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(Hypertension. 2006;47:609.)
© 2006 American Heart Association, Inc.
Part 2 Original Articles |
From the Department of Medicine, Michigan State University, East Lansing.
Correspondence to Donna H. Wang, Department of Medicine, B316 Clinical Center, Michigan State University, East Lansing, MI 48824. E-mail donna.wang{at}ht.msu.edu
To determine the role of the transient receptor potential vanilloid type 1 (TRPV1) channels in development of hypertension in Dahl saltsensitive (DS) rats fed a high-salt diet (HS), male DS and Dahl saltresistant (DR) rats were maintained on a low-salt diet (LS) or HS for 3 weeks. HS significantly increased systolic blood pressure in DS+HS rats compared with DS+LS, DR+HS, and DR+LS rats. Intravenous bolus injection of capsazepine (3 mg/kg), a selective TRPV1 antagonist, significantly increased mean arterial pressure in conscious DR+HS rats compared with DR+LS, DS±HS, and DS±LS rats. In contrast, capsaicin (10 or 30 µg/kg), a selective TRPV1 agonist, dose-dependently decreased mean arterial pressure in all of the groups with the most profound magnitude in DR+HS rats compared with the other 3 groups. TRPV1 expression in mesenteric resistance arteries and the renal cortex and medulla, calcitonin generelated peptide levels in dorsal root ganglia, and calcitonin generelated peptidepositive sensory nerve density in mesenteric resistance arteries were significantly decreased in DS+HS rats compared with DS+LS, DR+HS, and DR+LS rats. Taken together, our data indicate that the TRPV1 receptor is activated and its expression upregulated during HS intake in DR rats, which acts to prevent salt-induced increases in blood pressure. In contrast, TRPV1 expression and function are impaired in DS rats, which renders DS rats sensitive to salt load in terms of blood pressure regulation.
Key Words: peptides rats, Dahl hypertension, sodium-dependent blood pressure
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