A3299 TRPV1 activation by dietary capsaicin improves high salt diet-induced hypertension

Abstract

Objectives: High-salt intake contributes to the development of hypertension. We have reported that transient receptor potential vanilloid type 1 (TRPV1) activation by dietary capsaicin improves endothelial function in genetically hypertensive rats. We investigate whether TRPV1 activation also antagonizes high-salt induced hypertension. Methods: C57BL/6J (WT) and TRPV1−/− mice were randomized into three groups (n = 8) and were fed with normal diet (ND), high-salt diet (8% salt, HS) or high-salt plus 0.01% capsaicin diet (HSC). Mouse systolic blood pressure (SBP) was measured by tail-cuff plethysmography and 24-hour ambulatory arterial pressure was measured with telemetric transmitters. Results: The study showed that TRPV1 activation inhibited the increased αENaC activity, and increased urinary sodium excretion through reducing sodium reabsorption in WT mice on a HS but not in TRPV1−/− mice. TRPV1 activation significantly lowered tail SBP in WT mice on a HS after the 8 month. TRPV1 activation also lowered 24-hour ambulatory arterial pressure in WT HS group mice after 10-month treatment. Importantly, the hypotensive effect of capsaicin was absent in TRPV1−/− mice. Plasma aldosterone levels were lower in mice on a HS compared with mice on a ND in WT and TRPV1−/−mice. The urinary sodium excretion and volume of water intake were higher in mice on a HS compared with in WT and TRPV1−/−mice on ND. However, the plasma sodium, potassium and chloride, urinary potassium, and food intake were not different among each group of WT and TRPV1−/− mice. Conclusion: TRPV1 activation by capsaicin increases urinary sodium excretion and prevents high-salt diet induced hypertension through antagonizing αENaC-mediated urinary sodium reabsorption.