The influence of ruthenium on vascular tone

Pauwels, Bart; Boydens, Charlotte; Voorde, Johan Van de

doi:10.1111/jphp.12417

Cited by 3 publications

(1 citation statement)

References 29 publications

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“…Furthermore, these CORMs have shown to elicit effects independently of CO release . Recently, it was also found that ruthenium as such exerts some effects . Although in most cases these CO‐independent effects seem to be beneficial, possible undesired side effects should be kept in mind.…”

Section: Ruthenium‐based Co‐donating Moleculesmentioning

confidence: 99%

Ruthenium-based nitric oxide-donating and carbon monoxide-donating molecules

Pauwels

Boydens

Daele

et al. 2016

Journal of Pharmacy and Pharmacology

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Objectives Over the past few years, the use of metallocomplexes for medical purposes has considerably grown. Because of its favourable characteristics, ruthenium has taken a significant place in this expanding field of research. Several ruthenium-containing metal compounds have been developed as delivery agents of physiological important molecules such as nitric oxide (NO) and carbon monoxide (CO). Key findings This review focuses on the (vaso)relaxant capacity of rutheniumbased NO-donating and CO-donating molecules in view of their potential usefulness in the treatment of cardiovascular diseases and erectile dysfunction. Summary Ruthenium seems to be a valuable candidate for the design of NOdonating and CO-donating molecules. To date, ruthenium remains of interest in drug research as the search for new alternatives is still necessary.

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Section: Ruthenium‐based Co‐donating Moleculesmentioning

confidence: 99%

Ruthenium-based nitric oxide-donating and carbon monoxide-donating molecules

Pauwels

Boydens

Daele

et al. 2016

Journal of Pharmacy and Pharmacology

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Carbon Monoxide-Releasing Molecule-2 Inhibits Connexin 43-Hemichannel Activity in Spinal Cord Astrocytes to Attenuate Neuropathic Pain

Wang

Sun

2017

J Mol Neurosci

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Carbon monoxide-releasing molecule (CORM-2) acts as a carbon monoxide (CO) deliverer in a more controlled manner without altering carboxyhemoglobin level and exerts potential function in inhibiting inflammation and/or acute nociception. However, the regulatory mechanism of CORM-2 on spinal nerve ligation (SNL)-induced neuropathic pain is not currently clear. Our study aims to investigate the role of CORM-2 in neuropathic pain and the underlying mechanism. We found that spinal cord astrocytes were dramatically activated on day 7 after SNL. L-α-aminoadipate (L-α-AA), an astroglial toxin, reversed SNL-induced astrocyte activation at sub-toxic dose. Intrathecal administration of CO donor CORM-2 induced antiallodynic and antihyperalgesic effects in neuropathic animals induced by SNL and suppressed SNL-induced spontaneous excitatory postsynaptic current (EPSC) frequency in lamina II neurons of spinal cord slices. CORM-2 administration markedly inhibited SNL-induced connexin 43 (Cx43) expression, hemichannel function, and gap junction function on spinal astrocyte membranes. Moreover, exogenous CORM-2 could attenuate HO-1 expression, while overexpressed heme oxygenase-1 (HO-1) increased intracellular CO production, attenuated Cx43 expression, hemichannel function, and gap junction function on spinal astrocyte membranes. Additionally, Cx43 over-expression markedly reduced CORM-2-induced mechanical threshold and thermal hyperalgesia and elevated CORM-2-induced spontaneous EPSC frequency. In conclusion, CORM-2 attenuated SNL-induced neuropathic pain via suppressing Cx43-hemichannel function, which may contribute to understanding of the pathology of neuropathic pain.

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Vascular responses to compound 48/80 in rat mesenteric vascular beds

Jin

Takatori

et al. 2016

Can. J. Physiol. Pharmacol.

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A further investigation was performed on the vascular effect of endogenous histamine using the histamine releaser, compound 48/80, in rat mesenteric vascular beds with active tone. In preparations with intact endothelium, low concentrations of compound 48/80 (1.53 × 10(-5) - 3 × 1.53 × 10(-5) mg/mL) perfusion for 1 min only induced a small vasodilation. High concentrations of compound 48/80 (1.53 × 10(-4) - 3 × 1.53 × 10(-2) mg/mL) induced a biphasic vascular responses, an initial vasoconstriction followed a subsequent long-lasting vasodilation. The vasodilation induced by low concentrations of compound 48/80 and the vasoconstriction induced by high concentration of compound 48/80 was inhibited by olopatadine. However, cimetidine did not affect the responses induced by compound 48/80. Endothelium removal enlarged the compound 48/80-induced phase-2 vasoconstriction, while it attenuated the phase-3 vasodilation. Additionally, indomethacin and seratrodast significantly inhibited vasoconstriction but it did not affect the long-lasting vasodilation induced by high concentrations of compound 48/80. Ruthenium red inhibited the vasodilation induced by low concentrations and high concentrations of compound 48/80. These results suggest that the vasoconstriction induce by high concentrations of compound 48/80 is mediated by endogenous histamine released from mast cells. It is also suggested that thromboxane A2 released from mast cells is related to the vasoconstriction.

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The influence of ruthenium on vascular tone

Abstract: Ruthenium-containing molecules can influence vascular tone induced by norepinephrine due to oxidative inactivation. Moreover, they can undermine NO-mediated responses. This should be considered when developing ruthenium-containing drugs.

Cited by 3 publications

References 29 publications

Ruthenium-based nitric oxide-donating and carbon monoxide-donating molecules

Ruthenium-based nitric oxide-donating and carbon monoxide-donating molecules

Carbon Monoxide-Releasing Molecule-2 Inhibits Connexin 43-Hemichannel Activity in Spinal Cord Astrocytes to Attenuate Neuropathic Pain

Vascular responses to compound 48/80 in rat mesenteric vascular beds

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