What effect does increased cAMP in cardiac muscle cells result in?

Increased levels of cyclic adenosine monophosphate (cAMP) in cardiac muscle cells lead to enhanced contractility, also known as positive inotropy. This occurs because cAMP acts as a secondary messenger that activates protein kinase A (PKA). When PKA is activated, it phosphorylates various proteins within the cardiac muscle cells, including calcium channels and phospholamban.

The phosphorylation of calcium channels on the sarcolemma leads to an increase in calcium influx during action potentials. Additionally, phosphorylation of phospholamban decreases its inhibitory effect on the sarcoplasmic reticulum calcium ATPase (SERCA), which enhances the uptake of calcium into the sarcoplasmic reticulum. This results in increased availability of calcium for the contractile processes, ultimately augmenting the force of contraction of the heart muscle.

Therefore, the correct choice reflects the physiological response of the heart to elevated cAMP levels, demonstrating how this signaling molecule plays a critical role in enhancing cardiac function.