title: Alpha-adrenergic and neuropeptide Y Y1 receptor control of collateral circuit conductance: influence of exercise training.
abstract: This study evaluated the role of alpha-adrenergic receptor- and neuropeptide Y (NPY) Y1 receptor-mediated vasoconstriction in the collateral circuit of the hind limb. Animals were evaluated either the same day (Acute) or 3 weeks following occlusion of the femoral artery; the 3-week animals were in turn limited to cage activity (Sed) or given daily exercise (Trained). Collateral-dependent blood flows (BFs) were measured during exercise with microspheres before and after alpha-receptor inhibition (phentolamine) and then NPY Y1 receptor inhibition (BIBP 3226) at the same running speed. Blood pressures (BPs) were measured above (caudal artery) and below (distal femoral artery) the collateral circuit. Arterial BPs were reduced by alpha-inhibition (50-60 mmHg) to approximately 75 mmHg, but not further by NPY Y1 receptor inhibition. Effective experimental sympatholysis was verified by 50-100% increases (P < 0.001) in conductance of active muscles not affected by femoral occlusion with receptor inhibition. In the absence of receptor inhibition, vascular conductance of the collateral circuit was minimal in the Acute group (0.13 +/- 0.02), increased over time in the Sed group (0.41 +/- 0.03; P < 0.001), and increased further in the Trained group (0.53 +/- 0.03; P < 0.02). Combined receptor inhibition increased collateral circuit conductances (P < 0.005), most in the Acute group (116 +/- 37%; P < 0.02), as compared to the Sed (41 +/- 6.6%; P < 0.001) and Trained (31 +/- 5.6%; P < 0.001) groups. Thus, while the sympathetic influence of the collateral circuit remained in the Sed and Trained animals, it became less influential with time post-occlusion. Collateral conductances were collectively greater (P < 0.01) in the Trained as compared to Sed group, irrespective of the presence or absence of receptor inhibition. Conductances of the active ischaemic calf muscle, with combined receptor inhibition, were suboptimal in the Acute group, but increased in Sed and Trained animals to exceptionally high values (e.g. red fibre section of the gastrocnemius: approximately 7 ml min(-1) (100 g)(-1) mmHg(-1)). Thus, occlusion of the femoral artery promulgated vascular adaptations, even in vessels that are not part of the collateral circuit. The presence of active sympathetic control of the collateral circuit, even with exercise training, raises the potential for reductions in collateral BF below that possible by the structure of the collateral circuit. However, even with release of this sympathetic vasoconstriction, conductance of the collateral circuit was significantly greater with exercise training, probably due to the network of structurally larger collateral vessels.
authors.affiliation: Department of Biomedical Sciences, E102 Vet. Medical Bldg, University of Missouri, Columbia, MO 65211, USA.
authors.forename: Jessica C
authors.initials: JC
authors.lastname: Taylor
authors.forename: H T
authors.initials: HT
authors.lastname: Yang
authors.forename: M Harold
authors.initials: MH
authors.lastname: Laughlin
authors.forename: Ronald L
authors.initials: RL
authors.lastname: Terjung
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001808:Blood Vessels / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D003097:Collateral Circulation / Q000187:drug effects / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006614:Hindlimb / Q000098:blood supply / Q000187:drug effects / Q000503:physiopathology; D007511:Ischemia / Q000503:physiopathology; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply / Q000187:drug effects; D010646:Phentolamine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D043562:Receptors, G-Protein-Coupled / Q000037:antagonists & inhibitors / Q000502:physiology*; D018013:Receptors, Neuropeptide / Q000037:antagonists & inhibitors / Q000502:physiology*; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; C092926:BIBP 3226; C066211:Npy1r protein, rat; D011942:Receptors, Adrenergic, alpha; D043562:Receptors, G-Protein-Coupled; D018013:Receptors, Neuropeptide; D014665:Vasodilator Agents; D010656:Phenylephrine; D001120:Arginine; D000109:Acetylcholine; D010646:Phentolamine