Vasomotor Effects of Acetylcholine, Bradykinin, Noradrenaline, 5-Hydroxytryptamine, Histamine and Angiotensin II on the Mouse Basilar Artery

Islam, Md. Zahorul; Watanabe, Yutaka; Nguyen, Ha Thi Thanh; Yamazaki-Himeno, Emi; Obi, Takeshi; Shiraishi, Masayuki; Miyamoto, Atsushi

doi:10.1292/jvms.14-0223

Cited by 17 publications

(10 citation statements)

References 29 publications

(32 reference statements)

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“…We have previously reported that vasodilation induced by acetylcholine, which is dependent on NO production from endothelial cells, was decreased in a basilar artery isolated from MeHg-exposed mice [14, 15]. In this study, we showed that treatment of 0.3 µ M MeHg significantly inhibited NO production, but not expression of eNOS, in a dose-dependent manner.…”

Section: Discussionsupporting

confidence: 50%

MARCKS is involved in methylmercury-induced decrease in cell viability and nitric oxide production in EA.hy926 cells

Dao

Islam

Sudo

et al. 2016

The Journal of Veterinary Medical Science

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Methylmercury (MeHg) is a persistent environmental contaminant that has been reported worldwide. MeHg exposure has been reported to lead to increased risk of cardiovascular diseases; however, the mechanisms underlying the toxic effects of MeHg on the cardiovascular system have not been well elucidated. We have previously reported that mice exposed to MeHg had increased blood pressure along with impaired endothelium-dependent vasodilation. In this study, we investigated the toxic effects of MeHg on a human endothelial cell line, EA.hy926. In addition, we have tried to elucidate the role of myristoylated alanine-rich C kinase substrate (MARCKS) in the MeHg toxicity mechanism in EA.hy926 cells. Cells exposed to MeHg (0.1–10 µM) for 24 hr showed decreased cell viability in a dose-dependent manner. Treatment with submaximal concentrations of MeHg decreased cell migration in the wound healing assay, tube formation on Matrigel and spontaneous nitric oxide (NO) production of EA.hy926 cells. MeHg exposure also elicited a decrease in MARCKS expression and an increase in MARCKS phosphorylation. MARCKS knockdown or MARCKS overexpression in EA.hy926 cells altered not only cell functions, such as migration, tube formation and NO production, but also MeHg-induced decrease in cell viability and NO production. These results suggest the broad role played by MARCKS in endothelial cell functions and the involvement of MARCKS in MeHg-induced toxicity.

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Section: Discussionsupporting

confidence: 50%

MARCKS is involved in methylmercury-induced decrease in cell viability and nitric oxide production in EA.hy926 cells

Dao

Islam

Sudo

et al. 2016

The Journal of Veterinary Medical Science

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“…This has been attributed to the relative expression of 5‐HT receptor subtypes in different tissues and species (Watts et al, 2012). In mice, the species under consideration in the present study, 5‐HT has been reported to have a contractile effect on isolated arteries (Islam et al, 2014; Matsumoto, Kobayashi, Ishida, Taguchi, & Kamata, 2010; McKune & Watts, 2001). The in vivo vascular response to 5‐HT, on the other hand, is typically vasodilation, reflecting an interplay between its direct vascular actions and its involvement in the neural regulation of cardiovascular function (Watts et al, 2012).…”

Section: Introductionmentioning

confidence: 76%

Deletion of murine slc29a4 modifies vascular responses to adenosine and 5‐hydroxytryptamine in a sexually dimorphic manner

et al. 2020

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Equilibrative nucleoside transporter 4 (ENT4), encoded by SLC29A4, mediates the flux of both 5‐hydroxytryptamine (5‐HT) and adenosine across cell membranes. We hypothesized that loss of ENT4 function in mice would modify the effects of these established regulators of vascular function. Male and female wild‐type (WT) and slc29a4‐null (ENT4‐KO) mice were compared with respect to their hemodynamics and mesenteric vascular function. Male ENT4‐KO mice had a complete loss of myogenic tone in their mesenteric resistance arteries. This was accompanied by a decrease in blood flow in the superior mesenteric artery in the male ENT4‐KO mice, and a reduced responsiveness to 5‐HT. In contrast, endothelium‐dependent relaxations of mesenteric arteries from female ENT4‐KO mice were more sensitive to Ca2+‐activated K+ (KCa) channel blockade than WT mice. Female ENT4‐KO mice also demonstrated an enhanced vasodilatory response to adenosine in vivo that was not seen in males. Ketanserin (5‐HT2A inhibitor) and GR55562 (5‐HT1B/1D inhibitor) decreased 5‐HT‐induced tone, but only ketanserin inhibited the relaxant effect of 5‐HT in mesenteric arteries. 5‐HT‐evoked increases in tone were elevated in arteries from ENT4‐KO mice upon block of endothelial relaxant pathways, with arteries from female ENT4‐KO mice showing the greatest increase. Adenosine A2b receptor expression was decreased, while other adenosine transporter subtypes, as well as adenosine deaminase and adenosine kinase were increased in mesenteric arteries from male, but not female, ENT4‐KO mice. These findings indicate that deletion of slc29a4 leads to sex‐specific changes in vascular function with significant consequences for regulation of blood flow and pressure by adenosine and 5‐HT.

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“…Therefore, in addition to the increase in expression of tryptase, the increase in 5-HT and HA also occurs during acupoint sensitization. As neurotransmitters and immune mediators, 5-HT and HA are important regulators of the microcirculatory system [ 37 – 38 ] and involved in allergy [ 39 – 40 ]. These factors, 5-HT and HA, have been attributed a potential role in the exchange of information between MCs and nerve terminals [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

Mast cells are important regulator of acupoint sensitization via the secretion of tryptase, 5-hydroxytryptamine, and histamine

et al. 2018

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Mast cells (MCs) play a crucial role in mediating the establishment of networks among the circulatory, nervous and immune system at acupoints. However, the changes which occur in MCs during acupoint sensitization, i.e. the dynamic transformation of an acupoint from a "silenced" to an "activated" status, remain uncharacterized. To investigate the morphological and functional changes of MCs as an aid to understanding the cellular mechanism underlying acupoint sensitization, a rat model of knee osteoarthritis (OA) was induced by an injection of mono-iodoacetate (MIA) on day 0. On day 14, toluidine blue and immunofluorescence staining were used to observe the recruitment and degranulation of MCs and the release of mast cell co-expressed mediators: tryptase, 5-hydroxytryptamine (5-HT) and histamine (HA) at the acupoints Yanglingquan (GB34), Heding (EX-LE2) and Weizhong (BL40). Results showed that the number of MCs as well as the percentages of degranulated and extensively degranulated MCs at the acupoints GB34 and EX-LE2 in the light (A), mild (B), heavy (C) osteoarthritis groups were larger than those in the normal control (N) and normal saline (NS) groups (p < 0.01). Comparisons among the A, B and C groups suggested that the number and the degranulation extent of the MCs at the acupoints GB34 and EX-LE2 were positively correlated with the severity of the disease. Some MCs in the A, B and C group showed the release of 5-HT, HA, and tryptase in degranulation at the acupoints GB34 and EX-LE2. Such changes in MCs were not observed at the acupoint BL40. In conclusion, this study confirmed that acupoint sensitization is associated with the increase in recruitment and degranulation levels of MCs on a acupoint-specific and disease severity-dependent manner. The release of tryptase, 5-HT, and HA during MC degranulation is likely to be one of the cellular mechanisms occurring during acupoint sensitization.

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Vasomotor Effects of Acetylcholine, Bradykinin, Noradrenaline, 5-Hydroxytryptamine, Histamine and Angiotensin II on the Mouse Basilar Artery

Cited by 17 publications

References 29 publications

MARCKS is involved in methylmercury-induced decrease in cell viability and nitric oxide production in EA.hy926 cells

MARCKS is involved in methylmercury-induced decrease in cell viability and nitric oxide production in EA.hy926 cells

Deletion of murine slc29a4 modifies vascular responses to adenosine and 5‐hydroxytryptamine in a sexually dimorphic manner

Mast cells are important regulator of acupoint sensitization via the secretion of tryptase, 5-hydroxytryptamine, and histamine

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