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Dissection of the Effects of Quercetin on Mouse Myocardium
Author(s) -
Santos Michel Santana,
Oliveira Evaleide Diniz,
SantosMiranda Artur,
Cruz Jader Santos,
Gondim Antônio Nei Santana,
MenezesFilho José Evaldo Rodrigues,
Souza Diego Santos,
PinhodaSilva Leidiane,
Jesus Itamar Couto Guedes,
RomanCampos Danilo,
Guatimosim Silvia,
Lara Aline,
CondeGarcia Eduardo Antônio,
Vasconcelos Carla Maria Lins
Publication year - 2017
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/bcpt.12743
Subject(s) - quercetin , intracellular , chemistry , flavonoid , medicine , membrane potential , propranolol , electrophysiology , cardiac transient outward potassium current , calcium , calcium in biology , qrs complex , calcium channel , endocrinology , pharmacology , patch clamp , biochemistry , antioxidant
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 I Ca,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 (V 0.5 ) 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 [Ca 2+ ] i transient by 28% when compared to control. Quercetin accelerated [Ca 2+ ] i transient decay time, which could be attributed to SERCA activation. In resting cardiomyocytes, quercetin did not change amplitude or frequency of Ca 2+ 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 Ca 2+ current and cell‐wide intracellular Ca 2+ transient without visible changes in Ca 2+ sparks.