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To examine the role of transient receptor potential vanilloid type 4 (TRPV4) channels in the development of salt-sensitive hypertension, male Dahl salt-sensitive (DS) and -resistant (DR) rats were fed a low-salt (LS) or high-salt (HS) diet for 3 weeks. DS-HS but not DR-HS rats developed hypertension. 4alpha-Phorbol-12,13-didecanoate (a selective TRPV4 activator; 2.5 mg/kg IV) decreased mean arterial pressure in all of the groups with the greatest effects in DR-HS and the least in DS-HS rats (P&lt;0.05). Depressor effects of 4alpha-phorbol-12,13-didecanoate but not dihydrocapsaicin (a selective TRPV1 agonist; 30 microg/kg IV) were abolished by ruthenium red (a TRPV4 antagonist; 3 mg/kg IV) in all of the groups. Blockade of TRPV4 with ruthenium red increased mean arterial pressure in DR-HS rats only (P&lt;0.05). TRPV4 protein contents were decreased in the renal cortex, medulla, and dorsal root ganglia in DS-HS compared with DS-LS rats but increased in dorsal root ganglia and mesenteric arteries in DR-HS compared with DR-LS rats (P&lt;0.05). Mean arterial pressure responses to blockade of small- and large-/intermediate-conductance Ca(2+)-activated K(+) channels (Maxikappa channels) with apamin and charybdotoxin, respectively, were examined. Apamin (100 microg/kg) plus charybdotoxin (100 microg/kg) abolished 4alpha-phorbol-12,13-didecanoate-induced hypotension in DR-LS, DR-HS, and DS-LS rats only. Thus, HS-induced enhancement of TRPV4 function and expression in sensory neurons and resistant vessels in DR rats may prevent salt-induced hypertension possibly via activation of Maxikappa channels given that blockade of TRPV4 elevates mean arterial pressure. In contrast, HS-induced suppression of TRPV4 function and expression in sensory neurons and kidneys in DS rats may contribute to increased salt sensitivity.

Impairment in Function and Expression of Transient Receptor Potential Vanilloid Type 4 in Dahl Salt-Sensitive Rats