P4 SOCIAL STRESS-INDUCED BLOOD PRESSURE INCREASE IN BORDERLINE HYPERTENSIVE RATS IS ASSOCIATED WITH ENDOTHELIAL DYSFUNCTION IN THE RESISTANT ARTERIES

• Main Authors: Angelika Puzserova, Ruzena Sotnikova, Jozef Torok, Anna Zemancikova, Iveta Bernatova
• Format: Article
• Language: English
• Published: Atlantis Press 2017-12-01
• Series: Artery Research
• Online Access: https://www.atlantis-press.com/article/125930237/view

Objectives: Several studies have observed that altered endothelial function is involved in the development of stress-induced hypertension. The aim of this study was to investigate the effects of chronic social stress (crowding) on endothelium-dependent relaxation (EDR) of the superior mesenteric artery (SMA) and of small resistant mesenteric arteries (MA) as well as on neurogenic contractions of SMA in adult borderline hypertensive rats (BHR). Methods: Twelve-week-old BHR (offspring of spontaneously hypertensive dams and Wistar-Kyoto sires) males were exposed to crowding (living space: 200 cm2/rat) for eight weeks. Control BHR were kept in the groups of four rats per cage (living space: 480 cm2/rat). Systolic blood pressure (sBP) was determined by the tail-cuff method. Vascular function was investigated in the isolated arteries at isometric conditions. EDR was assessed using acetylcholine test. Results: Crowding significantly increased sBP of BHR to the hypertensive values. Results showed that stress did not affect total acetylcholine-induced relaxation and its nitric oxide (NO)-dependent and NO-independent components in the SMA. In the resistant MA, stress reduced total acetylcholine-induced relaxation by reducing NO-independent component, without the alterations of its NO-dependent component. However, stress failed to affect significantly neurogenic contractions of SMA elicited by electrical stimulation of perivascular sympathetic nerves and vasoconstriction induced by exogenous noradrenaline in SMA. Conclusion: In conclusion, chronic social stress can accelerate the development of hypertension in BHR, which seems to be associated with NO-independent endothelial dysfunction in small resistant arteries. Supported by the grants VEGA No. 2/0190/17 and APVV-16-0263.