Effects of chloride channel blockers on rat renal vascular responses to angiotensin II and norepinephrine.

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Effects of chloride channel blockers on rat renal vascular responses to angiotensin II and norepinephrine. / Steendahl, Joen; Sørensen, Charlotte Mehlin; Salomonsson, Max; Holstein-Rathlou, N.-H.

I: American Journal of Physiology - Renal Physiology, Bind 286, Nr. 2, 2003, s. F323-30.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Steendahl, J, Sørensen, CM, Salomonsson, M & Holstein-Rathlou, N-H 2003, 'Effects of chloride channel blockers on rat renal vascular responses to angiotensin II and norepinephrine.', American Journal of Physiology - Renal Physiology, bind 286, nr. 2, s. F323-30. https://doi.org/10.1152/ajprenal.00017.2003

APA

Steendahl, J., Sørensen, C. M., Salomonsson, M., & Holstein-Rathlou, N-H. (2003). Effects of chloride channel blockers on rat renal vascular responses to angiotensin II and norepinephrine. American Journal of Physiology - Renal Physiology, 286(2), F323-30. https://doi.org/10.1152/ajprenal.00017.2003

Vancouver

Steendahl J, Sørensen CM, Salomonsson M, Holstein-Rathlou N-H. Effects of chloride channel blockers on rat renal vascular responses to angiotensin II and norepinephrine. American Journal of Physiology - Renal Physiology. 2003;286(2):F323-30. https://doi.org/10.1152/ajprenal.00017.2003

Author

Steendahl, Joen ; Sørensen, Charlotte Mehlin ; Salomonsson, Max ; Holstein-Rathlou, N.-H. / Effects of chloride channel blockers on rat renal vascular responses to angiotensin II and norepinephrine. I: American Journal of Physiology - Renal Physiology. 2003 ; Bind 286, Nr. 2. s. F323-30.

Bibtex

@article{f5308cc0ab6111ddb5e9000ea68e967b,
title = "Effects of chloride channel blockers on rat renal vascular responses to angiotensin II and norepinephrine.",
abstract = "The aim of the present study was to investigate the role of Ca2+-activated Cl- channels in the renal vasoconstriction elicited by angiotensin II (ANG II) and norepinephrine (NE). Renal blood flow (RBF) was measured in vivo using electromagnetic flowmetry. Ratiometric photometry of fura 2 fluorescence was used to estimate intracellular free Ca2+ concentration ([Ca2+]i) in isolated preglomerular vessels from rat kidneys. Renal arterial injection of ANG II (2-4 ng) and NE (20-40 ng) produced a transient decrease in RBF. Administration of ANG II (10-7 M) and NE (5 x 10-6 M) to the isolated preglomerular vessels caused a prompt increase in [Ca2+]i. Renal preinfusion of DIDS (0.6 and 1.25 micromol/min) attenuated the ANG II-induced vasoconstriction to approximately 35% of the control response, whereas the effects of NE were unaltered. Niflumic acid (0.14 and 0.28 micromol/min) and 2-[(2-cyclopentenyl-6,7-dichloro-2,3-dihydro-2-methyl-1-oxo-1H-inden-5-yl)oxy]acetic acid (IAA-94; 0.045 and 0.09 micromol/min) did not affect the vasoconstrictive responses of these compounds. Pretreatment with niflumic acid (50 microM) or IAA-94 (30 microM) for 2 min decreased baseline [Ca2+]i but did not change the magnitude of the [Ca2+]i response to ANG II and NE in the isolated vessels. The present results do not support the hypothesis that Ca2+-activated Cl- channels play a crucial role in the hemodynamic effects of ANG II and NE in rat renal vasculature.",
author = "Joen Steendahl and S{\o}rensen, {Charlotte Mehlin} and Max Salomonsson and N.-H. Holstein-Rathlou",
note = "Keywords: 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; Angiotensin II; Animals; Antihypertensive Agents; Calcium; Chloride Channels; Cyclooxygenase Inhibitors; Diuretics; Fluorescent Dyes; Fura-2; Glycolates; Kidney Glomerulus; Magnetics; Male; Niflumic Acid; Norepinephrine; Prazosin; Rats; Rats, Sprague-Dawley; Renal Circulation; Vasoconstrictor Agents",
year = "2003",
doi = "10.1152/ajprenal.00017.2003",
language = "English",
volume = "286",
pages = "F323--30",
journal = "American Journal of Physiology: Renal Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "2",

}

RIS

TY - JOUR

T1 - Effects of chloride channel blockers on rat renal vascular responses to angiotensin II and norepinephrine.

AU - Steendahl, Joen

AU - Sørensen, Charlotte Mehlin

AU - Salomonsson, Max

AU - Holstein-Rathlou, N.-H.

N1 - Keywords: 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; Angiotensin II; Animals; Antihypertensive Agents; Calcium; Chloride Channels; Cyclooxygenase Inhibitors; Diuretics; Fluorescent Dyes; Fura-2; Glycolates; Kidney Glomerulus; Magnetics; Male; Niflumic Acid; Norepinephrine; Prazosin; Rats; Rats, Sprague-Dawley; Renal Circulation; Vasoconstrictor Agents

PY - 2003

Y1 - 2003

N2 - The aim of the present study was to investigate the role of Ca2+-activated Cl- channels in the renal vasoconstriction elicited by angiotensin II (ANG II) and norepinephrine (NE). Renal blood flow (RBF) was measured in vivo using electromagnetic flowmetry. Ratiometric photometry of fura 2 fluorescence was used to estimate intracellular free Ca2+ concentration ([Ca2+]i) in isolated preglomerular vessels from rat kidneys. Renal arterial injection of ANG II (2-4 ng) and NE (20-40 ng) produced a transient decrease in RBF. Administration of ANG II (10-7 M) and NE (5 x 10-6 M) to the isolated preglomerular vessels caused a prompt increase in [Ca2+]i. Renal preinfusion of DIDS (0.6 and 1.25 micromol/min) attenuated the ANG II-induced vasoconstriction to approximately 35% of the control response, whereas the effects of NE were unaltered. Niflumic acid (0.14 and 0.28 micromol/min) and 2-[(2-cyclopentenyl-6,7-dichloro-2,3-dihydro-2-methyl-1-oxo-1H-inden-5-yl)oxy]acetic acid (IAA-94; 0.045 and 0.09 micromol/min) did not affect the vasoconstrictive responses of these compounds. Pretreatment with niflumic acid (50 microM) or IAA-94 (30 microM) for 2 min decreased baseline [Ca2+]i but did not change the magnitude of the [Ca2+]i response to ANG II and NE in the isolated vessels. The present results do not support the hypothesis that Ca2+-activated Cl- channels play a crucial role in the hemodynamic effects of ANG II and NE in rat renal vasculature.

AB - The aim of the present study was to investigate the role of Ca2+-activated Cl- channels in the renal vasoconstriction elicited by angiotensin II (ANG II) and norepinephrine (NE). Renal blood flow (RBF) was measured in vivo using electromagnetic flowmetry. Ratiometric photometry of fura 2 fluorescence was used to estimate intracellular free Ca2+ concentration ([Ca2+]i) in isolated preglomerular vessels from rat kidneys. Renal arterial injection of ANG II (2-4 ng) and NE (20-40 ng) produced a transient decrease in RBF. Administration of ANG II (10-7 M) and NE (5 x 10-6 M) to the isolated preglomerular vessels caused a prompt increase in [Ca2+]i. Renal preinfusion of DIDS (0.6 and 1.25 micromol/min) attenuated the ANG II-induced vasoconstriction to approximately 35% of the control response, whereas the effects of NE were unaltered. Niflumic acid (0.14 and 0.28 micromol/min) and 2-[(2-cyclopentenyl-6,7-dichloro-2,3-dihydro-2-methyl-1-oxo-1H-inden-5-yl)oxy]acetic acid (IAA-94; 0.045 and 0.09 micromol/min) did not affect the vasoconstrictive responses of these compounds. Pretreatment with niflumic acid (50 microM) or IAA-94 (30 microM) for 2 min decreased baseline [Ca2+]i but did not change the magnitude of the [Ca2+]i response to ANG II and NE in the isolated vessels. The present results do not support the hypothesis that Ca2+-activated Cl- channels play a crucial role in the hemodynamic effects of ANG II and NE in rat renal vasculature.

U2 - 10.1152/ajprenal.00017.2003

DO - 10.1152/ajprenal.00017.2003

M3 - Journal article

C2 - 14506073

VL - 286

SP - F323-30

JO - American Journal of Physiology: Renal Physiology

JF - American Journal of Physiology: Renal Physiology

SN - 1931-857X

IS - 2

ER -

ID: 8420227