Polyclonal anti-histamine H 2 receptor antibodies detect differential expression of H 2 receptor protein in primary vascular cell types

Schneider, Annette; Rieß, Peter; Elbers, A.; Neugebauer, E.; Schaefer, U.

doi:10.1007/s00011-004-1246-4

Cited by 10 publications

(7 citation statements)

References 32 publications

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“…In the case of His, activation of H 1 receptors in HUA smooth muscle induces contraction by activation of phospholipase C and increase in IP 3 levels (Hawley et al 1995). The expression of H 2 receptors in human umbilical smooth muscle was also reported by Schneider et al (Schneider et al 2004). The activation of this receptor stimulates adenylyl cyclase activity producing an increase in cyclic AMP and relaxation.…”

Section: Discussionsupporting

confidence: 57%

Potassium channels are involved in testosterone-induced vasorelaxation of human umbilical artery

Cairrão

Álvarez

Santos-Silva

et al. 2007

Naunyn-Schmied Arch Pharmacol

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Recent studies have shown that testosterone induces relaxation of different arteries, although the mechanism of this action is still under debate. We investigated the involvement of potassium channels in this mechanism. Using standard organ bath techniques, rings of human umbilical arteries (HUA) without endothelium were contracted by serotonin (5-HT, 1 microM), histamine (10 microM) and potassium chloride (KCl, 30 and 60 mM), and the vasorelaxant effect of testosterone was analysed. Testosterone (100 microM) relaxed human umbilical arteries contracted with 5-HT (30.1 +/- 3.2%), histamine (55.1 +/- 2.6%), KCl 30 mM (52.9 +/- 8.3%) and KCl 60 mM (54.8 +/- 6.3%). Flutamide (10 microM), an inhibitor of classical intracellular testosterone receptor, and glibenclamide, an ATP-sensitive potassium-channels (K(ATP)) inhibitor, did not influence the testosterone relaxant effect. 4-aminopyridine, a voltage-sensitive potassium-channels (Kv) inhibitor, decreased the effect of testosterone on histamine- and 5-HT-contracted arteries. Tetraethylammonium (TEA), which inhibits Kv channels and large-conductance Ca(2+)-activated potassium channels (BK(Ca)), decreased the effect of testosterone on KCl (60 mM)-contracted and 5-HT-contracted HUA. In conclusion, testosterone induces relaxation of HUA, and this effect does not appear to be mediated via a classic intracellular testosterone receptor-dependent mechanism. Our results suggest that this relaxation is partially mediated by activation of BK(Ca) and K(V) channels. The involvement of these two channels in testosterone-relaxant mechanism is dependent on the pathways activated by the contractile agent used.

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Section: Discussionsupporting

confidence: 57%

Potassium channels are involved in testosterone-induced vasorelaxation of human umbilical artery

Cairrão

Álvarez

Santos-Silva

et al. 2007

Naunyn-Schmied Arch Pharmacol

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“…This receptor, coupled to G q protein, activates the PLC/IP 3 signalling cascade, leading to an increase in intracellular Ca 2+ levels and consequent contraction [40,41,42]. Schneider et al (2004) also reported the expression of the H 2 receptor in HUA smooth muscle [43]. This receptor, coupled to G s protein, stimulates adenyl cyclase, leading to an increase in cAMP levels and consequent relaxation.…”

Section: Discussionmentioning

confidence: 99%

UV-B Filter Octylmethoxycinnamate Induces Vasorelaxation by Ca2+ Channel Inhibition and Guanylyl Cyclase Activation in Human Umbilical Arteries

Lorigo

Quintaneiro

Lemos

et al. 2019

IJMS

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Ultraviolet (UV) filters are chemicals widely used in personal care products (PCPs). Due to their effect as endocrine disruptor compounds (EDCs), the toxicity of UV filters is a current concern for human health. EDC exposure may be correlated to cardiovascular diseases (CVD), but to our knowledge, no studies assessed the UV filters effects as human EDCs at the vascular level. Octylmethoxycinnamate (OMC) is the world’s most widely used UV-B filter, present in more than 90% of PCPs. Due to its demonstrated multiple hormonal activities in animal models, this substance is also suspected to be a human EDC. The purpose of this study was to assess the rapid/short-term effects of OMC on arterial tonus and analyse its mode of action (MOA). Using human umbilical arteries, the endocrine effects of OMC were evaluated in in vitro (cellular and organ) experiments by planar cell surface area (PCSA) and organ bath, respectively. Our data show that OMC induces a rapid/short-term smooth muscle relaxation acting through an endothelium-independent MOA, which seems to be shared with oestrogens, involving an activation of soluble guanylyl cyclase (sGC) that increases the cyclic guanosine monophosphate (cGMP) intracellular levels and an inhibition of L-type voltage-operated Ca2+ channels (L-Type VOCC).

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“…Vascular responses to histamine are mediated through H 1 and H 2 receptor subtypes (12), and the dissected mesenteric arteries contained both histamine H 1 and H 2 receptor mRNA (data not shown). Histamine H 2 receptors are present in cultured smooth muscle cells (28). In human radial and internal thoracic arteries, histamine evokes constriction and its concentration-response curve is shifted to the right by H 2 receptor antagonists (5).…”

Section: Discussionmentioning

confidence: 99%

Histamine-dependent prolongation by aldosterone of vasoconstriction in isolated small mesenteric arteries of the mouse

Schjerning

Uhrenholt

Svenningsen

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Schjerning J, Uhrenholt TR, Svenningsen P, Vanhoutte PM, Skøtt O, Jensen BL, Hansen PB. Histamine-dependent prolongation by aldosterone of vasoconstriction in isolated small mesenteric arteries of the mouse. Am J Physiol Heart Circ Physiol 304: H1094 -H1102, 2013. First published February 8, 2013 doi:10.1152/ajpheart.00524.2012.-In arterioles, aldosterone counteracts the rapid dilatation (recovery) following depolarization-induced contraction. The hypothesis was tested that this effect of aldosterone depends on cyclooxygenase (COX)-derived products and/or nitric oxide (NO) synthase (NOS) inhibition. Recovery of the response to high K ϩ was observed in mesenteric arteries of wild-type and COX-2 Ϫ/Ϫ mice but it was significantly diminished in preparations from endothelial NOS (eNOS) Ϫ/Ϫ mice. Aldosterone pretreatment inhibited recovery from wild-type and COX-2 Ϫ/Ϫ mice. The NO donor sodium nitroprusside (SNP) restored recovery in arteries from eNOS Ϫ/Ϫ mice, and this was inhibited by aldosterone. Actinomycin-D abolished the effect of aldosterone, indicating a genomic effect. The effect was blocked by indomethacin and by the COX-1 inhibitor valeryl salicylate but not by NS-398 (10 Ϫ6 mol/l) or the TP-receptor antagonist S18886 (10 Ϫ7 mol/l). The effect of aldosterone on recovery in arteries from wild-type mice and the SNPmediated dilatation in arteries from eNOS Ϫ/Ϫ mice was inhibited by the histamine H2 receptor antagonist cimetidine. RT-PCR showed expression of mast cell markers in mouse mesenteric arteries. The adventitia displayed granular cells positive for toluidine blue vital stain. Confocal microscopy of live mast cells showed loss of quinacrine fluorescence and swelling after aldosterone treatment, indicating degranulation. RT-PCR showed expression of mineralocorticoid receptors in mesenteric arteries and in isolated mast cells. These findings suggest that aldosterone inhibits recovery by stimulation of histamine release from mast cells along mesenteric arteries. The resulting activation of H2 receptors decreases the sensitivity to NO of vascular smooth muscle cells. Aldosterone may chronically affect vascular function through paracrine release of histamine. mast cells; mineralocorticoid; endothelial function; microcirculation CHANGES IN INTERNAL VASCULAR diameter and thus local peripheral resistance contribute to the regulation of arterial blood pressure and the distribution of blood flow to distal tissues. In renal arterioles, depolarization-elicited vasoconstriction is counter-regulated by a secondary, nitric oxide (NO)-mediated dilatation termed recovery (38). This phenomenon is associated with transfer of a calcium signal from the smooth muscle cells to the endothelial cells. Another type of rapid interference with vasoconstrictor responses occurs after 5 min of exposure to aldosterone, which inhibits depolarization-induced constriction in the afferent arteriole also in a NO-dependent manner (37). Longer (50 min) exposure of renal arterioles to aldosterone significantly inhibits recovery (37).Aldoste...

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Polyclonal anti-histamine H 2 receptor antibodies detect differential expression of H 2 receptor protein in primary vascular cell types

Cited by 10 publications

References 32 publications

Potassium channels are involved in testosterone-induced vasorelaxation of human umbilical artery

Potassium channels are involved in testosterone-induced vasorelaxation of human umbilical artery

UV-B Filter Octylmethoxycinnamate Induces Vasorelaxation by Ca2+ Channel Inhibition and Guanylyl Cyclase Activation in Human Umbilical Arteries

Histamine-dependent prolongation by aldosterone of vasoconstriction in isolated small mesenteric arteries of the mouse

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