Renal Na excretion consequent to pharmacogenetic activation of G-DREADD in principal cells.

Stimulation of metabotropic G-coupled purinergic P2Y receptors decreases activity of the epithelial Na channel (ENaC) in renal principal cells of the distal nephron. The physiological consequences of P2Y receptor signaling disruption in the P2Y receptor knockout mouse are decreased Na excretion and increased arterial blood pressure. However, because of the global nature of this knockout model, the quantitative contribution of ENaC and distal nephron compared with that of upstream renal vascular and tubular elements to changes in urinary excretion and arterial blood pressure is obscure.

Ankyrin-B protein in heart failure: identification of a new component of metazoan cardioprotection.

Ankyrins (ankyrin-R, -B, and -G) are adapter proteins linked with defects in metazoan physiology. Ankyrin-B (encoded by ANK2) loss-of-function mutations are directly associated with human cardiovascular phenotypes including sinus node disease, atrial fibrillation, ventricular tachycardia, and sudden cardiac death. Despite the link between ankyrin-B dysfunction and monogenic disease, there are no data linking ankyrin-B regulation with common forms of human heart failure.