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Updated: Feb 15, 2026

Cardiac Response to β-Adrenergic Stimulation Determined by Pressure-Volume Loop Analysis
Published on: May 19, 2021
Ghrelin potentiates cardiac reactivity to stress by modulating sympathetic control and beta-adrenergic response
Gabriel Camargo-Silva1, Larissa Córdova Turones1, Kellen Rosa da Cruz1
1Laboratory of Cardiovascular Physiology and Therapeutics, Department of Physiological Sciences, Institute of Biological Sciences, Federal University of Goiás, Goiania, GO, Brazil.
Abstract:
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.
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