Closure of multiple types of K+ channels is necessar to induce changes in renal vascular resistance in vivo in rats

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Closure of multiple types of K+ channels is necessar to induce changes in renal vascular resistance in vivo in rats. / Sørensen, Charlotte Mehlin; Giese, Isaiah; Braunstein, Thomas Hartig; von Holstein-Rathlou, Niels-Henrik; Salomonsson, Max.

I: Pflügers Archiv - European Journal of Physiology, Bind 462, Nr. 5, 11.2011, s. 655-667.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Sørensen, CM, Giese, I, Braunstein, TH, von Holstein-Rathlou, N-H & Salomonsson, M 2011, 'Closure of multiple types of K+ channels is necessar to induce changes in renal vascular resistance in vivo in rats', Pflügers Archiv - European Journal of Physiology, bind 462, nr. 5, s. 655-667. https://doi.org/10.1007/s00424-011-1018-2

APA

Sørensen, C. M., Giese, I., Braunstein, T. H., von Holstein-Rathlou, N-H., & Salomonsson, M. (2011). Closure of multiple types of K+ channels is necessar to induce changes in renal vascular resistance in vivo in rats. Pflügers Archiv - European Journal of Physiology, 462(5), 655-667. https://doi.org/10.1007/s00424-011-1018-2

Vancouver

Sørensen CM, Giese I, Braunstein TH, von Holstein-Rathlou N-H, Salomonsson M. Closure of multiple types of K+ channels is necessar to induce changes in renal vascular resistance in vivo in rats. Pflügers Archiv - European Journal of Physiology. 2011 nov;462(5):655-667. https://doi.org/10.1007/s00424-011-1018-2

Author

Sørensen, Charlotte Mehlin ; Giese, Isaiah ; Braunstein, Thomas Hartig ; von Holstein-Rathlou, Niels-Henrik ; Salomonsson, Max. / Closure of multiple types of K+ channels is necessar to induce changes in renal vascular resistance in vivo in rats. I: Pflügers Archiv - European Journal of Physiology. 2011 ; Bind 462, Nr. 5. s. 655-667.

Bibtex

@article{cb8bdadb634347e6a9f57d09d8e7a9b4,
title = "Closure of multiple types of K+ channels is necessar to induce changes in renal vascular resistance in vivo in rats",
abstract = "Inhibition of K(+) channels might mediate renal vasoconstriction. As inhibition of a single type of K(+) channel caused minor or no renal vasoconstriction in vivo in rats, we hypothesized that several classes of K(+) channels must be blocked to elicit renal vasoconstriction. We measured renal blood flow (RBF) in vivo in anesthetized Sprague-Dawley rats. Test agents were infused directly into the renal artery to avoid systemic effects. Inhibition of BK(Ca) and K(ir) channels (with TEA and Ba(2+), respectively) caused small and transient reductions in RBF (to 93¿±¿2% and 95¿±¿1% of baseline, respectively). K(ATP), SK(Ca) or K(v) channel blockade (with glibenclamide, apamin and 4-aminopyridine, respectively) was without effect. However, a cocktail of all blockers caused a massive reduction of RBF (to 15¿±¿10% of baseline). Nifedipine and mibefradil abolished and reduced, respectively, this RBF reduction. The effect of the cocktail of K(+) channel blockers was confirmed in mice using the isolated blood-perfused juxtamedullary nephron preparation. A cocktail of K(+) channel openers (K(+), NS309, NS1619 and pinacidil) had only a minor effect on baseline RBF in vivo in rats, but reduced the vasoconstriction induced by bolus injections of norepinephrine or angiotensin II (by 33¿±¿5% and 60¿±¿5%, respectively). Our results indicate that closure of numerous types of K(+) channels could participate in the mediation of agonist-induced renal vasoconstriction. Our results also suggest that renal vasoconstriction elicited by K(+) channel blockade is mediated by nifedipine-sensitive Ca(2+) channels and partly by mibefradil-sensitive Ca(2+) channels. ",
author = "S{\o}rensen, {Charlotte Mehlin} and Isaiah Giese and Braunstein, {Thomas Hartig} and {von Holstein-Rathlou}, Niels-Henrik and Max Salomonsson",
year = "2011",
month = nov,
doi = "10.1007/s00424-011-1018-2",
language = "English",
volume = "462",
pages = "655--667",
journal = "Pfl{\"u}gers Archiv - European Journal of Physiology",
issn = "0031-6768",
publisher = "Springer",
number = "5",

}

RIS

TY - JOUR

T1 - Closure of multiple types of K+ channels is necessar to induce changes in renal vascular resistance in vivo in rats

AU - Sørensen, Charlotte Mehlin

AU - Giese, Isaiah

AU - Braunstein, Thomas Hartig

AU - von Holstein-Rathlou, Niels-Henrik

AU - Salomonsson, Max

PY - 2011/11

Y1 - 2011/11

N2 - Inhibition of K(+) channels might mediate renal vasoconstriction. As inhibition of a single type of K(+) channel caused minor or no renal vasoconstriction in vivo in rats, we hypothesized that several classes of K(+) channels must be blocked to elicit renal vasoconstriction. We measured renal blood flow (RBF) in vivo in anesthetized Sprague-Dawley rats. Test agents were infused directly into the renal artery to avoid systemic effects. Inhibition of BK(Ca) and K(ir) channels (with TEA and Ba(2+), respectively) caused small and transient reductions in RBF (to 93¿±¿2% and 95¿±¿1% of baseline, respectively). K(ATP), SK(Ca) or K(v) channel blockade (with glibenclamide, apamin and 4-aminopyridine, respectively) was without effect. However, a cocktail of all blockers caused a massive reduction of RBF (to 15¿±¿10% of baseline). Nifedipine and mibefradil abolished and reduced, respectively, this RBF reduction. The effect of the cocktail of K(+) channel blockers was confirmed in mice using the isolated blood-perfused juxtamedullary nephron preparation. A cocktail of K(+) channel openers (K(+), NS309, NS1619 and pinacidil) had only a minor effect on baseline RBF in vivo in rats, but reduced the vasoconstriction induced by bolus injections of norepinephrine or angiotensin II (by 33¿±¿5% and 60¿±¿5%, respectively). Our results indicate that closure of numerous types of K(+) channels could participate in the mediation of agonist-induced renal vasoconstriction. Our results also suggest that renal vasoconstriction elicited by K(+) channel blockade is mediated by nifedipine-sensitive Ca(2+) channels and partly by mibefradil-sensitive Ca(2+) channels.

AB - Inhibition of K(+) channels might mediate renal vasoconstriction. As inhibition of a single type of K(+) channel caused minor or no renal vasoconstriction in vivo in rats, we hypothesized that several classes of K(+) channels must be blocked to elicit renal vasoconstriction. We measured renal blood flow (RBF) in vivo in anesthetized Sprague-Dawley rats. Test agents were infused directly into the renal artery to avoid systemic effects. Inhibition of BK(Ca) and K(ir) channels (with TEA and Ba(2+), respectively) caused small and transient reductions in RBF (to 93¿±¿2% and 95¿±¿1% of baseline, respectively). K(ATP), SK(Ca) or K(v) channel blockade (with glibenclamide, apamin and 4-aminopyridine, respectively) was without effect. However, a cocktail of all blockers caused a massive reduction of RBF (to 15¿±¿10% of baseline). Nifedipine and mibefradil abolished and reduced, respectively, this RBF reduction. The effect of the cocktail of K(+) channel blockers was confirmed in mice using the isolated blood-perfused juxtamedullary nephron preparation. A cocktail of K(+) channel openers (K(+), NS309, NS1619 and pinacidil) had only a minor effect on baseline RBF in vivo in rats, but reduced the vasoconstriction induced by bolus injections of norepinephrine or angiotensin II (by 33¿±¿5% and 60¿±¿5%, respectively). Our results indicate that closure of numerous types of K(+) channels could participate in the mediation of agonist-induced renal vasoconstriction. Our results also suggest that renal vasoconstriction elicited by K(+) channel blockade is mediated by nifedipine-sensitive Ca(2+) channels and partly by mibefradil-sensitive Ca(2+) channels.

U2 - 10.1007/s00424-011-1018-2

DO - 10.1007/s00424-011-1018-2

M3 - Journal article

VL - 462

SP - 655

EP - 667

JO - Pflügers Archiv - European Journal of Physiology

JF - Pflügers Archiv - European Journal of Physiology

SN - 0031-6768

IS - 5

ER -

ID: 38256569