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      Nitric oxide and the cerebral vascular function

      Journal of Biomedical Science

      Springer Nature America, Inc

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          Most cited references 47

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          The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine

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            Localization of nitric oxide synthase indicating a neural role for nitric oxide.

            Nitric oxide (NO), apparently identical to endothelium-derived relaxing factor in blood vessels, is also formed by cytotoxic macrophages, in adrenal gland and in brain tissue, where it mediates the stimulation by glutamate of cyclic GMP formation in the cerebellum. Stimulation of intestinal or anococcygeal nerves liberates NO, and the resultant muscle relaxation is blocked by arginine derivatives that inhibit NO synthesis. It is, however, unclear whether in brain or intestine, NO released following nerve stimulation is formed in neurons, glia, fibroblasts, muscle or blood cells, all of which occur in proximity to neurons and so could account for effects of nerve stimulation on cGMP and muscle tone. We have now localized NO synthase protein immunohistochemically in the rat using antisera to the purified enzyme. We demonstrate NO synthase in the brain to be exclusively associated with discrete neuronal populations. NO synthase is also concentrated in the neural innervation of the posterior pituitary, in autonomic nerve fibres in the retina, in cell bodies and nerve fibres in the myenteric plexus of the intestine, in adrenal medulla, and in vascular endothelial cells. These prominent neural localizations provide the first conclusive evidence for a strong association of NO with neurons.
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              Biological actions and properties of endothelium-derived nitric oxide formed and released from artery and vein.

               L. Ignarro (1989)
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                Author and article information

                Journal
                Journal of Biomedical Science
                J Biomed Sci
                Springer Nature America, Inc
                1021-7770
                1423-0127
                January 2000
                January 2000
                : 7
                : 1
                : 16-26
                Article
                10.1007/BF02255914
                © 2000
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