An analysis of the impact of buthionine sulfoximine and N-nitro-L-arginine on blood pressure


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Güngör B., Akdur S., Sılan C., Coşkun Ö., Aksulu H. E.

BIOMEDICAL RESEARCH AND THERAPY, vol.10, no.6, pp.5735-5743, 2023 (ESCI)

  • Publication Type: Article / Article
  • Volume: 10 Issue: 6
  • Publication Date: 2023
  • Doi Number: 10.15419/bmrat.v10i6.814
  • Journal Name: BIOMEDICAL RESEARCH AND THERAPY
  • Journal Indexes: Emerging Sources Citation Index (ESCI)
  • Page Numbers: pp.5735-5743
  • Çanakkale Onsekiz Mart University Affiliated: Yes

Abstract

Introduction: The presence of weaknesses in the efficacy of endogenous natriuretic and vasodilator agents plays a significant role in developing high blood pressure. It is often suggested that oxidative stress is critical in developing hypertension due to nitric oxide synthase (NOS) inhibition. This study aimed to investigate the intrarenal dopaminergic system activities, involvement of oxidative stress, and blood pressure changes resulting from NOS inhibition with N-nitro-L-arginine (L-NNA) and/or L-buthionine sulfoximine (BSO).Methods: Male Wistar albino rats (n = 24) were administered water containing 50 mg/L L-NNA for 21 days and/or intraperitoneal injections of BSO (125 mg/kg twice daily) for seven days; control rats were administered tap water. The rats' blood pressure; water and salt balance; total oxidant and antioxidant capacities; and urinary dopamine, adrenaline, and noradrenaline levels were measured.Results: While L-NNA and BSO alone did not significantly alter blood pressure, their coadministration caused rats to develop hypertension and significantly reduced the fractional excretion of sodium, increasing its tubular reabsorption. Urinary dopamine levels, indicators of intrarenal dopamine synthesis, did not change significantly Conclusion: These results indicate the importance of the weakness of endogenous natriuretic systems such as nitric oxide in hypertension development. While BSO did not induce oxidative stress in the measured parameters, it was shown for the first time as an actor in hypertension development in subjects with NOS inhibition to the extent that such inhibition did not increase blood pressure.