Key result
Chronic NO synthase inhibition with L-NAME in young spontaneously hypertensive rats induced adaptive mechanisms in the thoracic aorta, preserving NO-derived vasorelaxation and NOS activity.
Why the study?
Does chronic NO synthase inhibition with L-NAME affect vasoactive and structural properties of the thoracic aorta, NOS activity, and oxidative stress in young spontaneously hypertensive rats?
Does chronic NO synthase inhibition with L-NAME affect vasoactive and structural properties of the thoracic aorta, NOS activity, and oxidative stress in young spontaneously hypertensive rats?
In young spontaneously hypertensive rats, the thoracic aorta develops functional and molecular adaptive mechanisms in response to chronic NO deficiency.
Aortic adaptations to NO deficiency in young SHR models are hypothesis-generating; leaves clinical translation open pending human data.
Although the role of nitric oxide (NO) in essential hypertension is still unclear, the effects of long‐term NO deficiency have not yet been investigated during the critical juvenile period in spontaneously hypertensive rats (SHR). We aimed to analyze the effects of chronic NO synthase (NOS) inhibition on systolic blood pressure (sBP), vasoactivity, morphological changes and superoxide level in the thoracic aorta (TA), NOS activity in different tissues, and general biomarkers of oxidative stress in plasma of young SHR. Four‐week‐old SHR were treated with NG‐nitro‐L‐arginine methyl ester (L‐NAME, 50 mg/kg/day, p.o.) for 4‐5 weeks. L‐NAME treatment induced a transient sBP increase only, and surprisingly, slightly inhibited endothelium‐dependent relaxation of TA. Hereby, 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. In spite of an increased sensitivity of adrenergic receptors, the maximal adrenergic contraction of TA was unchanged, which was associated with changes in elastin arrangement and an increase in wall thickness. The production of reactive oxygen species in the TA was increased; however, the level of selected biomarkers of oxidative stress did not change. Our findings proved that the TA of young SHR responded to chronic NO deficiency by the development of adaptive mechanisms on the functional (preserved NO‐derived vasorelaxation, unincreased contraction) and molecular (preserved NOS activity) level.
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Berenyiová et al. (2018) studied Hypertension (Spontaneously hypertensive rats). NG-nitro-L-arginine methyl ester (L-NAME) was evaluated on Systolic blood pressure, vasoactivity, morphological changes, superoxide level, NOS activity, and oxidative stress biomarkers. Chronic NO synthase inhibition with L-NAME in young spontaneously hypertensive rats induced adaptive mechanisms in the thoracic aorta, preserving NO-derived vasorelaxation and NOS activity.
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