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The vanilloid receptor and hypertension.
Acta Pharmacol Sin. 2005 Mar; 26(3):286-94.AP

Abstract

Mammalian transient receptor potential (TRP) channels consist of six related protein sub-families that are involved in a variety of pathophysiological function, and disease development. The TRPV1 channel, a member of the TRPV sub-family, is identified by expression cloning using the "hot" pepper-derived vanilloid compound capsaicin as a ligand. Therefore, TRPV1 is also referred as the vanilloid receptor (VR1) or the capsaicin receptor. VR1 is mainly expressed in a subpopulation of primary afferent neurons that project to cardiovascular and renal tissues. These capsaicin-sensitive primary afferent neurons are not only involved in the perception of somatic and visceral pain, but also have a "sensory-effector" function. Regarding the latter, these neurons release stored neuropeptides through a calcium-dependent mechanism via the binding of capsaicin to VR1. The most studied sensory neuropeptides are calcitonin gene-related peptide (CGRP) and substance P (SP), which are potent vasodilators and natriuretic/diuretic factors. Recent evidence using the model of neonatal degeneration of capsaicin-sensitive sensory nerves revealed novel mechanisms that underlie increased salt sensitivity and several experimental models of hypertension. These mechanisms include insufficient suppression of plasma renin activity and plasma aldosterone levels subsequent to salt loading, enhancement of sympathoexcitatory response in the face of a salt challenge, activation of the endothelin-1 receptor, and impaired natriuretic response to salt loading in capsaicin-pretreated rats. These data indicate that sensory nerves counterbalance the prohypertensive effects of several neurohormonal systems to maintain normal blood pressure when challenged with salt loading. The therapeutic utilities of vanilloid compounds, endogenous agonists, and sensory neuropeptides are also discussed.

Authors+Show Affiliations

Department of Medicine, College of Human Medicine, Michigan State University, East Lansing, MI 48825, USA. donna.wang@ht.msu.edu

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

Language

eng

PubMed ID

15715923

Citation

Wang, Donna H.. "The Vanilloid Receptor and Hypertension." Acta Pharmacologica Sinica, vol. 26, no. 3, 2005, pp. 286-94.
Wang DH. The vanilloid receptor and hypertension. Acta Pharmacol Sin. 2005;26(3):286-94.
Wang, D. H. (2005). The vanilloid receptor and hypertension. Acta Pharmacologica Sinica, 26(3), 286-94.
Wang DH. The Vanilloid Receptor and Hypertension. Acta Pharmacol Sin. 2005;26(3):286-94. PubMed PMID: 15715923.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The vanilloid receptor and hypertension. A1 - Wang,Donna H, PY - 2005/2/18/pubmed PY - 2005/10/26/medline PY - 2005/2/18/entrez SP - 286 EP - 94 JF - Acta pharmacologica Sinica JO - Acta Pharmacol. Sin. VL - 26 IS - 3 N2 - Mammalian transient receptor potential (TRP) channels consist of six related protein sub-families that are involved in a variety of pathophysiological function, and disease development. The TRPV1 channel, a member of the TRPV sub-family, is identified by expression cloning using the "hot" pepper-derived vanilloid compound capsaicin as a ligand. Therefore, TRPV1 is also referred as the vanilloid receptor (VR1) or the capsaicin receptor. VR1 is mainly expressed in a subpopulation of primary afferent neurons that project to cardiovascular and renal tissues. These capsaicin-sensitive primary afferent neurons are not only involved in the perception of somatic and visceral pain, but also have a "sensory-effector" function. Regarding the latter, these neurons release stored neuropeptides through a calcium-dependent mechanism via the binding of capsaicin to VR1. The most studied sensory neuropeptides are calcitonin gene-related peptide (CGRP) and substance P (SP), which are potent vasodilators and natriuretic/diuretic factors. Recent evidence using the model of neonatal degeneration of capsaicin-sensitive sensory nerves revealed novel mechanisms that underlie increased salt sensitivity and several experimental models of hypertension. These mechanisms include insufficient suppression of plasma renin activity and plasma aldosterone levels subsequent to salt loading, enhancement of sympathoexcitatory response in the face of a salt challenge, activation of the endothelin-1 receptor, and impaired natriuretic response to salt loading in capsaicin-pretreated rats. These data indicate that sensory nerves counterbalance the prohypertensive effects of several neurohormonal systems to maintain normal blood pressure when challenged with salt loading. The therapeutic utilities of vanilloid compounds, endogenous agonists, and sensory neuropeptides are also discussed. SN - 1671-4083 UR - https://www.unboundmedicine.com/medline/citation/15715923/The_vanilloid_receptor_and_hypertension_ L2 - http://dx.doi.org/10.1111/j.1745-7254.2005.00057.x DB - PRIME DP - Unbound Medicine ER -