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(Hypertension. 2008;52:264.)
© 2008 American Heart Association, Inc.

Original Articles

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; 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.

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 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]

This article has been cited by other articles:

				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]

				C. Xie and D. H. Wang Ablation of Transient Receptor Potential Vanilloid 1 Abolishes Endothelin-Induced Increases in Afferent Renal Nerve Activity: Mechanisms and Functional Significance Hypertension, December 1, 2009; 54(6): 1298 - 1305. [Abstract] [Full Text] [PDF]

				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]