P9: The Participation of Nitric Oxide and Hydrogen Sulphide Signalisation in Vasoactive Responses of Rat Thoracic Aorta in Condition of Developed Spontaneous Hypertension

• Published in: Artery research Vol. 20; no. 1; p. 64
• Main Authors: Berenyiova, Andrea, Puzserova, Angelika, Grman, Marian, Kristek, Frantisek, Cacanyiova, Sona
• Format: Journal Article
• Language: English
• Published: Dordrecht Springer Netherlands 01.12.2017; Springer Nature B.V; BMC
• Subjects: ARTERY 17 Poster Presentation abstracts; Coronary vessels; Hypertension; Nitric oxide
• ISSN: 1872-9312; 1876-4401; 1876-4401
• DOI: 10.1016/j.artres.2017.10.062

Our previous study in young spontaneously hypertensive rats (SHR) confirmed a participation of nitric oxide (NO) and hydrogen sulphide (H 2 S) 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 H 2 S 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 H 2 S donor (Na 2 S) 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 Na 2 S effects. On the other hand, application of Na 2 S 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 H 2 S systems and their interaction (acute NO deficiency potentiated vasorelaxant effect of H 2 S). These effects could provide compensation of the increased vascular tone in adulthood.