Lack of Reactive Oxygen Species Deteriorates Blood Pressure Regulation in Acute Stress

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F16%3A00465946" target="_blank" >RIV/67985823:_____/16:00465946 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Lack of Reactive Oxygen Species Deteriorates Blood Pressure Regulation in Acute Stress

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

Lack of Reactive Oxygen Species Deteriorates Blood Pressure Regulation in Acute Stress

Popis výsledku anglicky

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.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FA - Kardiovaskulární nemoci včetně kardiochirurgie

OECD FORD obor

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Projekt

<a href="/cs/project/NV15-25396A" target="_blank" >NV15-25396A: Centrální a periferní modulace cévního tonu a vylučování sodíku: úloha mozku a ledvin v patofyziologii hypertenze</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2016

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Physiological Research

ISSN

0862-8408

e-ISSN

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Svazek periodika

65

Číslo periodika v rámci svazku

Suppl.3

Stát vydavatele periodika

CZ - Česká republika

Počet stran výsledku

10

Strana od-do

"S381"-"S390"

Kód UT WoS článku

000386689100008

EID výsledku v databázi Scopus

2-s2.0-84997542933