Titlebook: Nitric Oxide and the Kidney; Physiology and Patho Michael S. Goligorsky,Steven S. Gross Book 1997 Springer Science+Business Media Dordrecht

的闡明

成份

NO and the Medullary Circulation its vulnerability to hypoxic damage. Our observations and a literature review are presented, along with experimental data regarding the role of nitric oxide in the pathogenesis of radiocontrast nephropathy, a prototype of acute renal failure resulting from medullary hypoxia.

團(tuán)結(jié)

Regulation of the NOS Gene Familyys a role in basic cellular processes, in addition to the complex functions attributed to NO in mammalian cell biology. As there are several excellent reviews discussing the historical perspectives, pharmacology, and biochemistry of NOS and NO, this chapter will focus on recent advances in the molecular regulation of NOS expression [1-6-8].

鳥籠

Sinus-Node

ogy. This authoritative edited volume reviews theprogress to date and opens perspectives to novel diagnostic andtherapeutic strategies. The contributors are leading authorites, inmost cases the investigators who have pioneered the ideas explored inthe book.978-1-4613-7768-9978-1-4615-6039-5

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Coronation

Tubuloglomerular Feedback and Macula Densa-Derived NOnd initiation or release of vasoactive mediators occurs. TGF may also maintain homeostasis through regulation of sodium excretion, because increased delivery of sodium chloride to the macula densa activates TGF and decreases single-nephron GFR, thus adjusting the rate of sodium excretion.

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一大塊

Distribution of NOSs in the Kidney 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 Ca.levels for its activation; exceptions to this definition were reported for the kidney as detailed below.

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