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Adenylyl cyclase type V deletion increases basal left ventricular function and reduces left ventricular contractile

Tong Tang1, N Chin Lai, David M Roth

  • 1Veterans Affairs, San Diego Healthcare System, 9151A, 3350 La Jolla Village Drive, San Diego, California 92161, USA. ttang@vapop.ucsd.edu

Basic Research in Cardiology
|November 12, 2005
PubMed

Insights

Deletion of adenylyl cyclase type V (AC(V)) in mice improved basal cardiac function but reduced responsiveness to beta-adrenergic receptor (betaAR) stimulation, impacting cAMP levels and calcium handling.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Enzyme Function

Background:

  • Adenylyl cyclase type V (AC(V)) plays a critical role in cardiac cAMP production.
  • AC(V) is involved in regulating left ventricular (LV) contractility and beta-adrenergic receptor (betaAR) signaling.

Purpose of the Study:

  • To investigate the functional consequences of AC(V) deletion on cardiac performance.
  • To determine the impact of AC(V) absence on betaAR stimulation and intracellular calcium handling.

Main Methods:

  • Utilized AC(V)-deleted (AC(V) (-/-)) and control (CON) mice.
  • Assessed cardiac function using isolated perfused hearts (measuring LV +dP/dt).
  • Quantified cAMP production, sarcoplasmic reticulum calcium uptake (SERCA2a), and protein levels (phospholamban, protein phosphatase, Galphas).

Main Results:

  • AC(V) deletion increased basal LV +dP/dt but decreased dobutamine potency.
  • Absence of AC(V) led to reduced cAMP production and increased SERCA2a affinity for Ca(2+).
  • Observed increased phospholamban phosphorylation and reduced cardiac Galphas protein content.

Conclusions:

  • AC(V) deletion favorably impacts basal LV function despite reduced cAMP.
  • Enhanced Ca(2+) uptake via SERCA2a and phospholamban phosphorylation contribute to improved basal function.
  • AC(V) deletion impairs LV contractile responsiveness to betaAR stimulation due to reduced Galphas and cAMP capacity.

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