Mechanisms of K(+) induced renal vasodilation in normo- and hypertensive rats in vivo

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Mechanisms of K(+) induced renal vasodilation in normo- and hypertensive rats in vivo. / Magnusson, Linda Helena Margaretha; Sørensen, Charlotte Mehlin; Braunstein, T H; von Holstein-Rathlou, Niels-Henrik; Salomonsson, M.

I: Acta Physiologica (Print), Bind 202, Nr. 4, 01.08.2011, s. 703-12.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Magnusson, LHM, Sørensen, CM, Braunstein, TH, von Holstein-Rathlou, N-H & Salomonsson, M 2011, 'Mechanisms of K(+) induced renal vasodilation in normo- and hypertensive rats in vivo', Acta Physiologica (Print), bind 202, nr. 4, s. 703-12. https://doi.org/10.1111/j.1748-1716.2011.02304.x

APA

Magnusson, L. H. M., Sørensen, C. M., Braunstein, T. H., von Holstein-Rathlou, N-H., & Salomonsson, M. (2011). Mechanisms of K(+) induced renal vasodilation in normo- and hypertensive rats in vivo. Acta Physiologica (Print), 202(4), 703-12. https://doi.org/10.1111/j.1748-1716.2011.02304.x

Vancouver

Magnusson LHM, Sørensen CM, Braunstein TH, von Holstein-Rathlou N-H, Salomonsson M. Mechanisms of K(+) induced renal vasodilation in normo- and hypertensive rats in vivo. Acta Physiologica (Print). 2011 aug. 1;202(4):703-12. https://doi.org/10.1111/j.1748-1716.2011.02304.x

Author

Magnusson, Linda Helena Margaretha ; Sørensen, Charlotte Mehlin ; Braunstein, T H ; von Holstein-Rathlou, Niels-Henrik ; Salomonsson, M. / Mechanisms of K(+) induced renal vasodilation in normo- and hypertensive rats in vivo. I: Acta Physiologica (Print). 2011 ; Bind 202, Nr. 4. s. 703-12.

Bibtex

@article{fbfd5cd7cd8b431496eb44e87fcfc297,
title = "Mechanisms of K(+) induced renal vasodilation in normo- and hypertensive rats in vivo",
abstract = "Aim: We investigated the mechanisms behind K(+) -induced renal vasodilation in vivo in normotensive Sprague-Dawley (SD) rats and spontaneously hypertensive rats (SHR). Methods: Renal blood flow (RBF) was measured utilizing an ultrasonic Doppler flow probe. Renal vascular resistance (RVR) was calculated as the ratio of mean arterial pressure (MAP) and RBF (RVR = MAP/RBF). Test drugs were introduced directly into the renal artery. Inward rectifier K(+) (K(ir) ) channels and Na(+) ,K(+) -ATPase were blocked by Ba(2+) and ouabain (estimated plasma concentrations ~20 and ~7 µm) respectively. Results: Confocal immunofluorescence microscopy demonstrated K(ir) 2.1 channels in pre-glomerular vessels of SD and SHR. Ba(2+) caused a transient (6-13%) increase in baseline RVR in both SD and SHR. Ouabain had a similar effect. Elevated renal plasma [K(+) ] (~12 mm) caused a small and sustained decrease (5-13%) in RVR in both strains. This decrease was significantly larger in SHR than in SD. The K(+) -induced vasodilation was attenuated by Ba(2+) in control SD and SHR and by ouabain in SD. Nitric oxide (NO) blockade using l-NAME treatment increased MAP and decreased RBF in both rat strains, but did not affect the K(+) -induced renal vasodilation. Conclusion: K(+) -induced renal vasodilation is larger in SHR, mediated by K(ir) channels in SD and SHR, and in addition, by Na(+) ,K(+) -ATPase in SD. In addition, NO is not essential for K(+) -induced renal vasodilation.",
author = "Magnusson, {Linda Helena Margaretha} and S{\o}rensen, {Charlotte Mehlin} and Braunstein, {T H} and {von Holstein-Rathlou}, Niels-Henrik and M Salomonsson",
note = "{\textcopyright} 2011 The Authors. Acta Physiologica {\textcopyright} 2011 Scandinavian Physiological Society.",
year = "2011",
month = aug,
day = "1",
doi = "10.1111/j.1748-1716.2011.02304.x",
language = "English",
volume = "202",
pages = "703--12",
journal = "Acta Physiologica",
issn = "1748-1708",
publisher = "Wiley-Blackwell",
number = "4",

}

RIS

TY - JOUR

T1 - Mechanisms of K(+) induced renal vasodilation in normo- and hypertensive rats in vivo

AU - Magnusson, Linda Helena Margaretha

AU - Sørensen, Charlotte Mehlin

AU - Braunstein, T H

AU - von Holstein-Rathlou, Niels-Henrik

AU - Salomonsson, M

N1 - © 2011 The Authors. Acta Physiologica © 2011 Scandinavian Physiological Society.

PY - 2011/8/1

Y1 - 2011/8/1

N2 - Aim: We investigated the mechanisms behind K(+) -induced renal vasodilation in vivo in normotensive Sprague-Dawley (SD) rats and spontaneously hypertensive rats (SHR). Methods: Renal blood flow (RBF) was measured utilizing an ultrasonic Doppler flow probe. Renal vascular resistance (RVR) was calculated as the ratio of mean arterial pressure (MAP) and RBF (RVR = MAP/RBF). Test drugs were introduced directly into the renal artery. Inward rectifier K(+) (K(ir) ) channels and Na(+) ,K(+) -ATPase were blocked by Ba(2+) and ouabain (estimated plasma concentrations ~20 and ~7 µm) respectively. Results: Confocal immunofluorescence microscopy demonstrated K(ir) 2.1 channels in pre-glomerular vessels of SD and SHR. Ba(2+) caused a transient (6-13%) increase in baseline RVR in both SD and SHR. Ouabain had a similar effect. Elevated renal plasma [K(+) ] (~12 mm) caused a small and sustained decrease (5-13%) in RVR in both strains. This decrease was significantly larger in SHR than in SD. The K(+) -induced vasodilation was attenuated by Ba(2+) in control SD and SHR and by ouabain in SD. Nitric oxide (NO) blockade using l-NAME treatment increased MAP and decreased RBF in both rat strains, but did not affect the K(+) -induced renal vasodilation. Conclusion: K(+) -induced renal vasodilation is larger in SHR, mediated by K(ir) channels in SD and SHR, and in addition, by Na(+) ,K(+) -ATPase in SD. In addition, NO is not essential for K(+) -induced renal vasodilation.

AB - Aim: We investigated the mechanisms behind K(+) -induced renal vasodilation in vivo in normotensive Sprague-Dawley (SD) rats and spontaneously hypertensive rats (SHR). Methods: Renal blood flow (RBF) was measured utilizing an ultrasonic Doppler flow probe. Renal vascular resistance (RVR) was calculated as the ratio of mean arterial pressure (MAP) and RBF (RVR = MAP/RBF). Test drugs were introduced directly into the renal artery. Inward rectifier K(+) (K(ir) ) channels and Na(+) ,K(+) -ATPase were blocked by Ba(2+) and ouabain (estimated plasma concentrations ~20 and ~7 µm) respectively. Results: Confocal immunofluorescence microscopy demonstrated K(ir) 2.1 channels in pre-glomerular vessels of SD and SHR. Ba(2+) caused a transient (6-13%) increase in baseline RVR in both SD and SHR. Ouabain had a similar effect. Elevated renal plasma [K(+) ] (~12 mm) caused a small and sustained decrease (5-13%) in RVR in both strains. This decrease was significantly larger in SHR than in SD. The K(+) -induced vasodilation was attenuated by Ba(2+) in control SD and SHR and by ouabain in SD. Nitric oxide (NO) blockade using l-NAME treatment increased MAP and decreased RBF in both rat strains, but did not affect the K(+) -induced renal vasodilation. Conclusion: K(+) -induced renal vasodilation is larger in SHR, mediated by K(ir) channels in SD and SHR, and in addition, by Na(+) ,K(+) -ATPase in SD. In addition, NO is not essential for K(+) -induced renal vasodilation.

U2 - 10.1111/j.1748-1716.2011.02304.x

DO - 10.1111/j.1748-1716.2011.02304.x

M3 - Journal article

C2 - 21477070

VL - 202

SP - 703

EP - 712

JO - Acta Physiologica

JF - Acta Physiologica

SN - 1748-1708

IS - 4

ER -

ID: 33720379