| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Laboratory of Physiology, University of Angers, France
A transient increase in skin blood flow in response to an innocuous local pressure application, defined as pressure-induced vasodilatation (PIV), delays the occurrence of ischaemia, suggesting a protective feature against applied pressure. The PIV response depends on capsaicin-sensitive nerve fibres and calcitonin gene-related peptide (CGRP) has been shown to be involved. In these fibres, CGRP coexists with pituitary adenylate cyclase-activating polypeptide (PACAP). Three distinct receptors mediate the biological effects of PACAP: VPAC1 and VPAC2 receptors binding with the same affinity for PACAP and vasoactive intestinal peptide and PAC1 receptors showing high selectivity for PACAP. Because the receptors are widely expressed in the nervous system and in the skin, we hypothesized that at least one of them is involved in PIV development. To verify this hypothesis, we used [D-p-Cl-Phe6,Leu17]-VIP (nonspecific antagonist of VPAC1/VPAC2 receptors), PG 97-269 (antagonist of VPAC1 receptors), PACAP(6–38) (antagonist of VPAC2/PAC1 receptors) and Max.d.4 (antagonist of PAC1 receptors) in anaesthetized rodents. The blockade of VPAC1/VPAC2, VPAC1 or VPAC2/PAC1 receptors eliminated the PIV response, whereas PAC1 blockade had no effect, demonstrating an involvement of VPAC1/VPAC2 receptors in PIV development. Moreover, endothelium-independent and -dependent vasodilator responses were unchanged by the VPAC1/VPAC2 antagonist. Thus, the absence of a PIV response following VPAC1/VPAC2 blockade cannot be explained by any dysfunction of the vascular smooth muscle or endothelial vasodilator capacity. The involvement of VPAC1/VPAC2 receptors in the development of PIV seems to imply a series relationship in which each receptor type (CGRP, VPAC1, VPAC2) is necessary for the full transmission of the response.
(Received 15 September 2003;
accepted after revision 22 October 2003;
first published online 24 October 2003)
Corresponding author J. L. Saumet: Laboratory of Physiology, UPRES EA 2170, Medicine Department, University of Angers, F-49045 Angers cedex, France. Email: jeanlouis.saumet{at}univ-angers.fr
This article has been cited by other articles:
|
|
 |
|
  Y. Xie, D. W. Wolff, M.-F. Lin, and Y. Tu Vasoactive Intestinal Peptide Transactivates the Androgen Receptor through a Protein Kinase A-Dependent Extracellular Signal-Regulated Kinase Pathway in Prostate Cancer LNCaP Cells Mol. Pharmacol., July 1, 2007; 72(1): 73 - 85. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Fromy, D. Sigaudo-Roussel, C. Baron, Y. Roquelaure, G. Leftheriotis, and J. L. Saumet Neuroendocrine pathway involvement in the loss of the cutaneous pressure-induced vasodilatation during acute pain in rats J. Physiol., February 15, 2007; 579(1): 247 - 254. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Roosterman, T. Goerge, S. W. Schneider, N. W. Bunnett, and M. Steinhoff Neuronal control of skin function: the skin as a neuroimmunoendocrine organ. Physiol Rev, October 1, 2006; 86(4): 1309 - 1379. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. M. Braas, V. May, P. Zvara, B. Nausch, J. Kliment, J. D. Dunleavy, M. T. Nelson, and M. A. Vizzard Role for pituitary adenylate cyclase activating polypeptide in cystitis-induced plasticity of micturition reflexes Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2006; 290(4): R951 - R962. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Garry, D. Sigaudo-Roussel, S. Merzeau, O. Dumont, J. L. Saumet, and B. Fromy Cellular mechanisms underlying cutaneous pressure-induced vasodilation: in vivo involvement of potassium channels Am J Physiol Heart Circ Physiol, July 1, 2005; 289(1): H174 - H180. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
