Veratridine Induces Vasorelaxation in Mouse Cecocolic Mesenteric Arteries.

The vegetal alkaloid toxin veratridine (VTD) is a selective voltage-gated Na (Na) channel activator, widely used as a pharmacological tool in vascular physiology. We have previously shown that Na channels, expressed in arteries, contribute to vascular tone in mouse mesenteric arteries (MAs). Here, we aimed to better characterize the mechanisms of action of VTD using mouse cecocolic arteries (CAs), a model of resistance artery.

Tetrodotoxin Decreases the Contractility of Mesenteric Arteries, Revealing the Contribution of Voltage-Gated Na Channels in Vascular Tone Regulation.

Tetrodotoxin (TTX) poisoning through the consumption of contaminated fish leads to lethal symptoms, including severe hypotension. This TTX-induced hypotension is likely due to the downfall of peripheral arterial resistance through direct or indirect effects on adrenergic signaling. TTX is a high-affinity blocker of voltage-gated Na (Na) channels.

Understanding and preventing vaccination errors.

Introduction: Vaccine-related medication errors can occur at each step of the vaccination process: prescribing, dispensing, preparation, administration, monitoring, transport, and storage. We aimed to describe current knowledge of vaccination-related errors to identify areas for improvement.

Material And Methods: We performed a literature review on PubMed, using MeSH terms, from 1998 to 2020 to identify articles that would illustrate vaccine-related medication errors.

Pharmacological Dissection of the Crosstalk between Na and Ca Channels in GH3b6 Cells.

Thanks to the crosstalk between Na and Ca channels, Na and Ca homeostasis interplay in so-called excitable cells enables the generation of action potential in response to electrical stimulation. Here, we investigated the impact of persistent activation of voltage-gated Na (Na) channels by neurotoxins, such as veratridine (VTD), on intracellular Ca concentration ([Ca]) in a model of excitable cells, the rat pituitary GH3b6 cells, in order to identify the molecular actors involved in Na-Ca homeostasis crosstalk. By combining RT-qPCR, immunoblotting, immunocytochemistry, and patch-clamp techniques, we showed that GH3b6 cells predominantly express the Na1.

Membrane estrogen receptor alpha (ERα) participates in flow-mediated dilation in a ligand-independent manner.

Estrogen receptor alpha (ERα) activation by estrogens prevents atheroma through its nuclear action, whereas plasma membrane-located ERα accelerates endothelial healing. The genetic deficiency of ERα was associated with a reduction in flow-mediated dilation (FMD) in one man. Here, we evaluated ex vivo the role of ERα on FMD of resistance arteries.