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This research examines whether protein kinase A alters the economy of force maintenance and ATP consumption in cardiac muscle during contraction.

Protein Kinase A Does Not Alter Economy of Force Maintenance in Skinned Rat Cardiac Trabeculae

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This research examines whether protein kinase A alters the economy of force maintenance and ATP consumption in cardiac muscle during contraction.
Cardiac trabeculae were skinned with Triton X-100 and ATP consumption was measured via an enzyme-coupled optical technique.
Force-[Ca2+] relations were analyzed using a modified Hill equation, and ATP consumption rate was evaluated by multiple linear regression analysis.
Beta-adrenergic stimulation was simulated using protein kinase A treatment (3 micrograms/mL for 40 minutes).
PKA treatment increased the [Ca2+] needed for half-maximal force by 65% (P = .01) without affecting the steepness of the force-[Ca2+] relation.
The rate of ATP consumption correlated linearly with steady state force (P < .001), regardless of PKA treatment.
PKA did not change either the maximum rate of ATP consumption or the economy of force maintenance in the myocardium.

Population

Skinned rat cardiac trabeculae (Triton X-100)

Intervention

Incubation with the catalytic subunit of protein kinase A (PKA) (3 micrograms/mL, 40 minutes)

Comparator

No PKA treatment

Outcome

Rate of ATP consumption as a function of steady state force (economy of force maintenance)surrogate

Beta-adrenergic stimulation mimicked by PKA does not alter the rate-limiting step of cross-bridge cycling during isometric contraction in myocardium.

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PKA spares cross-bridge energetics in isolated myocardium; hypothesis-generating for beta-adrenergic effects in intact hearts.

Tombe et al. (1995) studied this question.

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