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Therapeutic Potential of L-Arginine, a Precursor of Nitric Oxide, in Focal Cerebral Ischemia

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The Human Brain Circulation

Part of the book series: Vascular Biomedicine ((VB))

Abstract

Nitric oxide (NO) is synthesized from the amino acid L-argin­ine by NO synthase, an enzyme present in cerebrovascular endo­thelium’ and perivascular nerve fibers.2 The synthesis of NO is calcium-dependent and requires NADPH. NO or a related thiol has been proposed as a mediator of endothelium-dependent relaxation.3 NO may also be neurotoxic and may be a mediator of cytotoxic effects of glutamate both in vitro4 and in vivo (see ref. 5 for a review). Both glutamate neurotoxicity and dilatation of blood vessels are important to the pathophysiology of focal cerebral ischemia, as is the NO-induced inhibition of platelet aggregation and adhesion.6’Current studies were undertaken to compare the effects of inhibiting NO synthase with the effects of providing sub­strate for NO synthesis, L-arginine, during the first 24 h after focal brain ischemia.

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Morikawa, E., Huang, Z., Rosenblatt, S., Yoshida, T., Moskowitz, M.A. (1994). Therapeutic Potential of L-Arginine, a Precursor of Nitric Oxide, in Focal Cerebral Ischemia. In: Bevan, R.D., Bevan, J.A. (eds) The Human Brain Circulation. Vascular Biomedicine. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-4612-0303-2_28

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  • DOI: https://doi.org/10.1007/978-1-4612-0303-2_28

  • Publisher Name: Humana Press, Totowa, NJ

  • Print ISBN: 978-1-4612-6700-3

  • Online ISBN: 978-1-4612-0303-2

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