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RENAL HEMODYNAMICS AND CARDIORENAL INTEGRATION

Renovascular BK_Ca channels are not activated in vivo under resting conditions and during agonist stimulation

Division of Renal and Cardiovascular Research, Department of Medical Physiology, The Panum Institute, University of Copenhagen, Copenhagen, Denmark

Submitted 18 May 2006 ; accepted in final form 1 September 2006

We investigated the role of large-conductance Ca²⁺-activated K⁺ (BK_Ca) channels for the basal renal vascular tone in vivo. Furthermore, the possible buffering by BK_Ca of the vasoconstriction elicited by angiotensin II (ANG II) or norepinephrine (NE) was investigated. The possible activation of renal vascular BK_Ca channels by cAMP was investigated by infusing forskolin. Renal blood flow (RBF) was measured in vivo using electromagnetic flowmetry or ultrasonic Doppler. Renal preinfusion of tetraethylammonium (TEA; 3.0 µmol/min) caused a small reduction of baseline RBF, but iberiotoxin (IBT; 0.3 nmol/min) did not have any effect. Renal injection of ANG II (1–4 ng) or NE (10–40 ng) produced a transient decrease in RBF. These responses were not affected by preinfusion of TEA or IBT. Renal infusion of the BK_Ca opener NS-1619 (90.0 nmol/min) did not affect basal RBF or the response to NE, but it attenuated the response to ANG II. Coadministration of NS-1619 with TEA or IBT abolished this effect. Forskolin caused renal vasodilation that was not inhibited by IBT. The presence of BK_Ca channels in the preglomerular vessels was confirmed by immunohistochemistry. Despite their presence, there is no indication for a major role for BK_Ca channels in the control of basal renal tone in vivo. Furthermore, BK_Ca channels do not have a buffering effect on the rat renal vascular responses to ANG II and NE. The fact that NS-1619 attenuates the ANG II response indicates that the renal vascular BK_Ca channels can be activated under certain conditions.

microcirculation; vascular smooth muscle; potassium channels; Sprague-Dawley rats

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