title: Gender-modulated endogenous baseline neuropeptide Y Y1-receptor activation in the hindlimb of Sprague-Dawley rats.
abstract: 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.
authors.affiliation: Neurovascular Research Laboratory, School of Kinesiology, University of Western Ontario, London, Ontario, Canada N6A 3K7.
authors.forename: Dwayne N
authors.initials: DN
authors.lastname: Jackson
authors.forename: Kevin J
authors.initials: KJ
authors.lastname: Milne
authors.forename: Earl G
authors.initials: EG
authors.lastname: Noble
authors.forename: J Kevin
authors.initials: JK
authors.lastname: Shoemaker
mesh_terms: D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D015153:Blotting, Western; D005260:Female; D005263:Femoral Artery / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects; D006614:Hindlimb / Q000098:blood supply / Q000502:physiology*; D007118:Immunoassay; D008297:Male; D009478:Neuropeptide Y / Q000378:metabolism; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017476:Receptors, Neuropeptide Y / Q000037:antagonists & inhibitors / Q000502:physiology*; D012039:Regional Blood Flow / Q000502:physiology; D012727:Sex Characteristics
chemical_list: D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists; C092926:BIBP 3226; D009478:Neuropeptide Y; D017476:Receptors, Neuropeptide Y; C097212:neuropeptide Y-Y1 receptor; D001120:Arginine; D011224:Prazosin