Acute and chronic effects of oxyhemoglobin on voltage-dependent ion channels in cerebral arteries

M Ishiguro, K Murakami, T Link, K Zvarova, B I Tranmer, A D Morielli, G C Wellman

Publikation: Bidrag til bog/antologi/rapport/konference-proceedingBidrag til bog/antologiForskningpeer review

Resumé

Voltage-dependent potassium (Kv) and calcium (VDCC) channels play an important role in the regulation of membrane potential and intracellular calcium concentration in cerebral artery myocytes. Recent evidence suggests VDCC activity is increased and Kv channel activity is decreased in cerebral arteries following subarachnoid hemorrhage (SAH), promoting enhanced constriction. We have examined the impact of the blood component oxyhemoglobin on Kv and VDCC function in small (100-200 microm) diameter cerebral arteries. Acute (10 min) exposure of oxyhemoglobin caused cerebral artery constriction and Kv current suppression that was abolished by tyrosine kinase inhibitors and a Kv channel blocker. Although short-term oxyhemoglobin application did not directly alter VDCC activity, five-day exposure to oxyhemoglobin was associated with enhanced expression of voltage-dependent calcium channels. This work suggests that acute and chronic effects of oxyhemoglobin act synergistically to promote membrane depolarization and increased VDCC activity in cerebral arteries. These actions of oxyhemoglobin may contribute to the development of cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

OriginalsprogEngelsk
TitelCerebral Vasospasm
RedaktørerT. Kırış, J.H. Zhang
ForlagSpringer
Publikationsdato2008
Sider99-102
ISBN (Trykt)978-3-211-75717-8
ISBN (Elektronisk)978-3-211-75718-5
DOI
StatusUdgivet - 2008
Udgivet eksterntJa
NavnActa Neurochirurgica Supplement
Vol/bind104
ISSN0065-1419

Fingeraftryk

Oxyhemoglobins
Constriction
Intracranial Vasospasm
Potassium
Membranes

Citer dette

Ishiguro, M., Murakami, K., Link, T., Zvarova, K., Tranmer, B. I., Morielli, A. D., & Wellman, G. C. (2008). Acute and chronic effects of oxyhemoglobin on voltage-dependent ion channels in cerebral arteries. I T. Kırış, & J. H. Zhang (red.), Cerebral Vasospasm (s. 99-102). Springer. Acta Neurochirurgica Supplement, Bind. 104 https://doi.org/10.1007/978-3-211-75718-5_19
Ishiguro, M ; Murakami, K ; Link, T ; Zvarova, K ; Tranmer, B I ; Morielli, A D ; Wellman, G C. / Acute and chronic effects of oxyhemoglobin on voltage-dependent ion channels in cerebral arteries. Cerebral Vasospasm. red. / T. Kırış ; J.H. Zhang. Springer, 2008. s. 99-102 (Acta Neurochirurgica Supplement, Bind 104).
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abstract = "Voltage-dependent potassium (Kv) and calcium (VDCC) channels play an important role in the regulation of membrane potential and intracellular calcium concentration in cerebral artery myocytes. Recent evidence suggests VDCC activity is increased and Kv channel activity is decreased in cerebral arteries following subarachnoid hemorrhage (SAH), promoting enhanced constriction. We have examined the impact of the blood component oxyhemoglobin on Kv and VDCC function in small (100-200 microm) diameter cerebral arteries. Acute (10 min) exposure of oxyhemoglobin caused cerebral artery constriction and Kv current suppression that was abolished by tyrosine kinase inhibitors and a Kv channel blocker. Although short-term oxyhemoglobin application did not directly alter VDCC activity, five-day exposure to oxyhemoglobin was associated with enhanced expression of voltage-dependent calcium channels. This work suggests that acute and chronic effects of oxyhemoglobin act synergistically to promote membrane depolarization and increased VDCC activity in cerebral arteries. These actions of oxyhemoglobin may contribute to the development of cerebral vasospasm following aneurysmal subarachnoid hemorrhage.",
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Ishiguro, M, Murakami, K, Link, T, Zvarova, K, Tranmer, BI, Morielli, AD & Wellman, GC 2008, Acute and chronic effects of oxyhemoglobin on voltage-dependent ion channels in cerebral arteries. i T Kırış & JH Zhang (red), Cerebral Vasospasm. Springer, Acta Neurochirurgica Supplement, bind 104, s. 99-102. https://doi.org/10.1007/978-3-211-75718-5_19

Acute and chronic effects of oxyhemoglobin on voltage-dependent ion channels in cerebral arteries. / Ishiguro, M; Murakami, K; Link, T; Zvarova, K; Tranmer, B I; Morielli, A D; Wellman, G C.

Cerebral Vasospasm. red. / T. Kırış; J.H. Zhang. Springer, 2008. s. 99-102 (Acta Neurochirurgica Supplement, Bind 104).

Publikation: Bidrag til bog/antologi/rapport/konference-proceedingBidrag til bog/antologiForskningpeer review

TY - CHAP

T1 - Acute and chronic effects of oxyhemoglobin on voltage-dependent ion channels in cerebral arteries

AU - Ishiguro, M

AU - Murakami, K

AU - Link, T

AU - Zvarova, K

AU - Tranmer, B I

AU - Morielli, A D

AU - Wellman, G C

PY - 2008

Y1 - 2008

N2 - Voltage-dependent potassium (Kv) and calcium (VDCC) channels play an important role in the regulation of membrane potential and intracellular calcium concentration in cerebral artery myocytes. Recent evidence suggests VDCC activity is increased and Kv channel activity is decreased in cerebral arteries following subarachnoid hemorrhage (SAH), promoting enhanced constriction. We have examined the impact of the blood component oxyhemoglobin on Kv and VDCC function in small (100-200 microm) diameter cerebral arteries. Acute (10 min) exposure of oxyhemoglobin caused cerebral artery constriction and Kv current suppression that was abolished by tyrosine kinase inhibitors and a Kv channel blocker. Although short-term oxyhemoglobin application did not directly alter VDCC activity, five-day exposure to oxyhemoglobin was associated with enhanced expression of voltage-dependent calcium channels. This work suggests that acute and chronic effects of oxyhemoglobin act synergistically to promote membrane depolarization and increased VDCC activity in cerebral arteries. These actions of oxyhemoglobin may contribute to the development of cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

AB - Voltage-dependent potassium (Kv) and calcium (VDCC) channels play an important role in the regulation of membrane potential and intracellular calcium concentration in cerebral artery myocytes. Recent evidence suggests VDCC activity is increased and Kv channel activity is decreased in cerebral arteries following subarachnoid hemorrhage (SAH), promoting enhanced constriction. We have examined the impact of the blood component oxyhemoglobin on Kv and VDCC function in small (100-200 microm) diameter cerebral arteries. Acute (10 min) exposure of oxyhemoglobin caused cerebral artery constriction and Kv current suppression that was abolished by tyrosine kinase inhibitors and a Kv channel blocker. Although short-term oxyhemoglobin application did not directly alter VDCC activity, five-day exposure to oxyhemoglobin was associated with enhanced expression of voltage-dependent calcium channels. This work suggests that acute and chronic effects of oxyhemoglobin act synergistically to promote membrane depolarization and increased VDCC activity in cerebral arteries. These actions of oxyhemoglobin may contribute to the development of cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

KW - Animals

KW - Calcium Channels, R-Type/drug effects

KW - Cerebral Arteries/drug effects

KW - Ion Channels/drug effects

KW - Models, Animal

KW - Organ Culture Techniques

KW - Oxyhemoglobins/pharmacology

KW - Rabbits

KW - Vasoconstriction/drug effects

U2 - 10.1007/978-3-211-75718-5_19

DO - 10.1007/978-3-211-75718-5_19

M3 - Book chapter

C2 - 18456998

SN - 978-3-211-75717-8

T3 - Acta Neurochirurgica Supplement

SP - 99

EP - 102

BT - Cerebral Vasospasm

A2 - Kırış, T.

A2 - Zhang, J.H.

PB - Springer

ER -

Ishiguro M, Murakami K, Link T, Zvarova K, Tranmer BI, Morielli AD et al. Acute and chronic effects of oxyhemoglobin on voltage-dependent ion channels in cerebral arteries. I Kırış T, Zhang JH, red., Cerebral Vasospasm. Springer. 2008. s. 99-102. (Acta Neurochirurgica Supplement, Bind 104). https://doi.org/10.1007/978-3-211-75718-5_19