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Tempol Intracerebroventricular Injection Abolishes the Hypertension and Mortality Arising from the Central Action of Scorpion Tityustoxin
Author(s) -
Silva Fernanda,
Guerra Joyce,
Menezes Rodrigo,
Guidine Patricia,
Chianca Deoclecio
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.986.4
Subject(s) - mean arterial pressure , ventricle , medicine , pharmacology , central nervous system , blockade , heart rate , endocrinology , anesthesia , receptor , blood pressure , chemistry
Studies address the high sensitivity of the central nervous system (CNS) to Tityustoxin action (TsTX, α‐toxin of the T.serrulatus scorpion venom). TsTX increases the sympathetic modulation due to masssive release of the excitatory aminoacids (EAA) in CNS. The EAA extracellular accumulation causing brain oxidative insults. Considering that central sympathetic activation is one of the mechanisms underlying hypertension, in which reactive oxygen species (ROS) is involved, we aimed to assess if the tempol (superoxide dismutase mimetic) injections in the left lateral ventricle (LLV) could influence the cardiovascular responses and mortality caused by TsTX central action. Urethane anesthetized wistar male rats were submitted to vessels femoral cannulation and to injections of PBS (Control group; n=4) or tempol (10 and 32µmol;2µL, respectively, n=5 and n=3), followed by TsTX injections (0.4µg;1μl) in LLV. Mean arterial pressure (MAP) and Heart Rate (HR) records were done before (10min for baseline; 20min for PBS or Tempol periods) and after TsTX injection (60min). Results expressed as mean±SEM; p<0.05. F ratio=mean square (MS) for the contrast/residual MS of the groups. Baseline MAP and HR were not different between groups.TsTX evoked hypertension and tachycardia (ΔMAP:35±5mmHg, ΔHR:121±22bpm, p<0.05) and 75% of death in control group. Tempol 32 µmol injection abolished the hypertension (for treatment; ΔMAP: F (2, 351) = 6, p<0.05) and the mortality (0%) arising from the TsTX central action. These results suggest that the pressor response and death could be mediated by ROS in CNS. Supported by: UFOP, CAPES and CNPq.