Hypoxia inhibits myogenic reactivity of renal afferent arterioles by activating ATP-sensitive K+ channels.
Recent findings implicate K+ channels as important modulators of myogenic tone and possible mediators of the vasodilatory effects of hypoxia. In the present report, we examined the effects of hypoxia on myogenic vasoconstriction of renal afferent arterioles. Using the in vitro perfused hydronephrotic rat kidney model, we observed precisely graded decreases in arteriolar diameter when renal perfusion pressure was increased. Normal myogenic reactivity was observed over PO2 levels of 150 to 80 mm Hg. Reducing PO2 to 60, 40, and 30 mm Hg resulted in a significant progressive inhibition of myogenic reactivity. At approximately 20 mm Hg, myogenic vasoconstriction was essentially abolished, whereas the vasoconstriction induced by 30 mmol/L KCl was unaffected. The addition of 1.0 mumol/L glibenclamide completely restored myogenic vasoconstriction during hypoxia. In contrast, 1.0 mmol/L tetraethylammonium did not alter the effects of hypoxia. To investigate the relation between hypoxia-induced vasodilation and smooth muscle oxidative phosphorylation, we monitored changes in arteriolar levels of reduced NADH during exposure to hypoxia. Arterioles preconstricted by elevated pressure were optically isolated for simultaneous monitoring of vessel diameter and NADH fluorescence (360-nm excitation, 450-nm emission). Reducing perfusate PO2 from 150 to 20 mm Hg resulted in progressive loss of myogenic tone with no change in arteriolar NADH. These findings indicate that lowering PO2 within a physiological range attenuates myogenic reactivity of the renal afferent arteriole by causing the activation of ATP-sensitive K+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)
- Copyright © 1994 by American Heart Association