title: Neural and humoral control of regional vascular beds via A1 adenosine receptors located in the nucleus tractus solitarii.
abstract: Our previous studies showed that stimulation of adenosine A(1) receptors located in the nucleus of the solitary tract (NTS) exerts counteracting effects on the iliac vascular bed: activation of the adrenal medulla and β-adrenergic vasodilation vs. sympathetic and vasopressinergic vasoconstriction. Because NTS A(1) adenosine receptors inhibit baroreflex transmission in the NTS and contribute to the pressor component of the HDR, we hypothesized that these receptors also contribute to the redistribution of blood from the visceral to the muscle vasculature via prevailing sympathetic and vasopressinergic vasoconstriction in the visceral (renal and mesenteric) vascular beds and prevailing β-adrenergic vasodilation in the somatic (iliac) vasculature. To test this hypothesis, we compared the A(1) adenosine-receptor-mediated effects of each vasoactive factor triggered by NTS A(1) adenosine receptor stimulation [N(6)-cyclopentyladenosine (CPA), 330 pmol in 50 nl] on the regional vascular responses in urethane/chloralose-anesthetized rats. The single-factor effects were separated using adrenalectomy, β-adrenergic blockade, V(1) vasopressin receptor blockade, and sinoaortic denervation. In intact animals, initial vasodilation was followed by large, sustained vasoconstriction with smaller responses observed in renal vs. mesenteric and iliac vascular beds. The initial β-adrenergic vasodilation prevailed in the iliac vs. mesenteric and renal vasculature. The large and sustained vasopressinergic vasoconstriction was similar in all vascular beds. Small sympathetic vasoconstriction was observed only in the iliac vasculature in this setting. We conclude that, although A(1) adenosine-receptor-mediated β-adrenergic vasodilation may contribute to the redistribution of blood from the visceral to the muscle vasculature, this effect is overridden by sympathetic and vasopressinergic vasoconstriction.
authors.affiliation: Dept. of Physiology, Wayne State Univ. School of Medicine, Detroit, MI 48201, USA.
authors.forename: Joseph M
authors.initials: JM
authors.lastname: McClure
authors.forename: Donal S
authors.initials: DS
authors.lastname: O'Leary
authors.forename: Tadeusz J
authors.initials: TJ
authors.lastname: Scislo
mesh_terms: D058907:Adenosine A1 Receptor Agonists / Q000494:pharmacology; D000313:Adrenal Medulla / Q000294:innervation / Q000378:metabolism / Q000601:surgery; D000315:Adrenalectomy; D000320:Adrenergic Fibers / Q000187:drug effects / Q000378:metabolism*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D065092:Antidiuretic Hormone Receptor Antagonists; D017763:Autonomic Denervation; D006439:Hemodynamics / Q000187:drug effects; D006727:Hormone Antagonists / Q000494:pharmacology; D007083:Iliac Artery / Q000187:drug effects / Q000294:innervation* / Q000378:metabolism; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000294:innervation* / Q000378:metabolism; D018482:Muscle, Skeletal / Q000098:blood supply*; D051381:Rats; D017207:Rats, Sprague-Dawley; D043682:Receptor, Adenosine A1 / Q000187:drug effects / Q000378:metabolism*; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000378:metabolism*; D017483:Receptors, Vasopressin / Q000378:metabolism; D012039:Regional Blood Flow; D012077:Renal Artery / Q000187:drug effects / Q000294:innervation* / Q000378:metabolism; D012079:Renal Circulation; D017552:Solitary Nucleus / Q000187:drug effects / Q000378:metabolism*; D013152:Splanchnic Circulation; D013997:Time Factors; D014661:Vasoconstriction; D014664:Vasodilation; D014667:Vasopressins / Q000378:metabolism
chemical_list: D058907:Adenosine A1 Receptor Agonists; D000319:Adrenergic beta-Antagonists; D065092:Antidiuretic Hormone Receptor Antagonists; D006727:Hormone Antagonists; D043682:Receptor, Adenosine A1; D011943:Receptors, Adrenergic, beta; D017483:Receptors, Vasopressin; D014667:Vasopressins