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1 Biology Department, Towson University, Towson 21252; and 2 Department of Medicine, Nephrology Division, University of Maryland School of Medicine, Baltimore, Maryland 21201
We tested whether dilation of outer medullary descending vasa recta
(OMDVR) is mediated by cAMP, nitric oxide (NO), and cyclooxygenase (COX). Adenosine (A; 10
6 M)-induced vasodilation of ANG
II (109 M)-preconstricted OMDVR was mimicked by the cAMP
analog 8-bromoadenosine 3',5'-cyclic monophosphate (1010
to 104 M) and reversed by the adenylate cyclase inhibitor
SQ-22536. Adenosine (104 M) stimulated OMDVR cAMP
production greater than threefold. NO synthase blockade with
NG-nitro-L-arginine methyl ester and
NG-monomethyl-L-arginine
(104 M) did not affect adenosine vasodilation. Adenosine
induced endothelial cytoplasmic calcium transients that were small.
Indomethacin (106 M) reversed adenonsine-induced dilation
of OMDVR preconstricted with ANG II, endothelin, 4-bromo-calcium
ionophore A23187, or carbocyclic thromboxane A2. In
contrast, selective A2-receptor activation dilated
endothelin-preconstricted OMDVR even in the presence of indomethacin.
We conclude that OMDVR vasodilation by adenosine involves cAMP and COX
but not NO. COX blockade does not fully inhibit selective
A2 receptor-mediated OMDVR dilation.
rat; microcirculation; microperfusion; fura 2; 8-cyclopentyl-1,3-dipropylxanthine; 2-p-[2-carboxyethyl]phenethyl-amino-5'-N-ethylcarboxamido-adenosine
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