Chronic activation of vasopressin-2 receptors induces hypertension in Liddle mice by promoting Na<sup>+</sup> and water retention
James D. Stockand, Elena Mironova, Hong Xiang, António G. Soares, Jorge Contreras, James A. McCormick, Susan B. Gurley, Alan C. Pao
Abstract
Liddle syndrome is a classic model for hypertension from high epithelial Na + channel (ENaC) activity. In the Liddle mouse model, vasopressin-2 receptors stimulate both ENaC and aquaporin-2, which increases Na + and water retention to such an extent that hypertension ensues. Liddle mice will preserve plasma tonicity at the expense of a higher blood pressure; these data highlight the inherent limitation in which the kidney must use ENaC as a pathway to regulate both plasma tonicity and blood pressure.
Topics & Concepts
Epithelial sodium channelEndocrinologyInternal medicineAquaporin 2VasopressinReabsorptionReceptorAldosteroneChemistryBlood pressurePlasma renin activityAgonistRenin–angiotensin systemArginine vasopressin receptor 2KidneyMedicineSodiumAntagonistEngineeringInletWater channelMechanical engineeringOrganic chemistryIon Transport and Channel RegulationElectrolyte and hormonal disordersNeuroendocrine regulation and behavior