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cotransporter in rat aorta
1 Renal Division,
Little is known
about the function and regulation of the
Na+-K+-2Cl
cotransporter NKCC1 in vascular smooth muscle. The
activity of NKCC1 was measured as the bumetanide-sensitive efflux of
86Rb+
from intact smooth muscle of the rat aorta. Hypertonic shrinkage (440 mosmol/kgH2O) rapidly
doubled cotransporter activity, consistent with its volume-regulatory
function. NKCC1 was also acutely activated by the vasoconstrictors ANG
II (52%), phenylephrine (50%), endothelin (53%), and 30 mM KCl
(54%). Both nitric oxide and nitroprusside inhibited basal NKCC1
activity (39 and 34%, respectively), and nitroprusside
completely reversed the stimulation by phenylephrine. The
phosphorylation of NKCC1 was increased by hypertonic shrinkage, phenylephrine, and KCl and was reduced by nitroprusside. The inhibition of NKCC1 significantly reduced the contraction of rat aorta induced by
phenylephrine (63% at 10 nM, 26% at 30 nM) but not by KCl. We
conclude that the
Na+-K+-2Cl
cotransporter in vascular smooth muscle is reciprocally regulated by
vasoconstrictors and nitrovasodilators and contributes to smooth muscle
contraction, indicating that alterations in NKCC1 could influence
vascular smooth muscle tone in vivo.
sodium-potassium-chloride cotransport; vascular smooth muscle; contraction; cell chloride; phenylephrine; angiotensin II; endothelin; nitric oxide
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