Abstract
CaV1.2 channels are essential in cardiac excitation-contraction coupling. They can be tuned by physiological signaling pathways and dysregulated in diseases such as heart failure (HF). One such regulatory pathway is stimulated by angiotensin II (AngII) signaling through Gq-coupled AT1 receptors (AT1R). AngII is a peptide hormone with physiological roles in blood pressure regulation and pathological roles in hypertension and HF. AT1R activation results in the hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2), a plasma membrane (PM) phospholipid which regulates several ion channels and exchangers including CaV1.2.
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