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Am J Physiol Heart Circ Physiol 278: H1248-H1255, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 4, H1248-H1255, April 2000

Inhibition of calcium signaling in descending vasa recta endothelia by ANG II

Thomas L. Pallone, Erik P. Silldorff, and Zhong Zhang

Division of Nephrology, University of Maryland School of Medicine, Baltimore 21201-1595; and Department of Biology, Towson University, Towson, Maryland 21252

The intracellular calcium ([Ca2+]i) response of outer medullary descending vasa recta (OMDVR) endothelia to ANG II was examined in fura 2-loaded vessels. Abluminal ANG II (10-8 M) caused [Ca2+]i to fall in proportion to the resting [Ca2+]i (r = 0.82) of the endothelium. ANG II (10-8 M) also inhibited both phases of the [Ca2+]i response generated by bradykinin (BK, 10-7 M), 835 ± 201 versus 159 ± 30 nM (peak phase) and 169 ± 26 versus 103 ± 14 nM (plateau phase) (means ± SE). Luminal ANG II reduced BK (10-7 M)-stimulated plateau [Ca2+]i from 180 ± 40 to 134 ± 22 nM without causing vasoconstriction. Abluminal ANG II added to the bath after luminal application further reduced [Ca2+]i to 113 ± 9 nM and constricted the vessels. After thapsigargin (TG) pretreatment, ANG II (10-8 M) caused [Ca2+]i to fall from 352 ± 149 to 105 ± 37 nM. This effect occurred at a threshold ANG II concentration of 10-10 M and was maximal at 10-8 M. ANG II inhibited both the rate of Ca2+ entry into [Ca2+]i-depleted endothelia and the rate of Mn2+ entry into [Ca2+]i-replete endothelia. In contrast, ANG II raised [Ca2+]i in the medullary thick ascending limb and outer medullary collecting duct, increasing [Ca2+]i from baselines of 99 ± 33 and 53 ± 11 to peaks of 200 ± 47 and 65 ± 11 nM, respectively. We conclude that OMDVR endothelia are unlikely to be the source of ANG II-stimulated NO production in the medulla but that interbundle nephrons might release Ca2+-dependent vasodilators to modulate vasomotor tone in vascular bundles.

microperfusion; kidney; fura 2; bradykinin; thapsigargin


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