Key result
Spontaneously hypertensive rats utilize adaptive mechanisms involving nitric oxide and hydrogen sulphide systems, where acute NO deficiency potentiates the vasorelaxant effect of H2S to compensate for increased vascular tone.
In adult spontaneously hypertensive rats, adaptive mechanisms involving NO and H2S systems and their interaction provide compensation for increased vascular tone.
Rat model reveals H2S compensation during NO deficiency; leaves open relevance to human hypertension.
Our previous study in young spontaneously hypertensive rats (SHR) confirmed a participation of nitric oxide (NO) and hydrogen sulphide (H2S) in probably inherent adaptive strategy of conduit arteries in condition of sustained hypertension. The aim of study was to confirm or refuse the compensatory mechanisms in developed phase of hypertension in SHR with an emphasis on manifestation of the NO and H2S signalisations. In the experiments 17–20-weeks-old normotensive Wistar rats and SHR were included. Systolic blood pressure (sBP) was measured by plethysmographic method and vasoactivity of isolated thoracic aorta (TA) was recorded by sensors of changes of isometric tension. We observed an increased sBP and hypertrophy of myocardium in SHR. The contractile response of TA to exogenous noradrenaline was reduced in SHR due to inhibition effect of endogenous NO. In SHR impaired endothelial functions were confirmed, however through a prevalence of vasoconstrictors produced by cyclooxygenase but not as a result of reduced NO synthesis. Dual effect of H2S donor (Na2S) was showed in both strains; however an increased maximal vasorelaxation was proved in SHR. Moreover, acute inhibition of NO production increased the relaxant phase of Na2S effects. On the other hand, application of Na2S modulatory dose increased the release of NO from exogenous NO donor, nitrosogluthation in Wistar rats but not in SHR. The data confirmed that SHR disposed with adaptive mechanisms including NO and H2S systems and their interaction (acute NO deficiency potentiated vasorelaxant effect of H2S). These effects could provide compensation of the increased vascular tone in adulthood.
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Berenyiová et al. (2017) studied Spontaneous hypertension (n=17). Spontaneous hypertension vs. Normotensive Wistar rats was evaluated on Vasoactive responses of isolated thoracic aorta. Spontaneously hypertensive rats utilize adaptive mechanisms involving nitric oxide and hydrogen sulphide systems, where acute NO deficiency potentiates the vasorelaxant effect of H2S to compensate for increased vascular tone.
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