scholarly journals Activation of angiotensin-converting enzyme 2/angiotensin-(1–7)/Mas axis attenuates the cardiac reactivity to acute emotional stress

2013 ◽  
Vol 305 (7) ◽  
pp. H1057-H1067 ◽  
Author(s):  
Augusto Martins Lima ◽  
Carlos Henrique Xavier ◽  
Anderson José Ferreira ◽  
Mohan K. Raizada ◽  
Gerd Wallukat ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Intravenous Injection ◽  
Emotional Stress ◽  
Acute Stress ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Air Jet ◽  
Acute Emotional Stress

Recent data indicate the brain angiotensin-converting enzyme/ANG II/AT1 receptor axis enhances emotional stress responses. In this study, we investigated whether its counterregulatory axis, the angiotensin-converting enzyme 2 (ACE2)/ANG-(1–7)/Mas axis, attenuate the cardiovascular responses to acute emotional stress. In conscious male Wistar rats, the tachycardia induced by acute stress (air jet 10 l/min) was attenuated by intravenous injection of ANG-(1–7) [Δ heart rate (HR): saline 136 ± 22 vs. ANG-(1–7) 61 ± 25 beats/min; P < 0.05]. Peripheral injection of the ACE2 activator compound, XNT, abolished the tachycardia induced by acute stress. We found a similar effect after intracerebroventricular injections of either ANG-(1–7) or XNT. Under urethane anesthesia, the tachycardia evoked by the beta-adrenergic agonist was markedly reduced by ANG-(1–7) [ΔHR: saline 100 ± 16 vs. ANG-(1–7) 18 ± 15 beats/min; P < 0.05]. The increase in renal sympathetic nerve activity (RSNA) evoked by isoproterenol was also abolished after the treatment with ANG-(1–7) [ΔRSNA: saline 39% vs. ANG-(1–7) −23%; P < 0.05]. The tachycardia evoked by disinhibition of dorsomedial hypothalamus neurons, a key nucleus for the cardiovascular response to emotional stress, was reduced by ∼45% after intravenous injection of ANG-(1–7). In cardiomyocyte, the incubation with ANG-(1–7) (1 μM) markedly attenuated the increases in beating rate induced by isoproterenol. Our data show that activation of the ACE2/ANG-(1–7)/Mas axis attenuates stress-induced tachycardia. This effect might be either via the central nervous system reducing anxiety level and/or interfering with the positive chronotropy mediated by activation of cardiac β adrenergic receptors. Therefore, ANG-(1–7) might contribute to reduce the sympathetic load to the heart during situations of emotional stress, reducing the cardiovascular risk.

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

Neuropeptides ◽  
2020 ◽  
Vol 83 ◽  
pp. 102076
Author(s):  
Carina Cunha Silva ◽  
Ana Maria Bernal Correa ◽  
Christopher Kushmerick ◽  
Neeru M. Sharma ◽  
Kaushik P. Patel ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Basolateral Amygdala ◽  
Acute Stress ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2

scholarly journals Hemodynamic response pattern predicts susceptibility to stress-induced elevation in arterial pressure in the rat

2001 ◽  
Vol 281 (1) ◽  
pp. R31-R37 ◽  
Author(s):  
Jay R. Muller ◽  
Khoi M. Le ◽  
William R. Haines ◽  
Qi Gan ◽  
Mark M. Knuepfer
Keyword(s):  
Cardiac Output ◽  
Conditioned Stimulus ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Acute Stress ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Response Patterns ◽  
Air Jet ◽  
Poststress Period

Cocaine or air jet stress evokes pressor responses due to either a large increase in systemic vascular resistance (vascular responders) or small increases in both cardiac output and vascular resistance (mixed responders) in conscious rats. Repeated cocaine administration results in elevated arterial pressure in vascular responders but not in mixed responders. The present study examined the hypothesis that the pattern of cardiovascular responses to an unconditioned stimulus (UCS; air jet) is related to responses to a conditioned stimulus (CS; tone followed by brief foot shock) in individual rats. Our data demonstrate that presentation of the UCS produced variable cardiac output responses that correlated with responses to the CS ( n = 60). We also determined whether individual cardiovascular response patterns to acute stress correlated with predisposition to a sustained stress-induced elevation in arterial pressure. Rats were exposed to three different stressors presented one per day successively for 4 wk and during a poststress period of 3 wk while arterial pressure was recorded periodically. Mean arterial pressure was elevated in all rats during chronic stress but, during the poststress period, remained at significantly higher levels in vascular responders but not mixed responders. Therefore, we conclude that acute behavioral stress to a conditioned stimulus elicits variable hemodynamic responses that predict the predisposition to a sustained stress-induced elevation in arterial pressure.

scholarly journals Angiotensin Converting Enzyme Inhibition Reduces Cardiovascular Responses to Acute Stress in Myocardially Infarcted and Chronically Stressed Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
A. Cudnoch-Jedrzejewska ◽  
K. Czarzasta ◽  
L. Puchalska ◽  
J. Dobruch ◽  
O. Borowik ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Acute Stress ◽  
Cardiovascular Responses ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Converting Enzyme Inhibition ◽  
Acute Stressor

Previous studies showed that chronically stressed and myocardially infarcted rats respond with exaggerated cardiovascular responses to acute stress. The present experiments were designed to elucidate whether this effect can be abolished by treatment with the angiotensin converting enzyme (ACE) inhibitor captopril. Sprague Dawley rats were subjected either to sham surgery (Groups 1 and 2) or to myocardial infarction (Groups 3 and 4). The rats of Groups 2 and 4 were also exposed to mild chronic stressing. Four weeks after the operation, mean arterial blood pressure (MABP) and heart rate (HR) were measured under resting conditions and after application of acute stress. The cardiovascular responses to the acute stress were determined again 24 h after administration of captopril orally. Captopril significantly reduced resting MABP in each group. Before administration of captopril, the maximum increases in MABP evoked by the acute stressor in all (infarcted and sham-operated) chronically stressed rats and also in the infarcted nonchronically stressed rats were significantly greater than in the sham-operated rats not exposed to chronic stressing. These differences were abolished by captopril. The results suggest that ACE may improve tolerance of acute stress in heart failure and during chronic stressing.

Thermodynamics of the interaction between the spike protein of severe acute respiratory syndrome- coronavirus-2 and the receptor of human angiotensin converting enzyme 2. Effects of possible ligands

2020 ◽  
Author(s):  
Cristina Garcia-Iriepa ◽  
Cecilia Hognon ◽  
Antonio Francés-Monerris ◽  
Isabel Iriepa ◽  
Tom Miclot ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Molecular Mechanisms ◽  
Molecular Design ◽  
Binding Free Energy ◽  
Transmembrane Protein ◽  
Spike Protein ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Rational Molecular Design ◽  
Rational Evaluation

<div><p>Since the end of 2019, the coronavirus SARS-CoV-2 has caused more than 180,000 deaths all over the world, still lacking a medical treatment despite the concerns of the whole scientific community. Human Angiotensin-Converting Enzyme 2 (ACE2) was recently recognized as the transmembrane protein serving as SARS-CoV-2 entry point into cells, thus constituting the first biomolecular event leading to COVID-19 disease. Here, by means of a state-of-the-art computational approach, we propose a rational evaluation of the molecular mechanisms behind the formation of the complex and of the effects of possible ligands. Moreover, binding free energy between ACE2 and the active Receptor Binding Domain (RBD) of the SARS-CoV-2 spike protein is evaluated quantitatively, assessing the molecular mechanisms at the basis of the recognition and the ligand-induced decreased affinity. These results boost the knowledge on the molecular grounds of the SARS-CoV-2 infection and allow to suggest rationales useful for the subsequent rational molecular design to treat severe COVID-19 cases.</p></div>

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