Published Online
on July 7, 2008

A more recent version of this article appeared on August 1, 2008

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Submitted on January 11, 2008
Revised on January 31, 2008

Deletion of Transient Receptor Potential Vanilloid Type 1 Receptors Exaggerates Renal Damage in Deoxycorticosterone Acetate-Salt Hypertension

Youping Wang; Dagmar Babánková; Jie Huang; Greg M. Swain; and Donna H. Wang^*

From the Departments of Medicine (Y.W., D.H.W.), Chemistry (D.B., G.M.S.), and Radiology (J.H.), and the Neuroscience Program (G.M.S., D.H.W.), Michigan State University, East Lansing.

^* To whom correspondence should be addressed. E-mail: donna.wang{at}ht.msu.edu.

Abstract—To determine whether the transient receptor potential vanilloid type 1 (TRPV1) channel provides protection against hypertension-induced renal damage, hypertension was induced by uninephrectomy and by giving deoxycorticosterone acetate (DOCA)-salt in wild-type (WT) and TRPV1-null mutant (TRPV1^-/-) mice. Mean arterial pressure, as determined by radiotelemetry, increased significantly and reached the peak 7 days after DOCA-salt treatment in both WT and TRPV1^-/- mice. There was no difference in mean arterial pressure between the 2 strains at the baseline or at the peak that lasted for 4 treatment weeks. DOCA-salt treatment in both WT and TRPV1^-/- mice led to increased urinary excretion of albumin and 8-isoprostane, glomerulosclerosis, renal cortical tubulointerstitial injury, tubulointerstitial fibrosis, increased number of tubular proliferating cell nuclear antigen–positive cells, and renal monocyte/macrophage infiltration, all of which were much more severe in DOCA-salt–treated TRPV1^-/- compared with DOCA-salt-treated WT mice. Renal TRPV1 protein expression, but not the renal anandamide content, was elevated in DOCA-salt–treated WT compared with vehicle-treated WT mice. Renal anandamide levels were markedly elevated in DOCA-salt–treated TRPV1^-/- but not in vehicle-treated TRPV1^-/- mice. Thus, our data show that ablation of the TRPV1 gene exacerbates renal damage induced by DOCA-salt hypertension, indicating that TRPV1 may constitute a protective mechanism against end-organ damage induced by hypertension.

Key words: transient receptor potential vanilloid type 1 channel • hypertension • renal injury • deoxycorticosterone • mice

Related Article:

Transient Receptor Potential Vanilloid Type 1 Receptors in Hypertensive Renal Damage: A Promising Therapeutic Target?

Tilmann Ditting, Roland Veelken, and Karl F. Hilgers
Hypertension 2008 52: 213-214. [Extract] [Full Text] [PDF]

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				Y. Wang and D. H. Wang Aggravated renal inflammatory responses in TRPV1 gene knockout mice subjected to DOCA-salt hypertension Am J Physiol Renal Physiol, December 1, 2009; 297(6): F1550 - F1559. [Abstract] [Full Text] [PDF]

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				T. Ditting, R. Veelken, and K. F. Hilgers Transient Receptor Potential Vanilloid Type 1 Receptors in Hypertensive Renal Damage: A Promising Therapeutic Target? Hypertension, August 1, 2008; 52(2): 213 - 214. [Full Text] [PDF]