N-Acetylcysteine Prevents Hypertension via Regulation of the ADMA-DDAH Pathway in Young Spontaneously Hypertensive Rats.

Asymmetric dimethylarginine (ADMA) reduces nitric oxide (NO), thus causing hypertension. ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH), which can be inhibited by oxidative stress. N-Acetylcysteine (NAC), an antioxidant, can facilitate glutathione (GSH) synthesis. We aimed to...

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Publicado en:BioMed Research International Vol. 2013; pp. 696317 - 696318
Autores principales: Fan, Nai-Chia, Tsai, Chih-Min, Hsu, Chien-Ning, Huang, Li-Tung, Tain, You-Lin
Formato: research Journal Article
Publicado: Wiley-Blackwell 2013
Acceso en línea:Ver este registro en EBSCOhost
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      dt: 2013
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      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        atl: N-Acetylcysteine Prevents Hypertension via Regulation of the ADMA-DDAH Pathway in Young Spontaneously Hypertensive Rats.
      aug:
        au:
          Fan, Nai-Chia
          Tsai, Chih-Min
          Hsu, Chien-Ning
          Huang, Li-Tung
          Tain, You-Lin
        affil: Department of Pediatrics, Chang Gung Memorial Hospital at Linkou, Chang Gung University College of Medicine, Taoyuan, Taiwan.
      sug:
        subj:
          Acetylcysteine Administration and Dosage
          Amidohydrolases Metabolism
          Hypertension Metabolism
          Hypertension Physiopathology
          Animal Studies
          Arginine
          Arginine Metabolism
          Blood Pressure Drug Effects
          Glutathione
          Human
          Hypertension Etiology
          Metabolic Networks and Pathways
          Nitric Oxide Metabolism
          Oxidative Stress
          Peroxides Metabolism
          Rats
      ab: Asymmetric dimethylarginine (ADMA) reduces nitric oxide (NO), thus causing hypertension. ADMA is metabolized by dimethylarginine dimethylaminohydrolase (DDAH), which can be inhibited by oxidative stress. N-Acetylcysteine (NAC), an antioxidant, can facilitate glutathione (GSH) synthesis. We aimed to determine whether NAC can prevent hypertension by regulating the ADMA-DDAH pathway in spontaneously hypertensive rats (SHR). Rats aged 4 weeks were assigned into 3 groups (n = 8/group): control Wistar Kyoto rats (WKY), SHR, and SHR receiving 2% NAC in drinking water. All rats were sacrificed at 12 weeks of age. SHR had higher blood pressure than WKY, whereas NAC-treated animals did not. SHR had elevated plasma ADMA levels, which was prevented by NAC therapy. SHR had lower renal DDAH activity than WKY, whereas NAC-treated animals did not. Renal superoxide production was higher in SHR than in WKY, whereas NAC therapy prevented it. NAC therapy was also associated with higher GSH-to-oxidized GSH ratio in SHR kidneys. Moreover, NAC reduced oxidative stress damage in SHR. The observed antihypertensive effects of NAC in young SHR might be due to restoration of DDAH activity to reduce ADMA, leading to attenuation of oxidative stress. Our findings highlight the impact of NAC on the development of hypertension by regulating ADMADDAH pathway.
      pubtype: Academic Journal
      doctype:
        research
        Journal Article
      ougenre: Article
    language: English
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