TY - JOUR
T1 - Ghrelin potentiates cardiac reactivity to stress by modulating sympathetic control and beta-adrenergic response
AU - Camargo-Silva, Gabriel
AU - Turones, Larissa Córdova
AU - da Cruz, Kellen Rosa
AU - Gomes, Karina Pereira
AU - Mendonça, Michelle Mendanha
AU - Nunes, Allancer
AU - de Jesus, Itamar Guedes
AU - Colugnati, Diego Basile
AU - Pansani, Aline Priscila
AU - Pobbe, Roger Luis Henschel
AU - Santos, Robson
AU - Fontes, Marco Antônio Peliky
AU - Guatimosim, Silvia
AU - de Castro, Carlos Henrique
AU - Ianzer, Danielle
AU - Ferreira, Reginaldo Nassar
AU - Xavier, Carlos Henrique
N1 - Publisher Copyright:
© 2018 Elsevier Inc.
PY - 2018/3/1
Y1 - 2018/3/1
N2 - Prior evidence indicates that ghrelin is involved in the integration of cardiovascular functions and behavioral responses. Ghrelin actions are mediated by the growth hormone secretagogue receptor subtype 1a (GHS-R1a), which is expressed in peripheral tissues and central areas involved in the control of cardiovascular responses to stress. Aims: In the present study, we assessed the role of ghrelin – GHS-R1a axis in the cardiovascular reactivity to acute emotional stress in rats. Main methods and key findings: Ghrelin potentiated the tachycardia evoked by restraint and air jet stresses, which was reverted by GHS-R1a blockade. Evaluation of the autonomic balance revealed that the sympathetic branch modulates the ghrelin-evoked positive chronotropy. In isolated hearts, the perfusion with ghrelin potentiated the contractile responses caused by stimulation of the beta-adrenergic receptor, without altering the amplitude of the responses evoked by acetylcholine. Experiments in isolated cardiomyocytes revealed that ghrelin amplified the increases in calcium transient changes evoked by isoproterenol. Significance: Taken together, our results indicate that the Ghrelin-GHS-R1a axis potentiates the magnitude of stress-evoked tachycardia by modulating the autonomic nervous system and peripheral mechanisms, strongly relying on the activation of cardiac calcium transient and beta-adrenergic receptors.
AB - Prior evidence indicates that ghrelin is involved in the integration of cardiovascular functions and behavioral responses. Ghrelin actions are mediated by the growth hormone secretagogue receptor subtype 1a (GHS-R1a), which is expressed in peripheral tissues and central areas involved in the control of cardiovascular responses to stress. Aims: In the present study, we assessed the role of ghrelin – GHS-R1a axis in the cardiovascular reactivity to acute emotional stress in rats. Main methods and key findings: Ghrelin potentiated the tachycardia evoked by restraint and air jet stresses, which was reverted by GHS-R1a blockade. Evaluation of the autonomic balance revealed that the sympathetic branch modulates the ghrelin-evoked positive chronotropy. In isolated hearts, the perfusion with ghrelin potentiated the contractile responses caused by stimulation of the beta-adrenergic receptor, without altering the amplitude of the responses evoked by acetylcholine. Experiments in isolated cardiomyocytes revealed that ghrelin amplified the increases in calcium transient changes evoked by isoproterenol. Significance: Taken together, our results indicate that the Ghrelin-GHS-R1a axis potentiates the magnitude of stress-evoked tachycardia by modulating the autonomic nervous system and peripheral mechanisms, strongly relying on the activation of cardiac calcium transient and beta-adrenergic receptors.
KW - Beta-adrenergic receptors
KW - Cardiac calcium transient
KW - Emotional stress
KW - Ghrelin
KW - GHS-R1a receptor
KW - Heart rate
UR - https://www.scopus.com/pages/publications/85041496874
UR - https://www.scopus.com/pages/publications/85041496874#tab=citedBy
U2 - 10.1016/j.lfs.2018.01.019
DO - 10.1016/j.lfs.2018.01.019
M3 - Article
C2 - 29366747
AN - SCOPUS:85041496874
SN - 0024-3205
VL - 196
SP - 84
EP - 92
JO - Life Sciences
JF - Life Sciences
ER -