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cotransport via 20-HETE and PKC in medullary thick ascending
limb
1 Physiologie et Endocrinologie Cellulaire Rénale, Institut National de la Santé et de la Recherche Médicale Unité 356, Université Pierre et Marie Curie and Hôpital Broussais, 75270 Paris Cedex 06, France; and 2 Department of Internal Medicine and Molecular Genetics, University of Cincinnati School of Medicine, Cincinnati, Ohio 45267
Cell pH was monitored in medullary thick ascending limbs to
determine effects of ANG II on
Na+-K+(NH+4)-2Cl
cotransport. ANG II at 1016
to 1012 M inhibited
30-50% (P < 0.005),
but higher ANG II concentrations were stimulatory compared with the
1012 M ANG II level
cotransport activity; eventually,
106 M ANG II stimulated
34% cotransport activity (P < 0.003). Inhibition by 1012
M ANG II was abolished by phospholipase C (PLC), diacylglycerol lipase,
or cytochrome P-450-dependent
monooxygenase blockade; 1012 M ANG II had no effect
additive to inhibition by 20-hydroxyeicosatetranoic acid (20-HETE).
Stimulation by 106 M ANG II
was abolished by PLC and protein kinase C (PKC) blockade and was
partially suppressed when the rise in cytosolic
Ca2+ was prevented. All ANG II
effects were abolished by DUP-753 (losartan) but not by PD-123319. Thus
1012 M ANG II inhibits
via 20-HETE, whereas 
5 × 1011 M ANG II stimulates
via PKC
Na+-K+(NH+4)-2Cl
cotransport; all ANG II effects involve
AT1 receptors and PLC activation.
intracellular pH; intracellular calcium; cytochrome P-450-dependent monooxygenase; phospholipase C; diacylglycerol lipase; protein kinase C; angiotensin II receptors; DUP-753; PD-123319
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