Stimulation of metabotropic G_q-coupled purinergic P2Y_2 receptors decreases activity of the epithelial Na+ channel (ENaC) in renal principal cells of the distal nephron. The physiological consequences of P2Y_2 receptor signaling disruption in the P2Y_2 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.
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