Ghrelin potentiates cardiac reactivity to stress by modulating sympathetic control and beta-adrenergic response

Camargo-Silva, Gabriel; Turones, Larissa Córdova; Cruz, Kellen Rosa da; Gomes, Karina Pereira; Mendonça, Michelle Mendanha; Nunes, Allancer D C; Jesus, Itamar Couto Guedes de; Colugnati, Diego Basile; Pansani, Aline Priscila; Pobbe, Roger L.H.; Santos, Robson Augusto Souza; Fontes, Marco Antônio Peliky; Guatimosim, Sílvia; Castro, Carlos H.; Ianzer, Danielle; Ferreira, Reginaldo Nassar; Xavier, Carlos Henrique

doi:10.1016/j.lfs.2018.01.019

Cited by 9 publications

(3 citation statements)

References 63 publications

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“…We observed an initial rise in HR (by approximately 50%) in the stress group, with high values (at approximately 25% above baseline) persisting during the entire period of restraint and air-jet. These findings compare favorably with those previously observed in a similar protocol, consisting of 10 minutes of restraint followed by 10 minutes of air-jet stress [11]. Likewise, HR increased (by approximately 30%) during air-jet stress in another study [12], albeit no change was noted during an initial 10-minute restraint period.…”

Section: Heart Ratesupporting

confidence: 88%

Sympathetic and Vagal Responses Elicited by Acute Stress in Rats

Mouchtouri¹,

Lekkas²,

Delis³

et al. 2020

Cureus

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Introduction Acute emotional stress triggers autonomic responses that affect sympathovagal balance. However, the temporal pattern of changes in each autonomic arm during stress and recovery remains unclear. Therefore, we analyzed separately sympathetic and vagal activity, elicited by acute unpredictable stress in a rat model. Methods Continuous electrocardiographic recording was performed during (32 minutes) and after (two hours) successive use of restraint and air-jet stress in 10 rats, whereas five rats served as controls. Sympathetic and vagal indices were calculated non-invasively after heart rate variability analysis. Voluntary motion was quantified during recovery, as an index of continuing anxiety. Results The sympathetic nervous system index increased during stress and remained elevated during the initial stage of recovery. The parasympathetic nervous system index decreased immediately after the onset of stress and remained low throughout the observational period. During recovery, voluntary activity was more pronounced in the stress group than in the controls. Conclusion Successive restraint and air-jet stress in rats increased sympathetic activity and decreased vagal activity. These changes displayed only partial recovery post-stress and were accompanied by enhanced voluntary motion. Our findings may be important in the evaluation of the cardiac electrophysiologic implications of autonomic changes elicited by acute emotional stress.

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Section: Heart Ratesupporting

confidence: 88%

Sympathetic and Vagal Responses Elicited by Acute Stress in Rats

Mouchtouri¹,

Lekkas²,

Delis³

et al. 2020

Cureus

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“…The vibrotactile stress trial was conducted as described previously [43,44]. The animals were stimulated into an acrylic restrainer and exposed to the air-jet stress procedure, in which a stream of air (10 L/min) was directed to the animals' nose, for 10 min.…”

Section: Air-jetmentioning

confidence: 99%

Centrally acting antihypertensives change the psychogenic cardiovascular reactivity

Mendonça

Costa

Moraes

et al. 2021

Fundamemntal Clinical Pharma

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Clonidine (CL) and Rilmenidine (RI) are among the most frequently prescribed centrally acting antihypertensives. Here, we compared CL and RI effects on psychogenic cardiovascular reactivity to sonant, luminous, motosensory, and vibrotactile stimuli during neurogenic hypertension. The femoral artery and vein of Wistar (WT – normotensive) and spontaneously hypertensive rats (SHR) were catheterized before (24 h interval) i.p. injection of vehicle (NaCl 0.9%, control ‐ CT group), CL (10 µg/kg), or RI (10 µg/kg) and acute exposure to luminous (5000 lm), sonant (75 dB sudden tap), motor (180° cage twist), and air‐jet (10 L/min – restraint and vibrotactile). Findings showed that: (i) CL or RI reduced the arterial pressure of SHR, without affecting basal heart rate in WT and SHR; (ii) different stimuli evoked pressor and tachycardic responses; (iii) CL and RI reduced pressor response to sound; (iv) CL or RI reduced pressor responses to luminous stimulus without a change in peak tachycardia in SHR; (v) cage twist increased blood pressure in SHR, which was attenuated by CL or RI; (vi) air‐jet increased pressure and heart rate; (vii) CL or RI attenuated the pressor responses to air‐jet in SHR while RI reduced the chronotropic reactivity in both strains. Altogether, both antihypertensives relieved the psychogenic cardiovascular responses to different stimuli. The RI elicited higher cardioprotective effects through a reduction in air‐jet‐induced tachycardia.

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“…• Neuregulin-1 [134][135][136][137][138] • Ghrelin [139] • Vasopressin [140] • Anesthetic preconditioning [141] Non-pharmacological interventions…”

Section: Pharmacological Interventionsmentioning

confidence: 99%

Autonomic Nervous System and Neurocardiac Physiopathology

Kingma¹,

Simard²,

Rouleau³

2018

Autonomic Nervous System

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The autonomic nervous system regulates multiple physiological functions; how distinct neurons in peripheral autonomic and intrathoracic ganglia communicate remains to be established. Increasing focus is being paid to functionality of the neurocardiac axis and crosstalk between the intrinsic nervous system and diverse organ systems. Current findings indicate that progression of cardiovascular disease comprises peripheral and central aspects of the cardiac nervous system hierarchy. Indeed, autonomic neuronal dysfunction is known to participate in arrhythmogenesis and sudden cardiac death; diverse interventions (pharmacological, non-pharmacological) that affect neuronal remodeling in the heart following injury caused by cardiovascular disease (congestive heart failure, etc.) or acute myocardial infarction are being investigated. Herein we examine recent findings from clinical and animal studies on the role of the intrinsic cardiac nervous system on regulation of myocardial perfusion and the consequences of cardiac injury. We also discuss different interventions that target the autonomic nervous system, stimulate neuronal remodeling and adaptation, and thereby optimize patient outcomes.

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Ghrelin potentiates cardiac reactivity to stress by modulating sympathetic control and beta-adrenergic response

Cited by 9 publications

References 63 publications

Sympathetic and Vagal Responses Elicited by Acute Stress in Rats

Sympathetic and Vagal Responses Elicited by Acute Stress in Rats

Centrally acting antihypertensives change the psychogenic cardiovascular reactivity

Autonomic Nervous System and Neurocardiac Physiopathology

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