PHYSIOLOGICAL RESEARCH • ISSN 0862-8408 (print) • ISSN 1802-9973 (online)  2016 Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic Fax +420 241 062 164, e-mail: physres@biomed.cas.cz, www.biomed.cas.cz/physiolres Physiol. Res. 65 (Suppl. 3): S381-S390, 2016 Lack of Reactive Oxygen Species Deteriorates Blood Pressure Regulation in Acute Stress I. BERNÁTOVÁ 1 , P. BALIŠ 1 , R. GOGA 2 , M. BEHULIAK 3 , J. ZICHA 3 , I. SEKAJ 2 1 Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovak Republic, 2 Institute of Robotics and Cybernetics, Faculty of Electrical Engineering and Information Technology, Slovak University of Technology, Bratislava, Slovak Republic, 3 Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic Received May 14, 2016 Accepted September 5, 2016 Summary This study investigated the contribution of reactive oxygen species (ROS) to blood pressure regulation in conscious adult male Wistar rats exposed to acute stress. Role of ROS was investigated in rats with temporally impaired principal blood pressure regulation systems using ganglionic blocker pentolinium (P, 5 mg/kg), angiotensin converting enzyme inhibitor captopril (C, 10 mg/kg), nitric oxide synthase inhibitor L-NAME (L, 30 mg/kg) and superoxide dismutase mimeticum tempol (T, 25 mg/kg). Mean arterial pressure (MAP) was measured by the carotid artery catheter and inhibitors were administered intravenously. MAP was disturbed by a 3-s air jet, which increased MAP by 35.2±3.0 % vs. basal MAP after the first exposure. Air jet increased MAP in captopril- and tempol-treated rats similarly as observed in saline-treated rats. In pentolinium- treated rats stress significantly decreased MAP vs. pre-stress value. In L-NAME-treated rats stress failed to affect MAP significantly. Treatment of rats with P+L+C resulted in stress- induced MAP decrease by 17.3±1.3 % vs. pre-stress value and settling time (20.1±4.2 s). In P+L+C+T-treated rats stress led to maximal MAP decrease by 26.4±2.2 % (p<0.005 vs. P+L+C) and prolongation of settling time to 32.6±3.3 s (p<0.05 vs. P+L+C). Area under the MAP curve was significantly smaller in P+L+C- treated rats compared to P+L+C+T-treated ones (167±43 vs. 433±69 a.u., p<0.008). In conclusion, in rats with temporally impaired blood pressure regulation, the lack of ROS resulted in greater stress-induced MAP alterations and prolongation of time required to reach new post-stress steady state. Key words Air-jet stress • Superoxide • Nitric oxide • Sympathetic nervous system • Renin-angiotensin system Corresponding author I. Bernatova, Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Sienkiewiczova 1, 813 71 Bratislava, Slovak Republic. E-mail: iveta.bernatova@savba.sk Introduction Blood pressure (BP) is one of the principal vital signs and the maintenance of normal BP is critical in order to keep optimal oxygenation of tissues and organs in all vertebrates, including humans. That is why BP is continually controlled and regulated on optimal levels by the central, peripheral and local tissue mechanisms. All these levels of BP regulation, including endothelium-derived factors, play a significant role in the modulation of final BP level. However, among all components of BP regulatory system the sympathetic nervous system (SNS), renin-angiotensin system (RAS) and nitric oxide (NO) seem to be the most powerful regulators. When exposed to sudden stressor the autonomic nervous system is activated for fight or flight reaction. The stress-induced increase in heart rate (HR) by sympathetic stimulation of cardiac β-adrenergic receptors is accompanied by a rise in BP mediated mainly by α-adrenergic stimulation. On the other hand, NO is the major depressor factor attenuating BP. In fact, NO, well https://doi.org/10.33549/physiolres.933433