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NEUROHUMORAL CONTROL OF CIRCULATION AND HYPERTENSION

Bovine lactoferrin has a nitric oxide-dependent hypotensive effect in rats

¹Department of Veterinary Physiology, Faculty of Agriculture, Tottori University, Tottori 680-0945; ²National Institute for Physiological Science, Okazaki 444-8585; ³Nuclear Receptor Ligand, Kawasaki, Kanagawa 213-0012; and ⁴Department of Veterinary Pharmacology, Faculty of Agriculture, Kagoshima University, Kagoshima 890-0065, Japan

Submitted 23 April 2003 ; accepted in final form 7 October 2003

Lactoferrin (LF) is a multifunctional protein that is found in milk, neutrophils, and other biological fluids. Under inflammatory conditions, LF production is increased in the periphery by neutrophils. However, the cardiovascular function of LF is still unknown. In the present study, we investigated the effect of bovine LF (BLF) on the mean blood pressure (MBP) and heart rate (HR) in urethane-anesthetized rats and the vascular function of BLF in the rat thoracic aorta. Intravenous injection of BLF produced dose-dependent decreases in MBP but did not affect HR, while the opioid agonist morphine decreased both MBP and HR. The hypotensive effect of BLF was not altered by naloxone methiodide, which cannot pass through the blood-brain barrier, but was significantly reduced by naloxone hydrochloride, which does pass through the blood-brain barrier. BLF-induced hypotension was completely blocked by the NO synthase inhibitor N^G-nitro-L-arginine methyl ester (L-NAME) but not by the inactive enantiomer of L-NAME, N^G-nitro-D-arginine methyl ester (D-NAME). BLF-induced hypotension was not altered by the muscarinic ACh receptor antagonist atropine or the cyclooxygenase inhibitor diclofenac. BLF produced relaxation in endothelium-intact but not endothelium-denuded aortic rings precontracted with phenylephrine. The relaxation evoked by BLF was completely blocked by L-NAME but not by D-NAME or the ATP-sensitive potassium channel blocker glibenclamide. These results suggest that BLF causes hypotension via an endothelium-dependent vasodilation that is strongly mediated by NO production and that BLF-induced hypotension also may be mediated by the central opioidergic system.

N^G-nitro-L-arginine methyl ester; naloxone hydrochloride; naloxone methiodide; endothelium cell

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