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

Autor: Silvia Guatimosim, Marco Antônio Peliky Fontes, Allancer D C Nunes, Robson A.S. Santos, Roger Luis Henschel Pobbe, Gabriel Camargo-Silva, Larissa Córdova Turones, Reginaldo Nassar Ferreira, Itamar Couto Guedes de Jesus, Kellen Rosa da Cruz, Carlos Henrique Xavier, Aline Priscila Pansani, Diego Basile Colugnati, Michelle Mendanha Mendonça, Karina Pereira Gomes, Danielle Ianzer, Carlos H. Castro
Rok vydání: 2018
Předmět:
Male
Restraint
Physical
0301 basic medicine
medicine.medical_specialty
Sympathetic Nervous System
Adrenergic receptor
Growth hormone secretagogue receptor
Stimulation
In Vitro Techniques
Muscarinic Agonists
General Biochemistry
Genetics and Molecular Biology
03 medical and health sciences
0302 clinical medicine
Heart Rate
Tachycardia
Internal medicine
Receptors
Adrenergic
beta
Heart rate
medicine
Animals
Arterial Pressure
Rats
Wistar
General Pharmacology
Toxicology and Pharmaceutics
Receptors
Ghrelin
Receptor
business.industry
digestive
oral
and skin physiology
Heart
General Medicine
Adrenergic beta-Agonists
Ghrelin
Rats
Autonomic nervous system
030104 developmental biology
Endocrinology
Calcium Channels
business
Stress
Psychological
hormones
hormone substitutes
and hormone antagonists
030217 neurology & neurosurgery
Acetylcholine
medicine.drug
Zdroj: Life Sciences. 196:84-92
ISSN: 0024-3205
Popis: 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.
Databáze: OpenAIRE
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