Chronic Vasodilation Mimics Renal Sodium Transporter Profile Seen In Pregnancy

A healthy pregnancy is associated with marked plasma volume expansion (PVE) mediated primarily by Na and water retention. This study tests the Underfill Hypothesis of pregnancy which proposes systemic vasodilation initiates PVE. Chronic vasodilation in virgin rats was induced by 14 days administration of NaNO2 or nifedipine (NIF) that led to sustained falls in BP of 4‐6 mmHg. We performed a Na transporter profile in kidney cortex homogenates. Only the protein abundance of the α subunit epithelial Na channel (ENaC) increased with NaNO2 and NIF (204+/−13% and 203+/‐11% of control respectively). No change was seen in the Na‐H‐exchanger type 3 (NHE3), Na‐K‐2Cl cotransporter (NKCC2), Na‐2Cl cotransporter (NCC), β ENaC or γ ENaC. We also noted an increase in the abundance of aquaporin 2 water channel (AQP2) (128+/−4% and 141+/−9% of control respectively). We previously conducted Na transporter profiles of whole kidney homogenates in early (day 6‐9), mid (day 13–15) and late (day 18–20) pregnant rats. Chronic vasodilation mimics the profiles seen in mid and late pregnancy where only α ENaC was upregulated (167+/−29% and 168+/−17% of control respectively). Others have shown increases in AQP2 in pregnancy. This suggests that 14 days chronic vasodilation mimics renal collecting duct adaptations, which enhance Na and water retention, seen in mid and late pregnancy thus supporting the Underfill Hypothesis of pregnancy.