Figure 4.

AVP-V1aR signaling contributes to weaker myocardial contractions and cardiac remodeling in heart failure (HF). (A) AVP binding to V1aR during HF activates G_αq protein-mediated signaling, which amplifies IP₃ signaling and triggers Ca²⁺ release (dashed) from the sarcoplasmic reticulum (SR). Prolonged Ca²⁺ mobilization leads to myocardial hypertrophy. (B) G_αq-independent signaling promotes GRK recruitment to the plasma membrane (PM) decreasing catecholamine-β adrenergic receptor (βAR) activation and Ca²⁺ mobilization. When prolonged, this condition impairs myocardial contractions.