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Angiotensinergic neurotransmission in the medial amygdaloid nucleus modulates the cardiovascular responses to emotional stress in rats.
Author(s) -
Crestani CARLOS C.,
CostaFerreira Willian,
GomesdeSouza Lucas
Publication year - 2018
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.2018.32.1_supplement.554.14
Subject(s) - microinjection , losartan , neurochemical , medicine , microinjections , angiotensin ii , endocrinology , amygdala , limbic system , anesthesia , receptor antagonist , neuroscience , central nervous system , receptor , blood pressure , antagonist , psychology
The physiological and behavioral responses observed during aversive threats are coodinated by overlapping circuits in the central nervous system. The medial amygdaloid nucleus (MeA) is a limbic structures implicated in the control of cardiovascular responses to stress. However, the local neurochemical mechanisms involved in such control has not been fully elucidated. In this sense, angiotensin II and their receptors were identified within the MeA. Nevertheless, a possible involvement of this neurochemical mechanism in MeA control of stress‐evoked cardiovascular responses has never been evaluated. Thus, the aim of this study was to investigate the involvement of AT 1 receptor within the MeA in control of cardiovascular responses evoked by an acute session of restraint stress in rats. For this, male Wistar rats (240g–260g) had cannula‐guide bilaterally implanted within the MeA. A catheter was also implanted in the femoral artery for mean arterial pressure (MAP) and heart rate (HR) recording. The restraint stress was performed by placing the animals in a plastic cylindrical tube for 60 minutes. Independent group of animals received bilateral microinjections into the MeA of the selective AT 1 receptor antagonist losartan (1nmol/100nL), angiotensin II (0.05nmol/100nL) or vehicle (saline, 100nL) 10 min before the onset of the restraint stress session. We observed that bilateral microinjection of losartan into the MeA enhanced the tachycardia evoked by restraint stress (F (1,11) =7, P<0.02), but without affecting the MAP increase (F (1,11) =1, P>0.05). Similarly, bilateral treatment of the Mea with angiotensin II enhanced restraint‐evoked HR increase (F (1,12) =6.5, P<0.02) without affecting the MAP response (F (1,12) =0.5, P>0.05). Taken together, these results provide evidence of an inhibitory role of the AT 1 receptor within the MeA in cardiac responses to emotional stress. Besides, results indicate that angiotensin II acting via mechanisms other than the AT 1 receptor plays a facilitatory influence on HR response. Support or Funding Information FAPESP, CNPq and PADC‐FCF/UNESP. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .