Angiotensin-converting enzyme 2 activator, DIZE in the basolateral amygdala attenuates the tachycardic response to acute stress by modulating glutamatergic tone

Silva, Carina Cunha; Correa, Ana M.; Kushmerick, Christopher; Sharma, Neeru M.; Patel, Kaushik P.; Almeida, Jaci de; Moreira, Fabrício A.; Ferreira, Anderson J.; Fontes, Marco Antônio Peliky

doi:10.1016/j.npep.2020.102076

Cited by 9 publications

(5 citation statements)

References 68 publications

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“…Our findings along with those of Hall et al invoke the possibility that accumulation of Ang II and/or insufficient Ang 1-7 could contribute to loss of pericyte survival, and that this cascade of events is at least in part responsible for the impaired CBF that continues following reperfusion in a stroke patient. This is further supported by previous work showing that Ang II, via ATR1, stimulates glutamate release [70], whereas an ACE2 activator can reduce the excitatory synaptic activity of neurons, in association with decreased expression of the NMDA receptor (ionotropic glutamate receptor) [71]. Thus, it is plausible that the shift in balance between the ACE-Ang II-AT1R and ACE2-Ang (1-7)-MasR axes during stroke leads to increased glutamate signaling that Hall et al showed contributed to pericyte death.…”

Section: Pericytes Constrict Capillaries and Then Die In Rigorsupporting

confidence: 82%

The Role of the ACE2/MasR Axis in Ischemic Stroke: New Insights for Therapy

et al. 2021

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Ischemic stroke remains the leading cause of neurologically based morbidity and mortality. Current stroke treatment is limited to two classes of FDA-approved drugs: thrombolytic agents (tissue plasminogen activator (tPA)) and antithrombotic agents (aspirin and heparin), which have a narrow time-window (<4.5 h) for administration after onset of stroke symptoms. While thrombolytic agents restore perfusion, they carry serious risks for hemorrhage, and do not influence damage responses during reperfusion. Consequently, stroke therapies that can suppress deleterious effects of ischemic injury are desperately needed. Angiotensin converting enzyme-2 (ACE2) has been recently suggested to beneficially influence experimental stroke outcomes by converting the vasoconstrictor Ang II into the vasodilator Ang 1–7. In this review, we extensively discuss the protective functions of ACE2-Ang (1–7)-MasR axis of renin angiotensin system (RAS) in ischemic stroke.

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Section: Pericytes Constrict Capillaries and Then Die In Rigorsupporting

confidence: 82%

The Role of the ACE2/MasR Axis in Ischemic Stroke: New Insights for Therapy

et al. 2021

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“…The previous studies indicated that the lesion of the CeA of borderline hypertensive rats reduced the increase in arterial pressure evoked by the intermittent foot shock (Sanders et al, 1994). Regarding the BLA, in addition to a role of local angiotensin-converting enzyme 2 (ACE2)/Ang-(1-7)/Mas receptor axis pathway (Oscar et al, 2015;Silva et al, 2020), the previous studies using the chemical blockade with muscimol in non-human primates and rodents have indicated a facilitatory role of this amygdaloid nucleus in the cardiovascular responses to stress (Salomé et al, 2007;Elorette et al, 2020). As for the projections to the BNST, the results indicating a facilitatory role of the CeA and BLA in the cardiovascular responses to stress do not support the hypothesis of an involvement of these amygdaloid nuclei in the control of the cardiovascular responses to stress by the PL noradrenergic neurotransmission.…”

Section: Discussionmentioning

confidence: 99%

Both Prelimbic and Infralimbic Noradrenergic Neurotransmissions Modulate Cardiovascular Responses to Restraint Stress in Rats

et al. 2021

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The prelimbic (PL) and infralimbic (IL) subareas of the medial prefrontal cortex (mPFC) have been implicated in physiological and behavioral responses during aversive threats. The previous studies reported the noradrenaline release within the mPFC during stressful events, and the lesions of catecholaminergic terminals in this cortical structure affected stress-evoked local neuronal activation. Nevertheless, the role of mPFC adrenoceptors on cardiovascular responses during emotional stress is unknown. Thus, we investigated the role of adrenoceptors present within the PL and IL on the increase in both arterial pressure and heart rate (HR) and on the sympathetically mediated cutaneous vasoconstriction evoked by acute restraint stress. For this, bilateral guide cannulas were implanted into either the PL or IL of male rats. All animals were also subjected to catheter implantation into the femoral artery for cardiovascular recording. The increase in both arterial pressure and HR and the decrease in the tail skin temperature as an indirect measurement of sympathetically mediated cutaneous vasoconstriction were recorded during the restraint session. We observed that the microinjection of the selective α2-adrenoceptor antagonist RX821002 into either the PL or IL decreased the pressor response during restraint stress. Treatment of the PL or IL with either the α1-adrenoceptor antagonist WB4101 or the α2-adrenoceptor antagonist reduced the restraint-evoked tachycardia. The drop in the tail skin temperature was decreased by PL treatment with the β-adrenoceptor antagonist propranolol and with the α1- or α2-adrenoceptor antagonists. The α2-adrenoceptor antagonist into the IL also decreased the skin temperature response. Our results suggest that the noradrenergic neurotransmission in both PL and IL mediates the cardiovascular responses to aversive threats.

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“…More recent evidence indicated that these projections are mainly glutamatergic ( Centanni et al, 2019 ; McGinnis et al, 2020 ; Girven et al, 2021 ), and some of these structures (e.g., LH) have already been implicated in cardiovascular regulation by IC under resting conditions ( Cechetto and Chen, 1990 ; Oppenheimer et al, 1992 ). Furthermore, all these limbic structures are involved in the regulation of stress-evoked cardiovascular changes ( Tavares et al, 2009 ; Deolindo et al, 2013 ; Oscar et al, 2015 ; Barretto-de-Souza et al, 2018 ; Gomes-de-Souza et al, 2019 ; Silva et al, 2020 ). Therefore, these regions might constitute intermediate sites connecting the rostral posterior IC to autonomic centers in the medulla for control of the pressor response during aversive threats.…”

Section: Discussionmentioning

confidence: 99%

Site-Specific Regulation of Stress Responses Along the Rostrocaudal Axis of the Insular Cortex in Rats

et al. 2022

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The insular cortex (IC) has been described as a part of the central network implicated in the integration and processing of limbic information, being related to the behavioral and physiological responses to stressful events. Besides, a site-specific control of physiological functions has been reported along the rostrocaudal axis of the IC. However, a functional topography of the IC in the regulation of stress responses has never been reported. Therefore, this study aimed to investigate the impact of acute restraint stress in neuronal activation at different sites along the rostrocaudal axis of the IC. Furthermore, we evaluated the involvement of IC rostrocaudal subregions in the cardiovascular responses to acute restraint stress. We observed that an acute session of restraint stress increased the number of Fos-immunoreactive cells in the rostral posterior region of the IC, while fewer activated cells were identified in the anterior and caudal posterior regions. Bilateral injection of the non-selective synaptic inhibitor CoCl2 into the anterior region of the IC did not affect the blood pressure and heart rate increases and the sympathetically mediated cutaneous vasoconstriction to acute restraint stress. However, synaptic ablation of the rostral posterior IC decreased the restraint-evoked arterial pressure increase, whereas tachycardia was reduced in animals in which the caudal posterior IC was inhibited. Taken together, these pieces of evidence indicate a site-specific regulation of cardiovascular stress response along the rostrocaudal axis of the IC.

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Angiotensin-converting enzyme 2 activator, DIZE in the basolateral amygdala attenuates the tachycardic response to acute stress by modulating glutamatergic tone

Cited by 9 publications

References 68 publications

The Role of the ACE2/MasR Axis in Ischemic Stroke: New Insights for Therapy

The Role of the ACE2/MasR Axis in Ischemic Stroke: New Insights for Therapy

Both Prelimbic and Infralimbic Noradrenergic Neurotransmissions Modulate Cardiovascular Responses to Restraint Stress in Rats

Site-Specific Regulation of Stress Responses Along the Rostrocaudal Axis of the Insular Cortex in Rats

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