Modied sympathetic nerve regulation in AKAP5-null mice

Chong Han, Hirofumi Tomita, Takayoshi Ohba, Kimitaka Nishizaki, Yoshiki Ogata, Yasushi Matsuzaki, Daisuke Sawamura, Teruyuki Yanagisawa, Tomohiro Osanai, Tadaatsu Imaizumi, Atsushi Matsubara, Takeshi Adachi, Kyoichi Ono, Ken Okumura, Manabu Murakami

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)


Genetic analyses have revealed an important association between A-kinase anchoring proteins (AKAPs) and the intracellular calcium modulating system. AKAP5, also known as AKAP79/150, is an anchoring protein between PKA and voltage-dependent calcium channels, ryanodine receptor-2, phospholamban and other molecules. The aim of the present study was to elucidate the physiological importance of AKAP5 in the creation of cardiac rhythm using AKAP5-null mice. ECG analysis showed a normal sinus rhythm and a decreased responsiveness to isoproterenol in AKAP5-null mice compared with wild-type mice. Analysis of heart rate variability revealed that the R-R interval was unstable in AKAP5-null mutants and that the low-frequency components had decreased, indicating that the tonus of the sympathetic nervous system was affected. Furthermore, the atrium of the AKAP5-null mice showed a decreased positive inotropic response to isoproterenol, indicating the involvement of AKAP5 in a PKA-dependent pathway. Thus, our present study revealed that AKAP5 plays a signicant role in the regulation of sympathetic nerve activities.

Original languageEnglish
Pages (from-to)897-902
Number of pages6
JournalBiochemical and biophysical research communications
Issue number4
Publication statusPublished - 2016 Jan 22


  • Heart rate
  • Mouse
  • PKA
  • Parasympathetic nerve
  • Sympathetic nerve

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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