Magnesium increases iberiotoxin-sensitive large conductance calcium activated potassium currents on the basilar artery smooth muscle cells in rabbits

Dhungel, Kshitiz Upadhyay; Kim, Tae Woon; Sharma, Naveen; Bhattarai, Janardhan P.; Park, Seon Ah; Han, Seong Kyu; Kim, Chul Jin

doi:10.1179/1743132811y.0000000049

Cited by 7 publications

(4 citation statements)

References 32 publications

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“…Thus, it has been proposed that under conditions in which Ca 2+ ic does not exceed a few micromolar, Mg 2+ tonically activates BK channels in vascular SM [209]. Consistently, 5 mM Mg 2+ increases whole-cell BK currents in rabbit basilar cerebral artery myocytes [42].…”

Section: Regulation By Intracellular Signals Other Than Ca2+icmentioning

confidence: 96%

Calcium- and voltage-gated BK channels in vascular smooth muscle

Dopico

Bukiya

Jaggar

2018

Pflugers Arch - Eur J Physiol

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Ion channels in vascular smooth muscle regulate myogenic tone and vessel contractility. In particular, activation of calcium- and voltage-gated potassium channels of large conductance (BK channels) results in outward current that shifts the membrane potential toward more negative values, triggering a negative feed-back loop on depolarization-induced calcium influx and SM contraction. In this short review, we first present the molecular basis of vascular smooth muscle BK channels and the role of subunit composition and trafficking in the regulation of myogenic tone and vascular contractility. BK channel modulation by endogenous signaling molecules, and paracrine and endocrine mediators follows. Lastly, we describe the functional changes in smooth muscle BK channels that contribute to, or are triggered by, common physiological conditions and pathologies, including obesity, diabetes, and systemic hypertension.

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Section: Regulation By Intracellular Signals Other Than Ca2+icmentioning

confidence: 96%

Calcium- and voltage-gated BK channels in vascular smooth muscle

Dopico

Bukiya

Jaggar

2018

Pflugers Arch - Eur J Physiol

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“…Proposed mechanisms of Mg 2+ -induced relaxation include direct effects on VSMCs via Ca 2+ antagonism, K + channel activation, 29,49,97 and activation of adenosine A 2 receptor. 98 Mg 2+ has been shown to be a Ca 2+ antagonist in different cell types, such as neurons, 99 cardiomyocytes, 100 skeletal muscle, 101 and VSMCs.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, direct effects of Mg 2+ on VSMCs have been described 46–49 . Proposed mechanisms of Mg 2+ ‐induced relaxation include direct effects on VSMCs via Ca 2+ antagonism, 46–48 activation of hyperpolarizing BK Ca K + channels, 29,49 with a potentially crucial role of the divalent cation channel TRPM7.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, direct effects of Mg 2+ on VSMCs have been described. [46][47][48][49] Proposed mechanisms of Mg 2+induced relaxation include direct effects on VSMCs via Ca 2+ antagonism, [46][47][48] activation of hyperpolarizing BK Ca K + channels, 29,49 with a potentially crucial role of the divalent cation channel TRPM7. TRPM7 has been implicated in the Mg 2+ -dependent influx into VSMCs in vitro, 50 and aortic Trpm7 expression is regulated by dietary Mg 2+ , 51 but no direct contribution of this channel to the Mg 2+dependent vasodilation has been described in intact vessels.…”

Section: Introductionmentioning

confidence: 99%

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Nitric oxide, endothelium‐derived hyperpolarizing factor, and smooth muscle‐dependent mechanisms contribute to magnesium‐dependent vascular relaxation in mouse arteries

Kudryavtseva,

Lyngsø,

Jensen

et al. 2024

Acta Physiologica

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AimMagnesium (Mg2+) is a vasorelaxant. The underlying physiological mechanisms driving this vasorelaxation remain unclear. Studies were designed to test the hypothesis that multiple signaling pathways including nitric oxide (NO) and endothelium‐derived hyperpolarizing factor (EDHF) in endothelial cells as well as Ca2+ antagonization and TRPM7 channels in vascular smooth muscle cells mediate Mg2+‐dependent vessel relaxation.MethodsTo uncover these mechanisms, force development was measured ex vivo in aorta rings from mice using isometric wire myography. Concentration responses to Mg2+ were studied in intact and endothelium‐denuded aortas. Key findings were confirmed in second‐order mesenteric resistance arteries perfused ex vivo using pressure myography. Effects of Mg2+ on NO formation were measured in Chinese Hamster Ovary (CHO) cells, isolated mesenteric vessels, and mouse urine.ResultsMg2+ caused a significant concentration‐dependent relaxation of aorta rings. This relaxation was attenuated significantly in endothelium‐denuded aortas. The endothelium‐dependent portion was inhibited by NO and cGMP blockade but not by cyclooxygenase inhibition. Mg2+ stimulated local NO formation in CHO cells and isolated mesenteric vessels without changing urinary NOx levels. High extracellular Mg2+ augmented acetylcholine‐induced relaxation. SKCa and IKCa channel blockers apamin and TRAM34 inhibited Mg2+‐dependent relaxation. The endothelium‐independent relaxation in aorta rings was inhibited by high extracellular Ca2+. Combined blockade of NO, SKCa, and IKCa channels significantly reduced Mg2+‐dependent dilatation in mesenteric resistance vessels.ConclusionsIn mouse conductance and resistance arteries Mg2+‐induced relaxation is contributed by endothelial NO formation, EDHF pathways, antagonism of Ca2+ in smooth muscle cells, and additional unidentified mechanisms.

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