HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 568/2/573    most recent jphysiol.2005.092700v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jackson, D. N Articles by Shoemaker, J. K. Search for Related Content PubMed PubMed Citation Articles by Jackson, D. N Articles by Shoemaker, J. K.

¹ Neurovascular Research Laboratory, School of Kinesiology
² Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada, N6A 3K7

We recently reported that male, but not female, rats exhibit basal endogenous neuropeptide Y Y₁-receptor modulation of hindlimb vasculature. The lack of baseline endo-genous Y₁-receptor control in females was evident despite the expression of Y₁-receptors and neuropeptide Y in hindlimb skeletal muscle tissue. The following study addressed the hypothesis that neuropeptide Y bioavailability is blunted in female rats under baseline conditions. It was further hypothesized that enhanced prejunctional autoinhibitory neuropeptide Y Y₂-receptor expression and/or proteolytic processing of released neuropeptide Y may persist in female rats. Using western blot analysis, it was observed that females had greater overall neuropeptide Y Y₂-receptor expression in skeletal muscle compared to males (P < 0.05). To address the prevalence/impact of baseline endogenous Y₂-receptor activation on neuropeptide Y release in hindlimb vasculature, an arterial infusion of BIIE0246 (specific non-peptide Y₂-receptor antagonist; 170 µg kg^–1) was carried out on female and male rats. Y₂-receptor blockade resulted in a decrease in hindlimb vascular conductance in females and males (P < 0.05). However, the BIIE0246-induced decrease in vascular conductance was Y₁-receptor dependent in females, but not males (P < 0.05). In addition, compared to baseline, BIIE0246 infusion resulted in increased plasma neuropeptide Y concentration in females (P < 0.05), while there was no observable change in males. In a final experiment, systemic inhibition of proteolytic enzymes dipeptidylpeptidase IV (via 500 nM diprotin A) and aminopeptidase P (via 180 nM 2-mercaptoethanol) elicited a Y₁-receptor-dependent decrease in hindlimb vascular conductance in females (P < 0.05). It was concluded that our previously reported lack of basal endogenous Y₁-receptor activation in female hindlimb vasculature was (at least partially) due to prejunctional Y₂-receptor autoinhibition and proteolytic processing of neuropeptide Y.

(Received 15 June 2005; accepted after revision 2 August 2005; first published online 4 August 2005)
Corresponding author J.K. Shoemaker, Ph.D. Neurovascular Research Laboratory, School of Kinesiology, Rm 3110, Thames Hall, University of Western Ontario London, Ontario, Canada, N6A 3K7. Email: kshoemak{at}uwo.ca

This article has been cited by other articles:

				M. J. S. Chee, K. Morl, D. Lindner, N. Merten, G. W. Zamponi, P. E. Light, A. G. Beck-Sickinger, and W. F. Colmers The Third Intracellular Loop Stabilizes the Inactive State of the Neuropeptide Y1 Receptor J. Biol. Chem., November 28, 2008; 283(48): 33337 - 33346. [Abstract] [Full Text] [PDF]