Temporal profile of potassium channel dysfunction in cerebrovascular smooth muscle after experimental subarachnoid haemorrhage

Jahromi, Babak S.; Aihara, Yasuo; Ai, Jinglu; Zhang, Zhen Du; Weyer, George; Nikitina, Elena; Yassari, Reza; Houamed, Khaled M.; Macdonald, R. Loch

doi:10.1016/j.neulet.2008.05.015

Cited by 15 publications

(9 citation statements)

References 24 publications

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“…Recently, the function and expression of ion channels, particularly the Ca 2+ -activated K + channels, have been investigated in SAH-induced vasospasm. In the present study, the expression of Ca 2+ -activated K + channels in MCA was largely reduced after SAH in both Ntg and GET-1 mice, which is in agreement with others findings that elevated PKC activity after SAH causes dysfunction in K + channel activity and expression [78,79]. …”

Section: Discussionsupporting

confidence: 93%

Targeted over-expression of endothelin-1 in astrocytes leads to more severe brain damage and vasospasm after subarachnoid hemorrhage

et al. 2013

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BackgroundEndothelin-1 (ET-1) is a potent vasoconstrictor, and astrocytic ET-1 is reported to play a role in the pathogenesis of cerebral ischemic injury and cytotoxic edema. However, it is still unknown whether astrocytic ET-1 also contributes to vasogenic edema and vasospasm during subarachnoid hemorrhage (SAH). In the present study, transgenic mice with astrocytic endothelin-1 over-expression (GET-1 mice) were used to investigate the pathophysiological role of ET-1 in SAH pathogenesis.ResultsThe GET-1 mice experienced a higher mortality rate and significantly more severe neurological deficits, blood–brain barrier breakdown and vasogenic edema compared to the non-transgenic (Ntg) mice following SAH. Oral administration of vasopressin V1a receptor antagonist, SR 49059, significantly reduced the cerebral water content in the GET-1 mice. Furthermore, the GET-1 mice showed significantly more pronounced middle cerebral arterial (MCA) constriction after SAH. Immunocytochemical analysis showed that the calcium-activated potassium channels and the phospho-eNOS were significantly downregulated, whereas PKC-α expression was significantly upregulated in the MCA of the GET-1 mice when compared to Ntg mice after SAH. Administration of ABT-627 (ETA receptor antagonist) significantly down-regulated PKC-α expression in the MCA of the GET-1 mice following SAH.ConclusionsThe present study suggests that astrocytic ET-1 involves in SAH-induced cerebral injury, edema and vasospasm, through ETA receptor and PKC-mediated potassium channel dysfunction. Administration of ABT-627 (ETA receptor antagonist) and SR 49059 (vasopressin V1a receptor antagonist) resulted in amelioration of edema and vasospasm in mice following SAH. These data provide a strong rationale to investigate SR 49059 and ABT-627 as therapeutic drugs for the treatment of SAH patients.

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Section: Discussionsupporting

confidence: 93%

Targeted over-expression of endothelin-1 in astrocytes leads to more severe brain damage and vasospasm after subarachnoid hemorrhage

et al. 2013

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“…Ishiguro et al [116] have found that oxyhemoglobin suppresses voltage-dependent potassium channels in the rabbit cerebral arteries. Of note is that there is little change in the expression of calcium-activated potassium channels after SAH in laboratory dogs, whereas a significant decrease in voltage-gated potassium channels occurs in the arterial smooth muscle cells due to the impact of the oxyhemoglobin [117]. …”

Section: Discussion and Future Perspectivesmentioning

confidence: 99%

Hyperbaric Oxygen for Cerebral Vasospasm and Brain Injury Following Subarachnoid Hemorrhage

Ostrowski

Zhang

2011

Transl. Stroke Res.

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The impact of acute brain injury and delayed neurological deficits due to cerebral vasospasm (CVS) are major determinants of outcomes after subarachnoid hemorrhage (SAH). Although hyperbaric oxygen (HBO) had been used to treat patients with SAH, the supporting evidence and underlying mechanisms have not been systematically reviewed. In the present paper, the overview of studies of HBO for cerebral vasospasm is followed by a discussion of HBO molecular mechanisms involved in the protection against SAH-induced brain injury and even, as hypothesized, in attenuating vascular spasm alone. Faced with the paucity of information as to what degree HBO is capable of antagonizing vasospasm after SAH, the authors postulate that the major beneficial effects of HBO in SAH include a reduction of acute brain injury and combating brain damage caused by CVS. Consequently, authors reviewed the effects of HBO on SAH-induced hypoxic signaling and other mechanisms of neurovascular injury. Moreover, authors hypothesize that HBO administered after SAH may “precondition” the brain against the detrimental sequelae of vasospasm. In conclusion, the existing evidence speaks in favor of administering HBO in both acute and delayed phase after SAH; however, further studies are needed to understand the underlying mechanisms and to establish the optimal regimen of treatment.

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“…Reduced K V channel function is also observed in dog models of subarachnoid hemorrhage (685) that may be related to decreased expression of K V 2 channel subunits (22, 685). …”

Section: Kv Channelsmentioning

confidence: 98%

Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

Tykocki

Boerman

Jackson

2017

Comprehensive Physiology

282

347

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Vascular tone of resistance arteries and arterioles determines peripheral vascular resistance, contributing to the regulation of blood pressure and blood flow to, and within the body’s tissues and organs. Ion channels in the plasma membrane and endoplasmic reticulum of vascular smooth muscle cells (SMCs) in these blood vessels importantly contribute to the regulation of intracellular Ca2+ concentration, the primary determinant of SMC contractile activity and vascular tone. Ion channels provide the main source of activator Ca2+ that determines vascular tone, and strongly contribute to setting and regulating membrane potential, which, in turn, regulates the open-state-probability of voltage gated Ca2+ channels (VGCCs), the primary source of Ca2+ in resistance artery and arteriolar SMCs. Ion channel function is also modulated by vasoconstrictors and vasodilators, contributing to all aspects of the regulation of vascular tone. This review will focus on the physiology of VGCCs, voltage-gated K+ (KV) channels, large-conductance Ca2+-activated K+ (BKCa) channels, strong-inward-rectifier K+ (KIR) channels, ATP-sensitive K+ (KATP) channels, ryanodine receptors (RyRs), inositol 1,4,5-trisphosphate receptors (IP3Rs), and a variety of transient receptor potential (TRP) channels that contribute to pressure-induced myogenic tone in resistance arteries and arterioles, the modulation of the function of these ion channels by vasoconstrictors and vasodilators, their role in the functional regulation of tissue blood flow and their dysfunction in diseases such as hypertension, obesity, and diabetes.

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Temporal profile of potassium channel dysfunction in cerebrovascular smooth muscle after experimental subarachnoid haemorrhage

Cited by 15 publications

References 24 publications

Targeted over-expression of endothelin-1 in astrocytes leads to more severe brain damage and vasospasm after subarachnoid hemorrhage

Targeted over-expression of endothelin-1 in astrocytes leads to more severe brain damage and vasospasm after subarachnoid hemorrhage

Hyperbaric Oxygen for Cerebral Vasospasm and Brain Injury Following Subarachnoid Hemorrhage

Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

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