Dissection of the Effects of Quercetin on Mouse Myocardium

• Published in: Basic & clinical pharmacology & toxicology Vol. 120; no. 6; pp. 550 - 559
• Main Authors: Santos, Michel Santana, Oliveira, Evaleide Diniz, Santos‐Miranda, Artur, Cruz, Jader Santos, Gondim, Antônio Nei Santana, Menezes‐Filho, José Evaldo Rodrigues, Souza, Diego Santos, Pinho‐da‐Silva, Leidiane, Jesus, Itamar Couto Guedes, Roman‐Campos, Danilo, Guatimosim, Silvia, Lara, Aline, Conde‐Garcia, Eduardo Antônio, Vasconcelos, Carla Maria Lins
• Format: Journal Article
• Language: English
• Published: England Wiley Subscription Services, Inc 01.06.2017
• Subjects: Animals; Ca2+-transporting ATPase; Calcium (intracellular); Calcium - metabolism; Calcium channels (L-type); Calcium Channels, L-Type - drug effects; Calcium Channels, L-Type - physiology; Calcium ions; Calcium signalling; Cardiac muscle; Cardiomyocytes; Electrocardiography - drug effects; Heart - drug effects; Heart - physiology; Heart diseases; Heart rate; Inotropism; Male; Membrane potential; Mice; Mice, Inbred C57BL; Muscle contraction; Muscles; Myocardial Contraction - drug effects; Myocardium; Myocardium - metabolism; Propranolol; Quercetin; Quercetin - pharmacology; Receptors (physiology); Rodents; Sympathetic nervous system
• ISSN: 1742-7835; 1742-7843
• DOI: 10.1111/bcpt.12743

Quercetin is a plant flavonoid with several biological activities. This study aimed to describe quercetin effects on contractile and electrophysiological properties of the cardiac muscle as well as on calcium handling. Quercetin elicited positive inotropism that was significantly reduced by propranolol indicating an involvement of the sympathetic nervous system. In cardiomyocytes, 30 μM quercetin increased ICa,L at 0 mV from −0.95 ± 0.01 A/F to −1.21 ± 0.08 A/F. The membrane potential at which 50% of the channels are activated (V0.5) shifted towards more negative potentials from −13.06 ± 1.52 mV to −19.26 ± 1.72 mV and did not alter the slope factor. Furthermore, quercetin increased [Ca2+]i transient by 28% when compared to control. Quercetin accelerated [Ca2+]i transient decay time, which could be attributed to SERCA activation. In resting cardiomyocytes, quercetin did not change amplitude or frequency of Ca2+ sparks. In isolated heart, quercetin increased heart rate and decreased PRi, QTc and duration of the QRS complex. Thus, we showed that quercetin activates β‐adrenoceptors, leading to increased L‐type Ca2+ current and cell‐wide intracellular Ca2+ transient without visible changes in Ca2+ sparks.