Abstract
A variety of renal cell types are capable of synthesizing nitric oxide (NO). Three isoforms have been identified to date. There are the constitutive isoforms NOS I also termed neurona I (n) or brain (b) type NOS based on its first identification in the brain of various speciesl and NOS III or endothelial (ec) NOS, although this isoform is not solely expressed in endothelia but has now also been detected in epithelial cells, see below], and the inducible isoform NOS II (or iNOS) which appears to occur in the kidney as a macrophage-type and a vascular smooth muscle cell-type NOS II [1]. NOS I and NOS III, although constitutively expressed, are quiescent until activated by increased Ca2+levels that sustain calmodulin binding [2-6]. In contrast, NOS II, the inducible form, is present after transcriptional activation by cytokines or lipopolysaccharide (LPS), the principal component of bacterial endotoxin [7-11]. This NOS isoform remains active for longer periods and does not require Ca2+levels for its activation; exceptions to this definition were reported for the kidney as detailed below.
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Bachmann, S. (1997). Distribution of NOSs in the Kidney. In: Goligorsky, M.S., Gross, S.S. (eds) Nitric Oxide and the Kidney. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-6039-5_7
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