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 ␤-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 ␤-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, ␤-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 ␤-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 ␤-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. purinergic receptors; V 1 receptor blockade; ␤-adrenergic blockade; adrenalectomy; sinoaortic denervation; iliac vascular conductance; mesenteric vascular conductance; renal vascular conductance RECENT STUDIES HAVE FIRMLY established that adenosine operating as a neuromodulator in the nucleus of the solitary tract (NTS) modifies cardiovascular control (14, 20, 24, 25, 34, 40 -44). The NTS is a major integrative center for visceral and autonomic reflexes and contains the greatest density of adenosine uptake sites within the central nervous system (4). Adenosine operates in the NTS in both physiological and pathological situations. Under normal, physiological conditions, a natural source of adenosine is ATP released from neurons and glial cells (6). This occurs, for example, during the stress or hypothalamic defense response (HDR) (42-44). Extracellular ATP is catabolized via ectonucleotidases to adeno-

How does adenosine control neuronal dysfunction and neurodegeneration?

“…; McClure et al . ), contributing to the fine‐tuning of neurovascular coupling that critically impacts on the sustainability of function of neuronal networks (Chen et al . ; Kimbrough et al .…”

“…; McClure et al . ), it is possible that the A 2A R‐mediated vascular control might also contribute to neuroprotection.…”

Angiotensin II control of regional haemodynamics in rats with aortocaval fistula

“…After a recovery period (5-7 weeks), experiments were conducted with surgical preparation similar to other studies (McClure et al 2011). Rats (sham group, 485 ± 5 g, n = 38; fistula group, 475 ± 5 g, n = 32) were anaesthetized with isoflurane (induction, 5% in 100% oxygen; maintenance, 1.5% in 100% oxygen with adjustments to maintain surgical anaesthesia).…”

Activation of NTS A1adenosine receptors inhibits regional sympathetic responses evoked by activation of cardiopulmonary chemoreflex

“…However, when adenosine is released into the NTS (i.e., during stress or severe hypotension/ischemia), it may serve as negative feedback regulator for depressor and sympathoinhibitory reflexes integrated in the NTS. nucleus of the solitary tract; purinergic receptors; renal nerve; adrenal nerve; lumbar nerve NUMEROUS STUDIES have shown that adenosine operates as a central neuromodulator of cardiovascular control at the level of the nucleus tractus solitarii (NTS) (1,4,30,33,39,41,56,58,59,61,64). In the central nervous system adenosine serves as an inhibiting or stimulating neuromodulator operating via A 1 and A 2a receptors, respectively (46).…”