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Vasoconstrictor Factors in Hindlimb Vascular Responses to Stimulation of Adenosine A1 Receptors in the Nucleus of the Solitary Tract (NTS)
Author(s) -
McClure Joseph M,
Scislo Tadeusz J,
O’Leary Donal S
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a363-c
Subject(s) - vasopressin , vasoconstriction , endocrinology , medicine , vasodilation , stimulation , adenosine , chemistry
Our previous study showed that stimulation of NTS adenosine A1 receptors exerts variable, counteracting effects on the iliac vascular bed: activation of the adrenal medulla and β‐adrenergic vasodilation vs. vasoconstriction mediated by neural and unknown humoral factors (McClure et al. Am J Physiol Heart Circ Physiol 289, 2005). Stimulation of NTS A1 receptors increases sympathetic nerve activity releasing norepinephrine and may attenuate the baroreflex, thus increasing circulating vasopressin. Therefore we investigated the role of vasopressin and sympathetic nerves in NTS A1 receptor mediated iliac vasoconstriction. We compared the integral responses (∫Δ%) of mean arterial pressure (MAP) and iliac conductance (IVC) in 5 groups of chloralose/urethane anesthetized rats: intact (INT), following vasopressin V1 receptor blockade (VX), VX and lumbar sympathectomy (VX+LX), ganglionic blockade and adrenalectomy (GX+ADX) and combined GX+ADX+VX. In INT, typical variable responses were observed (MAP=93.0±90.9, IVC=−127.1±101.6). VX reversed the responses to depressor (−136.2±60.5) and vasodilatory ones (95.5±85.0). VX+LX accentuated the depressor (−279.9±50.2) and vasodilatory responses (426.9±110.4). GX+ADX accentuated the pressor (353.6±69.1) and vasoconstrictor (−624.9±103.3) responses. GX+ADX+VX abolished this accentuation (MAP=64.9±37.0, ICV‐200.8±35.6). We conclude that the release of vasopressin triggered by stimulation of NTS A1 receptors is a major vasoconstrictor factor opposing β‐adrenergic vasodilation in the iliac vasculature. Supported by NIH HL‐67814.