BÖBREK HASTALIKLARINDA NİTRİK OKSİT SENTAZ AKTİVİTESİ VE DÜZENLENME MEKANİZMALARI

Year 2023, Volume: 37 Issue: 3, 293 - 307, 25.01.2024

Aygül Cemre Şahin , Caner Çavdar , Zahide Çavdar

https://doi.org/10.18614/deutip.1231395

Abstract

Nitrik oksit (NO) gaz yapıda, 5-6 saniyelik yarılanma ömrüne sahip, birçok fizyolojik ve patolojik olayda görev alan bir moleküldür. Fizyolojik şartlarda böbrekte renal ve glomerüler hemodinamiğin düzenlenmesi, natriürezis, medullar perfüzyon, tübüloglomerüler feedback, tübüler sodyum reabsorbsiyonu ve renal sinir aktivitesi gibi birçok olayda rol almaktadır. NO sentezinin bozulması sonucu çeşitli böbrek hasarı hastalıkları ortaya çıktığından bu mekanizmaların bilinmesi böbrek hasarına yönelik geliştirilecek tedavi yöntemlerinde önemli bir kilit noktasıdır. NO sentezinden sorumlu olan nitrik oksit sentaz (NOS) enzimlerinin insanda tanımlanan üç izoformu; nöronal NOS (nNOS), indüklenebilir NOS (iNOS) ve endotelyal NOS (eNOS)’dur. Bu enzimler ilk bulundukları doku ve işlevlerine göre adlandırılmış olsa da böbrekte geniş bir lokalizasyona sahip ve birçok böbrek hastalığıyla ilişkilendirilmiş enzimlerdir. Böbrek hastalıklarıyla ilgili yapılan çalışmalarda NO düzeyi ve NOS enzim aktivitesindeki değişiklikler önemli rol oynadığından, NOS’ların düzenlenmesinden sorumlu moleküler mekanizmalar birçok çalışmanın temelini oluşturmaktadır. Bu nedenle, bu derlemede NOS’ların moleküler düzenlenme mekanizmaları ve çeşitli böbrek hastalıklarıyla olan ilişkisi incelenmiş, bu mekanizmalara bütüncül bir bakış açısıyla böbrek patofizyolojisinde NO’nun rolü açıklanmaya çalışılmıştır.

Keywords

Nitrik oksit, nitrik oksit sentaz, kronik böbrek hastalığı

NITRIC OXIDE SYNTHASE ACTIVITY AND REGULATORY MECHANISMS IN RENAL DISEASES

Abstract

Nitric Oxide (NO) is a gaseous molecule with a half-life of 5-6 seconds, involved in many physiological and pathological events. Under physiological conditions, it plays a role in the regulation of renal and glomerular hemodynamics, natriuresis, medullary perfusion, tubuloglomerular feedback, tubular sodium reabsorption and renal nerve activity. Impairment of NO synthesis causes various kidney diseases. Therefore, the elucidation of these mechanisms is important in the treatment methods to be developed against kidney damage. Three isoforms of nitric oxide synthase (NOS) enzymes have been identified responsible for NO synthesis; neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). Although these enzymes are called according to the tissue and functions in which they were first found, they are enzymes that have a wide localization in the kidney and have been associated with many kidney diseases. In previous studies, it has been shown that kidney diseases are caused by changes in NO level and NOS enzyme activity. Therefore, the molecular mechanisms responsible for the regulation of NOSs form the basis of many studies. In this review, the molecular regulation mechanisms of NOS and their relationship with various kidney diseases were investigated, and the role of NO in the kidney pathophysiology was aimed to explain.

Keywords

nitric oxide, nitric oxide synthase, chronic kidney disease

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