Angiotensin II-induced vasoconstriction in the descending vasa recta is buffered by nitric oxide produced from surrounding tubular elements like medullary thick ascending limbs, rather than the vasa recta pericytes themselves.
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Implicates tubular elements as NO source buffering Ang II vasoconstriction; hypothesis-generating for medullary hemodynamics in hypertension.
Dickhout et al. (2002) studied this question.
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