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Experimental Physiology 93.8 pp 945-953
DOI: 10.1113/expphysiol.2008.042036
© The Physiological Society 2008
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Role of TRPV1 channels in renal haemodynamics and function in Dahl salt-sensitive hypertensive rats

Jianping Li1 and Donna H. Wang1

1 Department of Medicine, Neuroscience Program and Cell and Molecular Biology Program, Michigan State University, East Lansing, MI 48824, USA

This study tests the hypothesis that dysfunction of transient receptor potential vanilloid type 1 (TRPV1) channels occurs and contributes to the decrease in the glomerular filtration rate (GFR) and sodium/water excretion in Dahl salt-sensitive hypertensive rats. Recirculating Krebs–Henseleit buffer added with inulin was perfused at a constant flow in the isolated kidneys of Dahl salt-sensitive (DS) or Dahl salt-resistant (DR) rats fed a high-salt (HS) or low-salt (LS) diet for 3 weeks. Perfusion pressures (PP) were pre-adjusted to three levels (~100, ~150 or ~190 mmHg) with or without phenylephrine. Capsaicin, a selective TRPV1 agonist, in the presence or absence of capsazepine, a selective TRPV1 antagonist, was perfused. Basal GFR, urine flow rate (UFR) and Na+ excretion (UNaV) were significantly lower in DS-HS than in DR-HS, DS-LS and DR-LS rats. Capsaicin caused pressure-dependent decreases in PP and increases in GFR, UFR and UNaV in all groups, with less magnitude of decreases in PP and increases in GFR, UFR and UNaV in DS-HS than in DR-HS, DS-LS and DR-LS rats. Capsazepine completely blocked the effect of capsaicin on PP, GFR, UFR and UNaV in all groups. Thus, these results show that TRPV1 function is impaired in the kidney of DS rats fed a high-salt diet, which may contribute to the decrease in GFR and renal excretory function in DS rats in the face of salt challenge.

(Received 9 January 2008; accepted after revision 7 April 2008; first published online 10 April 2008)
Corresponding author D. H. Wang: B 316 Clinical Center, Department of Medicine, Michigan State University, East Lansing, MI 48824, USA. Email: donna.wang{at}ht.msu.edu







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