ArticleProceedings of the National Academy of Sciences of the United States of America2002
Decreased intracellular calcium mediates the histamine H3-receptor-induced attenuation of norepinephrine exocytosis from cardiac sympathetic nerve endings.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 73 citations in OpenAlex.
- Cardioprotective effects of H3 receptor activation could be double-sided: insights from isoproterenol-induced cardiac injury.Pflugers Archiv : European journal of physiology · 2025Article
- Histamine receptors in heart failure.Heart failure reviews · 2022Review
- Histamine and Microglia.Current topics in behavioral neurosciences · 2022Review
- Samelisant (SUVN-G3031), a potent, selective and orally active histamine H3 receptor inverse agonist for the potential treatment of narcolepsy: pharmacological and neurochemical characterisation.Psychopharmacology · 2021Article
- Associations of Polymorphisms in HRH2, HRH3, DAO, and HNMT Genes with Risk of Chronic Heart Failure.BioMed research international · 2016Article
- International Union of Basic and Clinical Pharmacology. XCVIII. Histamine Receptors.Pharmacological reviews · 2015Review
- Role of histamine H3 receptor in glucagon-secreting αTC1.6 cells.FEBS open bio · 2015Article
- A single-point mutation (Ala280Val) in the third intracellular loop alters the signalling properties of the human histamine H₃ receptor stably expressed in CHO-K1 cells.British journal of pharmacology · 2013Article
- Histamine H3 receptor antagonists in relation to epilepsy and neurodegeneration: a systemic consideration of recent progress and perspectives.British journal of pharmacology · 2012Review
- Natriuretic peptide-induced catecholamine release from cardiac sympathetic neurons: inhibition by histamine H3 and H4 receptor activation.The Journal of pharmacology and experimental therapeutics · 2012Article
- Effect of histamine on Ca(2+)-dependent signaling pathways in rat conjunctival goblet cells.Investigative ophthalmology & visual science · 2012Article
- Targeting cardiac mast cells: pharmacological modulation of the local renin-angiotensin system.Current pharmaceutical design · 2011Review
- Effects of sympathetic histamine on vasomotor responses of blood vessels in rabbit ear to electrical stimulation.Neuroscience bulletin · 2010Article
- IL-10 suppresses calcium-mediated costimulation of receptor activator NF-kappa B signaling during human osteoclast differentiation by inhibiting TREM-2 expression.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Cardioprotective effect of histamine H3-receptor activation: pivotal role of G beta gamma-dependent inhibition of voltage-operated Ca2+ channels.The Journal of pharmacology and experimental therapeutics · 2008Article
- Histamine H3-receptor signaling in cardiac sympathetic nerves: Identification of a novel MAPK-PLA2-COX-PGE2-EP3R pathway.Biochemical pharmacology · 2007Article
- Histamine receptors that influence blockage of the normal human nasal airway.British journal of pharmacology · 2005Article
- The histamine H3 receptor: from gene cloning to H3 receptor drugs.Nature reviews. Drug discovery · 2005Review
- Acute wake-promoting actions of JNJ-5207852, a novel, diamine-based H3 antagonist.British journal of pharmacology · 2004Article
- Central endogenous histamine modulates sympathetic outflow through H3 receptors in the conscious rabbit.British journal of pharmacology · 2003Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
Activation of presynatic histamine H(3) receptors (H(3)R) down-regulates norepinephrine exocytosis from cardiac sympathetic nerve terminals, in both normal and ischemic conditions. Analogous to the effects of alpha(2)-adrenoceptors, which also act prejunctionally to inhibit norepinephrine release, H(3)R-mediated antiexocytotic effects could result from a decreased Ca(2+) influx into nerve endings. We tested this hypothesis in sympathetic nerve terminals isolated from guinea pig heart (cardiac synaptosomes) and in a model human neuronal cell line (SH-SY5Y), which we stably transfected with human H(3)R cDNA (SH-SY5Y-H(3)). We found that reducing Ca(2+) influx in response to membrane depolarization by inhibiting N-type Ca(2+) channels with omega-conotoxin (omega-CTX) greatly attenuated the exocytosis of [(3)H]norepinephrine from both SH-SY5Y and SH-SY5Y-H(3) cells, as well as the exocytosis of endogenous norepinephrine from cardiac synaptosomes. Similar to omega-CTX, activation of H(3)R with the selective H(3)R-agonist imetit also reduced both the rise in intracellular Ca(2+) concentration (Ca(i)) and norepinephrine exocytosis in response to membrane depolarization. The selective H(3)R antagonist thioperamide prevented this effect of imetit. In the parent SH-SY5Y cells lacking H(3)R, imetit affected neither the rise in Ca(i) nor [(3)H]norepinephrine exocytosis, demonstrating that the presence of H(3)R is a prerequisite for a decrease in Ca(i) in response to imetit and that H(3)R activation modulates norepinephrine exocytosis by limiting the magnitude of the increase in Ca(i). Inasmuch as excessive norepinephrine exocytosis is a leading cause of cardiac dysfunction and arrhythmias during acute myocardial ischemia, attenuation of norepinephrine release by H(3)R agonists may offer a novel therapeutic approach to this condition.
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