Gender-modulated endogenous baseline neuropeptide Y Y1-receptor activation in the hindlimb of Sprague-Dawley rats.

This study examined the effect of neuropeptide Y Y(1)-receptor blockade both alone, and in interaction with alpha(1)-adrenoceptor antagonism, on basal hindlimb vascular conductance in male and female Sprague-Dawley rats. Hindlimb vascular conductance was measured during infusion of BIBP3226 (Y(1)-receptor antagonist; 100 microg kg(-1)), prazosin (alpha(1)-receptor antagonist; 20 microg kg(-1)), and combined blockade. In males, vascular conductance increased 1.1 +/- 0.3 microl min(-1) mmHg(-1) above baseline with BIBP3226, and 2.4 +/- 0.4 microl min(-1) mmHg(-1) above baseline with prazosin (both P < 0.05). The increase in vascular conductance during combined blockade (5.1 +/- 0.7 microl 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 Y(1)-receptor blockade. However, alpha(1)-receptor blockade resulted in a 3.5 +/- 0.6 microl 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 Y(1)-receptor expression (P < 0.05; Western blot). It was concluded that, under baseline conditions, agonist and receptor-based mechanisms for Y(1)-receptor dependent control of vascular conductance in skeletal muscle was greater in male versus female rats.