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No major role of BKCa channels in the modulation of renal blood flow in rats

The aim of the present study was to investigate the role of large calcium activated potassium (BKCa) channels in the maintenance of basal renal vascular tone in vivo in anesthetized adult Sprague‐Dawley rats. We also examined whether the vasoconstriction elicited by angiotensin II (Ang II) and norepinephrine (NE) was buffered by simultaneous activation of BKCa. Vasoactive agents, BKCa blockers or a stimulator were infused directly into the renal artery via a polyethylene (PE‐10) catheter introduced into the left femoral artery and advanced through the abdominal aorta and approximately 1 mm into the left renal artery. Renal blood flow (RBF) was measured by using an electromagnetic flow sensor. Renal preinfusion of BKCa blockers tetraethylammonium chlorid (TEA) (3.0 μmol/min) for 1 (n = 8) or 5 min (n = 5) and iberiotoxin for 5 min (n = 6) (3.3 nmol/min) did not significantly affect the RBF baseline. Renal arterial injection of a 10 μL bolus of Ang II (n = 18) (1‐4 ng/10 μL) or NE (n = 17) (10‐40 ng/10 μL) produced a significant dose dependent temporary decrease in RBF. These responses were not significantly affected by 1 or 4 min preinfusion of TEA (n = 8) or a 4 min preinfusion of iberiotoxin (n = 6). Renal addition of the BKCa opener NS 1619 (n = 5) (30 and 90 μmol/min) did not significantly affect basal renal blood flow or the responses to Ang II and NE. The present results do not indicate any major role for BKCa channels in the control of basal renal tone in vivo. Furthermore, there is no support for the hypothesis that BKCa channels have a buffering effect on the responses to Ang II and NE in rat renal vasculature.