Kamata K, Hosokawa M
Department of Physiology and Morphology, Hoshi University, Tokyo, Japan.
Res Commun Mol Pathol Pharmacol. 1997 May;96(2):147-56.
We examined the possible existence of a novel endothelium-derived relaxing factor in the endothelium of the perfused rat kidney. Acetylcholine-induced vasodilatation was abolished by treatment with NG-nitro-L-arginine (L-NNA) and methylene blue in isotonic high K+ (60 mM) medium, whereas cyclopiazonic acid (CPA)-induced vasodilatation of the perfused kidney was slightly increased by this treatment. When the kidney was perfused with 0.47% CHAPS solution for 1 min, acetylcholine- or cyclopiazonic acid-induced vasodilatation was almost abolished. Acetylcholine- or cyclopiazonic acid-induced vasodilatation was not affected by indomethacin. These results suggest that CPA may release a novel endothelium-derived relaxing factor, which is not prostanoids, nitric oxide nor endothelium-derived hyperpolarizing factor in the endothelium of the renal vascular bed.
