Cardiology Letters 2020, 29(5):303-309

The impact of long-term NO-deficiency on the vasoactive properties of thoracic aorta, NOS activity, and plasma biomarkers of oxidative stress in young SHR

Berényiová A¹, Dovinová I¹, Kvandová M¹, Kristek F¹, Jansen E², Majzúnová M¹, Čačányiová S¹

¹ Centrum experimentálnej medicíny Slovenskej akadémie vied, Ústav normálnej a patologickej fyziológie, Bratislava, Slovenská republika

² Centre for Health Protection, National Institute for Public Health and the Enviroment, Bilthoven, Holandsko

Aim: In this study we aimed to describe the effect of chronic NO-deficiency on the systolic blood pressure (sBP), the vasoactive responses of thoracic aorta (TA), activity of NO-synthase (NOS) and general biomarkers of oxidative stress in plasma of young spontaneously hypertensive rats (SHR).

Subjects and methods: A non-specific NOS inhibitor, NG-nitro-L-arginine (L-NAME, 50 mg/kg/day, p.o.) was administered for 4-5 weeks to four-week-old SHR (n = 8), age matched SHRs (n = 8) used as a control group. The sBP was measured by the non-invasive plethysmographic method, weekly. At the end of the treatment plasma samples were collected, the biometric parameters were calculated, and the TA was isolated. The vasoactive responses of TA were followed by sensors of isometric tension. NOS activity was measured by conversion of radioactive L-arginine to L-citruline.

Results: The L-NAME treatment induced a transient sBP increase only and had a moderated inhibitory effect on the endothelium-dependent relaxation of TA. Thereby, the inhibition of NOS activity varied from tissue to tissue, ranging from the lowest in the TA and the kidney to the highest in the brain stem. Despite an increased sensitivity of adrenergic receptors, the maximal adrenergic contraction of TA was unchanged, and also the level of general biomarkers of oxidative stress did not change.

Conclusions: Our findings proved that the TA of young SHR responded to chronic NO deficiency by a development of adaptive mechanisms on the functional (preserved NO-derived vasorelaxation, unincreased contraction) and molecular (preserved NOS activity) levels. Although these mechanisms could provide a local compensation of increased activity of the adrenergic system, they were not able to eliminate changes evoking serious systemic pathological consequences. Fig. 3, Tab. 3, Ref. 23, on-line full text (Free, PDF) www. cardiologyletters.sk

Keywords: NOS inhibition; young spontaneously hypertensive rats; vasoactivity; compensatory mechanisms

Published: May 1, 2020  Show citation