Transient receptor potential vanilloid‐1 (TRPV1) and TRPV4 Null Mice Display Normal Salt Appetite

Abstract

The forebrain lamina terminalis plays an important role in body fluid homeostasis. Recent evidence suggests that both TRPV1 and TRPV4 channels contribute to central osmoregulation during acute and chronic sodium loading. The purpose of the present study was to determine whether TRPV1 and TRPV4 channels contribute to salt appetite. Wild‐type (WT) mice and mice lacking the TRPV1 and TRPV4 genes (TRPV1xV4‐/‐, n=4 per group) were fed a sodium‐deficient diet (0.01%) and given access to water and 0.3M NaCl for 10 days. Average 24‐h intake of water (2.66±0.16 vs 2.78±0.05mL) and 0.3 M NaCl (0.58±0.13mL vs 0.23±0.07mL) were not different between TRPV1xV4‐/‐ and WT mice. Hypovolemia, produced by sc injection of 20% polyethylene glycol (0.5mL) stimulated the ingestion of water and salt in both groups; however, TRPV1xV4‐/‐ and WT mice ingested similar amounts of water (1.63±0.06 vs 1.40±0.09mL, respectively) and 0.3 M NaCl (0.59±0.09 vs 0.54±0.10mL respectively) at 8 hrs. TRPV1xV4‐/‐ and WT mice drank similar amounts of water (0.15±0.03 vs 0.28±0.05mL) and 0.3 M NaCl (0.14±0.06 vs 0.15±0.05mL) after injection of saline vehicle (0.5mL). These findings indicate that TRPV1 and TRPV4 channels do not contribute to salt appetite. Supported by NIH HL090826, AHA 0630202N