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
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