Rabbit brain contains an endogenous inhibitor of endothelium-dependent relaxation

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Abstract
1 Supernatants prepared from the rabbit brain, lung and liver caused an endothelium-dependent and volume-related contraction of the phenylephrine-pretreated rabbit aorta and inhibited relaxation due to acetylcholine (ACh). 2 Perfusion in situ of the rabbit lung or liver with Krebs solution substantially reduced or removed the endothelium-dependent inhibitor. Spectrophotometric analysis revealed the presence of substantial amounts of haemoglobin (1.8–2.1 μm) in these organ supernatants. 3 Supernatants prepared from the Krebs-perfused rabbit brain retained the ability to contract the phenylephrine-pretreated rabbit aorta and to inhibit relaxation due to ACh and substance P (SP). Rabbit brain supernatant did not reduce the vasodilator effect of sodum nitroprusside (NP) or nitric oxide (NO). 4 Rabbit brain supernatant contained low (< 0.35 μm) concentrations of haemoglobin. 5 The inhibitory effect of rabbit brain supernatant was reversed by l-arginine (500 μm) but not d-arginine (500 μm). 6 The inhibitor of endothelium-dependent vasodilatation present in rabbit brain was not removed by dialysis (24 h, 4°C) but was partially precipitated by ammonium sulphate (30% w/v). 7 Rabbit brain contains an endogenous inhibitor of vascular NO biosynthesis. The identity of this inhibitor is not known although it seems likely to be a large peptide or protein.