2010
DOI: 10.1007/s12264-010-1126-6
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Effects of sympathetic histamine on vasomotor responses of blood vessels in rabbit ear to electrical stimulation

Abstract: Stimulation on the auricular nerve may evoke histamine release from sympathetic nerves rather than from mast cells. Moreover, the functions of sympathetic histamine vary from pre-synaptic modulation to post-synaptic vasoconstriction or vasodilatation, via activation of different histamine receptors.

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Cited by 6 publications
(4 citation statements)
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“…Importantly, inversed hemodynamic or autonomic response after peripheral and central activation varies upon the neurotransmitter and is not always the fact. In case of histamine, type‐1 histamine receptor activation at both peripheral and central locations causes blood pressure up‐regulation . So far, the cellular mechanism and neural circuitry underlying NTS information processing in autonomic networks are poorly understood, while the neurotransmitters delivered by sensory terminals, the corresponding ligand‐specific receptors located at presynaptic and postsynaptic membranes, and the coupling of such receptors with a number of cellular effector systems in the respective neurons, as well as the subsequent transduction of given sensory signals via enzymatic cascades and ion channels, may all be associated with the complexity of autonomic activation at peripheral and central locations.…”
Section: Discussionmentioning
confidence: 99%
“…Importantly, inversed hemodynamic or autonomic response after peripheral and central activation varies upon the neurotransmitter and is not always the fact. In case of histamine, type‐1 histamine receptor activation at both peripheral and central locations causes blood pressure up‐regulation . So far, the cellular mechanism and neural circuitry underlying NTS information processing in autonomic networks are poorly understood, while the neurotransmitters delivered by sensory terminals, the corresponding ligand‐specific receptors located at presynaptic and postsynaptic membranes, and the coupling of such receptors with a number of cellular effector systems in the respective neurons, as well as the subsequent transduction of given sensory signals via enzymatic cascades and ion channels, may all be associated with the complexity of autonomic activation at peripheral and central locations.…”
Section: Discussionmentioning
confidence: 99%
“…The levels of blood pressure and epinephrine or norepinephrine in the blood that increase the blood pressure level under immobilization stress in rats were alleviated after rats were given electroacupuncture stimulus on acupuncture points HT3 and PC6 32) . Periodontal norepinephrine, dopamine, corticosterone, and ACTH, which increases the blood pressure under electric stimulus in rats, were also decreased by electroacupuncture stimulus to an acupuncture point (LI4) for 15 minutes 33) ; however, high intensity electrical stimulation is likely to have severe side-effects 12,13) . Our results that the increasing pain, which was caused by high intensity electrical stimulation, is closely correlated with the activation of norepinephrine and epinephrine.…”
Section: Discussionmentioning
confidence: 99%
“…However, it has been noted that these interventions can give rise to a contrary result, if the intervention method is flawed. For example, the induction of muscle cramps or pain that occurs due to an inappropriate treatment program using electric stimulus can actually lead to negative results by inappropriate increase of the sympathetic nervous activation 12,13) . A previous study focused on inducing fluctuation of hormones without any muscle cramp using an electronic stimulus device 14) .…”
Section: Introductionmentioning
confidence: 99%
“…The finding that the phasic/tonic tension ratio of a KCl-induced contraction was affected by hemorrhage suggests that VSM desensitization was a generalized phenomenon because KCl bypasses receptors to activate contraction by causing membrane depolarization (4). Histamine potency was reduced by both hemorrhage and tyramine, and although histamine is generally not considered a sympathetic neurotransmitter, there is limited evidence from one laboratory supporting the hypothesis that histamine is coreleased with norepinephrine in several species, including rabbit (12,24). Thus whether reduced sensitivity to HA was due to a generalized VSM desensitization, or to sympathetically released histamine activation of VSM histaminergic receptors followed by subsequent HA receptor desensitization, remains to be determined.…”
Section: H162mentioning
confidence: 99%