 3,4-diaminopyridine-induced Parasympathetic activation was stronger and more sustained in SHR, demonstrating an enhanced inhibitory control of K V on Parasympathetic Ganglion transmission. This enhanced K V activity may explain the dysfunctional vagal HR control in SHR.
