Produção Nacional
Revisado por pares
Ghrelin potentiates cardiac reactivity to stress by modulating sympathetic control and beta-adrenergic response
2018; Elsevier BV; Volume: 196; Linguagem: Inglês
10.1016/j.lfs.2018.01.019
ISSN1879-0631
AutoresGabriel Camargo-Silva, Larissa Córdova Turones, Kellen Rosa da Cruz, Karina Pereira Gomes, Michelle Mendanha Mendonça, Allancer Nunes, Itamar Couto Guedes de Jesus, Diego Basile Colugnati, Aline Priscila Pansani, Roger L.H. Pobbe, Robson A.S. Santos, Marco Antônio Peliky Fontes, Sílvia Guatimosim, Carlos H. Castro, Danielle Ianzer, Reginaldo Nassar Ferreira, Carlos Henrique Xavier,
Tópico(s)Adipose Tissue and Metabolism
ResumoPrior 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.In the present study, we assessed the role of ghrelin - GHS-R1a axis in the cardiovascular reactivity to acute emotional stress in rats.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.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.
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