Published online before print August 29, 2002, doi: 10.1161/01.RES.0000035243.66189.92
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Submitted on March 14, 2002
Revised on July 23, 2002
Accepted on August 16, 2002
Tubulovascular Nitric Oxide Crosstalk Buffers. Angiotensin II-Induced Medullary Vasoconstriction
Jeffrey G. Dickhout ;
From the Department of Physiology, Medical College of Wisconsin, Milwaukee, Wis.
* To whom correspondence should be addressed. E-mail: cowley{at}mcw.edu.
Studies were designed to determine the source of NO responsible for buffering of the angiotensin II (Ang II)-mediated decrease of blood flow in the renal medulla. Intracellular Ca2+ concentration ([Ca2+]i) and NO production ([NO]i) of pericytes and endothelium of the vasa recta were independently measured with the use of fura 2-AM and DAF-2DA, respectively, in microtissue strips of the vascular bundles of the outer medullary vasa recta. Disruption of the endothelium of the vasa recta by perfusion with latex microspheres enabled imaging of the pericytes. Ang II (1 µmol/L) produced an increase of [NO]i of 19±6 U in pericytes of the vasa recta when the vessels were adjacent to medullary thick ascending limbs (mTALs). Pericytes of isolated vasa recta without surrounding mTALs showed a rapid peak increase in [Ca2+]i of 248±107 nmol/L, with a sustained elevation of 107±75 nmol/L, but did not show an increase in [NO]i to either Ang II (1 µmol/L) or the Ca2+ ionophore 4-bromo-A23187 (5 µmol/L). These observations indicated the lack of Ang II and Ca2+-sensitive NO production in pericytes of the vasa recta. In isolated vasa recta with intact endothelium, Ang II reduced [Ca2+]i from 128±28 to 62±13 nmol/L and failed to increase [NO]i. However, the Ca2+ ionophore did increase [NO]i in the endothelium (47±8 U), indicating the presence of Ca2+-sensitive NO production. Significant increases of [NO]i were observed in single isolated mTALs in response to both Ang II (33±6 U) and the Ca2+ ionophore (51±18 U). We conclude that Ang II increases [Ca2+]i in pericytes of the descending vasa recta as part of its constrictor action and that this vasoconstriction is buffered by the NO from the surrounding tubular elements, such as mTALs.
Key words: vasa recta • pericytes • endothelium • nitric oxide synthase • intracellular Ca2+
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