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

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

SN - 1748-1708

VL - 202

SP - 703

EP - 712

JO - Acta Physiologica (Print)

JF - Acta Physiologica (Print)

IS - 4

ER -