Influence of K+-channels and gap junctions on endothelium derived hyperpolarization-induced renal vasodilation in rats

Kasper Møller Rasmussen; Jens Christian Brasen; Max Salomonsson; Charlotte Mehlin Sørensen

Influence of K+-channels and gap junctions on endothelium derived hyperpolarization-induced renal vasodilation in rats

Kasper Møller Rasmussen
, Jens Christian Brasen
, Max Salomonsson
, Charlotte Mehlin Sørensen

University of Copenhagen

Research output: Contribution to journal › Conference abstract in journal › Research › peer-review

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Abstract

We investigated the role of Ca2+-activated K+ -channels in the endothelial derived hyperpolarization-induced renal vasodilation in vitro and in vivo in rats. Also, the possible role of K+ - induced activation of inward rectifier K+ (Kir) channels and Na+ /K+ -ATPase was assessed. Furthermore, involvement of renal myoendothelial gap junctions was evaluated in vitro. Because assessment of endothelial derived hyperpolarization-induced renal vasodilation in vivo is hampered by experimental limitations, we have combined in vivo and in vitro experiments. Isometric tension in rat renal interlobar arteries was measured using a wire myograph. Renal blood flow was measured in isoflurane and pentobarbital anesthetized rats. The ACh-induced response was measured before and after inhibition of the nitric oxide synthase with L-NAME and cyclooxygenase using indomethacin. Blockade of small conductance Ca2+-activated K+ -channels (SKCa) by apamin and intermediate conductance Ca2+-activated K+ -channels (IKCa) by TRAM-34 significantly decreased the endothelial derived hyperpolarization-induced vasorelaxation in vitro but had no effect in vivo. Inhibition of Kir-channels by Ba2+ and Na+ / K+ -ATPases by ouabain significantly attenuated renal vasorelaxation in vitro but had no effect in vivo. In vitro, inhibition of gap junctions using carbenoxolone or 18a-glycyrrhetinic acid significantly reduced the endothelial derived hyperpolarization-induced vasorelaxation. In conclusion we found that in vitro, renal vascular SKCa and IKCa-channels are essential for the endothelial derived hyperpolarization-induced vasorelaxation. Furthermore, activation of Kir-channels, Na+ /K+ -ATPases and vascular gap junctions play a significant role in the renal vascular endothelial derived hyperpolarization-response in vitro. In vivo the endothelial derived hyperpolarization response seems unaffected by the present blockade of various K+ channels.

Original language	English
Journal	Acta Physiologica
Volume	215
Issue number	Suppl. 703 - Meeting abstract
Pages (from-to)	13-13
ISSN	1748-1708
Publication status	Published - 2015
Event	Meeting on Endothelium-Dependent Hyperpolarizations in Health and Disease - Nyborg, Denmark Duration: 14 Sept 2015 → 17 Sept 2015

Workshop

Workshop	Meeting on Endothelium-Dependent Hyperpolarizations in Health and Disease
Country/Territory	Denmark
City	Nyborg
Period	14/09/2015 → 17/09/2015

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@article{1353705ebaf64b1ea3a32e371b23a3c0,

title = "Influence of K+-channels and gap junctions on endothelium derived hyperpolarization-induced renal vasodilation in rats",

abstract = "We investigated the role of Ca2+-activated K+ -channels in the endothelial derived hyperpolarization-induced renal vasodilation in vitro and in vivo in rats. Also, the possible role of K+ - induced activation of inward rectifier K+ (Kir) channels and Na+ /K+ -ATPase was assessed. Furthermore, involvement of renal myoendothelial gap junctions was evaluated in vitro. Because assessment of endothelial derived hyperpolarization-induced renal vasodilation in vivo is hampered by experimental limitations, we have combined in vivo and in vitro experiments. Isometric tension in rat renal interlobar arteries was measured using a wire myograph. Renal blood flow was measured in isoflurane and pentobarbital anesthetized rats. The ACh-induced response was measured before and after inhibition of the nitric oxide synthase with L-NAME and cyclooxygenase using indomethacin. Blockade of small conductance Ca2+-activated K+ -channels (SKCa) by apamin and intermediate conductance Ca2+-activated K+ -channels (IKCa) by TRAM-34 significantly decreased the endothelial derived hyperpolarization-induced vasorelaxation in vitro but had no effect in vivo. Inhibition of Kir-channels by Ba2+ and Na+ / K+ -ATPases by ouabain significantly attenuated renal vasorelaxation in vitro but had no effect in vivo. In vitro, inhibition of gap junctions using carbenoxolone or 18a-glycyrrhetinic acid significantly reduced the endothelial derived hyperpolarization-induced vasorelaxation. In conclusion we found that in vitro, renal vascular SKCa and IKCa-channels are essential for the endothelial derived hyperpolarization-induced vasorelaxation. Furthermore, activation of Kir-channels, Na+ /K+ -ATPases and vascular gap junctions play a significant role in the renal vascular endothelial derived hyperpolarization-response in vitro. In vivo the endothelial derived hyperpolarization response seems unaffected by the present blockade of various K+ channels.",

author = "Rasmussen, \{Kasper M{\o}ller\} and Brasen, \{Jens Christian\} and Max Salomonsson and S{\o}rensen, \{Charlotte Mehlin\}",

year = "2015",

language = "English",

volume = "215",

pages = "13--13",

journal = "Acta Physiologica",

issn = "1748-1708",

publisher = "John Wiley and Sons Ltd",

number = "Suppl. 703 - Meeting abstract",

note = "Meeting on Endothelium-Dependent Hyperpolarizations in Health and Disease ; Conference date: 14-09-2015 Through 17-09-2015",

}

Influence of K+-channels and gap junctions on endothelium derived hyperpolarization-induced renal vasodilation in rats. / Rasmussen, Kasper Møller; Brasen, Jens Christian; Salomonsson, Max et al.
In: Acta Physiologica, Vol. 215, No. Suppl. 703 - Meeting abstract, 2015, p. 13-13.

Research output: Contribution to journal › Conference abstract in journal › Research › peer-review

TY - ABST

T1 - Influence of K+-channels and gap junctions on endothelium derived hyperpolarization-induced renal vasodilation in rats

AU - Rasmussen, Kasper Møller

AU - Brasen, Jens Christian

AU - Salomonsson, Max

AU - Sørensen, Charlotte Mehlin

PY - 2015

Y1 - 2015

N2 - We investigated the role of Ca2+-activated K+ -channels in the endothelial derived hyperpolarization-induced renal vasodilation in vitro and in vivo in rats. Also, the possible role of K+ - induced activation of inward rectifier K+ (Kir) channels and Na+ /K+ -ATPase was assessed. Furthermore, involvement of renal myoendothelial gap junctions was evaluated in vitro. Because assessment of endothelial derived hyperpolarization-induced renal vasodilation in vivo is hampered by experimental limitations, we have combined in vivo and in vitro experiments. Isometric tension in rat renal interlobar arteries was measured using a wire myograph. Renal blood flow was measured in isoflurane and pentobarbital anesthetized rats. The ACh-induced response was measured before and after inhibition of the nitric oxide synthase with L-NAME and cyclooxygenase using indomethacin. Blockade of small conductance Ca2+-activated K+ -channels (SKCa) by apamin and intermediate conductance Ca2+-activated K+ -channels (IKCa) by TRAM-34 significantly decreased the endothelial derived hyperpolarization-induced vasorelaxation in vitro but had no effect in vivo. Inhibition of Kir-channels by Ba2+ and Na+ / K+ -ATPases by ouabain significantly attenuated renal vasorelaxation in vitro but had no effect in vivo. In vitro, inhibition of gap junctions using carbenoxolone or 18a-glycyrrhetinic acid significantly reduced the endothelial derived hyperpolarization-induced vasorelaxation. In conclusion we found that in vitro, renal vascular SKCa and IKCa-channels are essential for the endothelial derived hyperpolarization-induced vasorelaxation. Furthermore, activation of Kir-channels, Na+ /K+ -ATPases and vascular gap junctions play a significant role in the renal vascular endothelial derived hyperpolarization-response in vitro. In vivo the endothelial derived hyperpolarization response seems unaffected by the present blockade of various K+ channels.

AB - We investigated the role of Ca2+-activated K+ -channels in the endothelial derived hyperpolarization-induced renal vasodilation in vitro and in vivo in rats. Also, the possible role of K+ - induced activation of inward rectifier K+ (Kir) channels and Na+ /K+ -ATPase was assessed. Furthermore, involvement of renal myoendothelial gap junctions was evaluated in vitro. Because assessment of endothelial derived hyperpolarization-induced renal vasodilation in vivo is hampered by experimental limitations, we have combined in vivo and in vitro experiments. Isometric tension in rat renal interlobar arteries was measured using a wire myograph. Renal blood flow was measured in isoflurane and pentobarbital anesthetized rats. The ACh-induced response was measured before and after inhibition of the nitric oxide synthase with L-NAME and cyclooxygenase using indomethacin. Blockade of small conductance Ca2+-activated K+ -channels (SKCa) by apamin and intermediate conductance Ca2+-activated K+ -channels (IKCa) by TRAM-34 significantly decreased the endothelial derived hyperpolarization-induced vasorelaxation in vitro but had no effect in vivo. Inhibition of Kir-channels by Ba2+ and Na+ / K+ -ATPases by ouabain significantly attenuated renal vasorelaxation in vitro but had no effect in vivo. In vitro, inhibition of gap junctions using carbenoxolone or 18a-glycyrrhetinic acid significantly reduced the endothelial derived hyperpolarization-induced vasorelaxation. In conclusion we found that in vitro, renal vascular SKCa and IKCa-channels are essential for the endothelial derived hyperpolarization-induced vasorelaxation. Furthermore, activation of Kir-channels, Na+ /K+ -ATPases and vascular gap junctions play a significant role in the renal vascular endothelial derived hyperpolarization-response in vitro. In vivo the endothelial derived hyperpolarization response seems unaffected by the present blockade of various K+ channels.

M3 - Conference abstract in journal

SN - 1748-1708

VL - 215

SP - 13

EP - 13

JO - Acta Physiologica

JF - Acta Physiologica

IS - Suppl. 703 - Meeting abstract

T2 - Meeting on Endothelium-Dependent Hyperpolarizations in Health and Disease

Y2 - 14 September 2015 through 17 September 2015

ER -

Influence of K+-channels and gap junctions on endothelium derived hyperpolarization-induced renal vasodilation in rats

Abstract

Workshop

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