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[$Ca^{2+}-induced$ $Ca^{2+}$ Release from Sarcoplasmic Reticulum Negatively Regulates Myocytic ANP Release in Beating Rabbit Atria

Li, Dan    (Department of Physiology, Institute for Medical Sciences, Institute for Basic Sciences, Jeonbug National University Medical School   ); Quan, He Xiu    (Department of Physiology, Institute for Medical Sciences, Institute for Basic Sciences, Jeonbug National University Medical School   ); Wen, Jin-Fu    (Department of Physiology, Institute for Medical Sciences, Institute for Basic Sciences, Jeonbug National University Medical School   ); Jin, Jing-Yu    (Department of Physiology, Institute for Medical Sciences, Institute for Basic Sciences, Jeonbug National University Medical School   ); Park, Sung-Hun    (Department of Physiology, Institute for Medical Sciences, Institute for Basic Sciences, Jeonbug National University Medical School   ); Kim, Sun-Young    (Department of Physiology, Institute for Medical Sciences, Institute for Basic Sciences, Jeonbug National University Medical School   ); Kim, Sung-Zoo    (Department of Physiology, Institute for Medical Sciences, Institute for Basic Sciences, Jeonbug National University Medical School   ); Cho, Kyung-Woo    (Department of Physiology, Institute for Medical Sciences, Institute f  );
  • 초록

    It is not clear whether $Ca^{2+}-induced$ $Ca^{2+}$ release from the sarcoplasmic reticulum (SR) is involved in the regulation of atrial natriuretic peptide (ANP) release. Previously, we have shown that nifedipine increased ANP release, indicating that $Ca^{2+}$ entry via voltage-gated L-type $Ca^{2+}$ channel activation decreases ANP release. The purpose of the present study was two-fold: to define the role of SR $Ca^{2+}$ release in the regulation of ANP release and whether $Ca^{2+}$ entry via L-type $Ca^{2+}$ channel is prerequisite for the SR-related effect on ANP release. Experiments were performed in perfused beating rabbit atria. Ryanodine, an inhibitor of SR $Ca^{2+}$ release, increased atrial myocytic ANP release ( $8.69{\pm}3.05$ , $19.55{\pm}1.09$ , $27.31{\pm}3.51$ , and $18.91{\pm}4.76$ % for 1, 2, 3, and $6{\mu}M$ ryanodine, respectively; all P $Ca^{2+}$ pump, ryanodine-induced increase in ANP release was not observed. Thapsigargin attenuated ryanodine-induced decrease in atrial dynamic changes. Blockade of L-type $Ca^{2+}$ channel with nifedipine abolished ryanodine-induced increase in ANP release ( $0.69{\pm}5.58$ % vs. $27.31{\pm}3.51$ %; P<0.001). In the presence of thapsigargin and ryanodine, nifedipine increased ANP release and decreased atrial dynamics. These data suggest that $Ca^{2+}$ -induced $Ca^{2+}$ release from the SR is inversely involved in the regulation of atrial myocytic ANP release.


  • 주제어

    Atrial natriuretic peptide .   L-type $Ca^{2+}$ channels .   Sarcoplasmic reticulum $Ca^{2+}$ release.  

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  • 이 논문을 인용한 문헌 (1)

    1. 2006. "" The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 10(3): 149~154     

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