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¹ Neurovascular Research Laboratory, Faculty of Health Science, School of Kinesiology, the University of Western Ontario, London, Ontario, Canada, N6A 3K7

This study examined the effect of neuropeptide Y Y₁-receptor blockade both alone, and in interaction with ₁-adrenoceptor antagonism, on basal hindlimb vascular conductance in male and female Sprague-Dawley rats. Hindlimb vascular conductance was measured during infusion of BIBP3226 (Y₁-receptor antagonist; 100 µg kg^–1), prazosin (₁-receptor antagonist; 20 µg kg^–1), and combined blockade. In males, vascular conductance increased 1.1 ± 0.3 µl min^–1 mmHg^–1 above baseline with BIBP3226, and 2.4 ± 0.4 µl min^–1 mmHg^–1 above baseline with prazosin (both P < 0.05). The increase in vascular conductance during combined blockade (5.1 ± 0.7 µl min^–1 mmHg^–1) was greater than the sum of the independent BIBP3226 and prazosin responses (P < 0.05). In females, basal hindlimb vascular conductance was unaffected by Y₁-receptor blockade. However, ₁-receptor blockade resulted in a 3.5 ± 0.6 µl min^–1 mmHg^–1 increase in vascular conductance above baseline, which was not different than the combined blockade condition. Males had greater skeletal muscle neuropeptide Y concentration (P < 0.05; ELISA) than females. Furthermore, compared with females, male skeletal muscle contained greater Y₁-receptor expression (P < 0.05; Western blot). It was concluded that, under baseline conditions, agonist and receptor-based mechanisms for Y₁-receptor dependent control of vascular conductance in skeletal muscle was greater in male versus female rats.

(Received 27 September 2004; accepted after revision 21 October 2004; first published online 28 October 2004)
Corresponding author J.K. Shoemaker: Neurovascular Research Laboratory, School of Kinesiology, Room 3110, Thames Hall, University of Western Ontario, London, Ontario, Canada, N6A 3K7. E-mail: kshoemak{at}uwo.ca

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