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Stimulation of adenosine A 1 receptors in the nucleus of the solitary tract (NTS) triggers the release of vasopressin into the circulation
Author(s) -
McClure Joseph M,
Rossi Noreen F,
Chen Haiping,
O'Leary Donal S,
Scislo Tadeusz J
Publication year - 2008
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.22.1_supplement.1171.12
Subject(s) - vasopressin , medicine , endocrinology , adenosine , vasopressin receptor , stimulation , agonist , receptor , chemistry , adenosine receptor , antagonist
Our previous study showed that stimulation of NTS A 1 adenosine receptors exerts 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 (Am J Physiol 289:H2536‐H2542, 2005). The follow up study identified vasopressin as a potential humoral factor involved: systemic blockade of V 1 vasopressin receptors abolished/reversed iliac vasoconstriction (FASEB 20: A363, 2006). Stimulation of NTS A 1 adenosine receptors attenuates the baroreflex (FASEB 21: A466, 2007), thus may increase circulating vasopressin. Therefore in the present study we compared circulating vasopressin levels before and after microinjections into the NTS of selective A 1 adenosine receptor agonist N 6 cyclopentyladenosine (CPA, 330 pmol/50nl) or vehicle (artificial cerebrospinal fluid, ACF, 50 nl), using the same experimental model as previously (chloralose/urethane anesthetized rats). CPA increased circulating vasopressin over 4‐fold (117.0±19.0 vs. 26.4±10.4 pg/ml, P=0.0006, n=8) whereas ACF did not increase vasopressin level significantly (50.9±11.3 vs. 25.0±7.2 pg/ml, P=0.083, n=5). We conclude that stimulation of NTS A 1 adenosine receptors increases circulating vasopressin probably via inhibition of NTS baroreflex mechanisms. NIH HL‐67814