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Elevated plasma levels of angiotensin II have been identified as a key determinant of cardiac hypertrophy and congestive heart failure. Angiotensin II signaling mediates its biological actions in part by altering intracellular sarcoplasmic reticulum/endoplasmic reticulum calcium stores and voltage-dependent L-type Ca2+ channels.1 Calcium concentration is directly involved in cardiac excitation–contraction coupling and plays a central role in intracellular signaling pathways. Because calcium is the physiological activator of the contractile proteins, chronic elevations of cardiac angiotensin II-altered calcium handling have been postulated to underlie the calcium overload and contractile dysfunction after myocardial infarction.2 Kamp and Hell3 have suggested involvement of protein kinase A (PKA) and protein kinase C (PKC) pathways in the modulation of intracellular calcium stores and contractility. This is consistent with the reported ability of angiotensin II to promote cardiac hypertrophy via the phosphoinositide 3-kinase (PI3K)/Akt-dependent pathway.4,5 In this regard, PI3K transduces extracellular signals into cellular function by regulating activity of several genes downstream of angiotensin II type 1 receptor (AT1R).6 Based on sequence homology and substrate preference, 8 members of the PI3K family have been identified. The most widely studied isoforms of the PI3K family include PI3Kα and PI3Kγ, which regulate a variety of biological actions, including L-type calcium channel activity7 and genes associated with cell growth and survival.5Although chronic angiotensin II stimulation reportedly leads to cardiac remodeling,8 metabolic alterations,9 cardiac fibrosis,10 and hypertrophy,5 little is known of the acute phase effects of angiotensin II on cardiomyocyte contractility. By definition, inotropy relates to alterations in contractile force generation independent of sarcomere length. It is mainly dictated by changes in activator calcium …

Negative Inotropy by Angiotensin II Is Mediated via Phosphoinositide 3-Kinase Alpha–Protein Kinase C-Coupled Signaling Pathway