TRPV1 activation prevents high-salt diet-induced nocturnal hypertension in mice

• Published in: Pflügers Archiv 2011-03, Vol.461 (3), p.345-353
• Main Authors: Hao, Xinzhong, Chen, Jing, Luo, Zhidan, He, Hongbo, Yu, Hao, Ma, Liqun, Ma, Shuangtao, Zhu, Tianqi, Liu, Daoyan, Zhu, Zhiming
• Format: Article
• Language: English
• Subjects: Animals; Biomedical and Life Sciences; Biomedicine; Capsaicin - pharmacology; Capsaicin - therapeutic use; Cell Biology; Circadian Rhythm; Human Physiology; Hydrogen Peroxide - metabolism; Hypertension - etiology; Hypertension - prevention & control; Ion Channels; Male; Malondialdehyde - metabolism; Mesenteric Arteries - drug effects; Mesenteric Arteries - metabolism; Mice; Mice, Inbred C57BL; Molecular Medicine; Neurosciences; Nitric Oxide - biosynthesis; Receptors; Receptors and Transporters; Sodium Chloride, Dietary - administration & dosage; TRPV Cation Channels - physiology
• ISSN: 0031-6768; 1432-2013
• DOI: 10.1007/s00424-011-0921-x

High dietary salt-caused hypertension is associated with increasing reactive oxygen species generation and reduced nitric oxide (NO) bioavailability. Transient receptor potential vanilloid type 1 (TRPV1), a specific receptor for capsaicin, is proposed to be involved in Dahl salt-sensitive hypertension, as determined in acute or short-term experiments. However, it remains unknown whether activation of TRPV1 by dietary capsaicin could prevent the vascular oxidative stress and hypertension induced by a high-salt diet. Here, we report that consumption of a high-salt diet blunted endothelium-dependent relaxation in mesenteric resistance arteries and elevated nocturnal blood pressure in mice. These effects were associated with increased superoxide anion generation and reduced NO levels in mesenteric vessels in mice on a high-salt diet. However, chronic administration of capsaicin reduced the high-salt diet-induced endothelial dysfunction and nocturnal hypertension in part by preventing the generation of superoxide anions and NO reduction of mesenteric arteries through vascular TRPV1 activation. Our findings provide new insights into the role of TRPV1 channels in the long-term regulation of blood pressure in response to high-salt intake. TRPV1 activation through chronic dietary capsaicin may represent a promising lifestyle intervention in populations with salt-sensitive hypertension.