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This Article Full Text Full Text (PDF) All Versions of this Article: 297/5/H1661    most recent 00432.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by McClure, J. M. Articles by Scislo, T. J. PubMed PubMed Citation Articles by McClure, J. M. Articles by Scislo, T. J.

Vasopressin is a major vasoconstrictor involved in hindlimb vascular responses to stimulation of adenosine A₁ receptors in the nucleus of the solitary tract

Departments of ¹Physiology and ²Internal Medicine, Wayne State University School of Medicine; and ³John D. Dingell Veterans Affairs Medical Center, Detroit, Michigan

Submitted May 8, 2009 ; accepted in final form September 8, 2009

Our previous study showed that stimulation of adenosine A₁ 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 versus vasoconstriction mediated by neural and unknown humoral factors. In the present study we investigated the relative contribution of three major potential humoral vasoconstrictors: vasopressin, angiotensin II, and norepinephrine in this response. In urethane-chloralose anesthetized rats we compared the integral changes in iliac vascular conductance evoked by microinjections into the NTS of the selective A₁ receptor agonist N⁶-cyclopentyladenosine (CPA; 330 pmol in 50 nl) in intact (Int) animals and following: V₁ vasopressin receptor blockade (VX), angiotensin II AT₁ receptor blockade (ATX), bilateral adrenalectomy + ganglionic blockade (ADX + GX; which eliminated the potential increases in circulating norepinephrine and epinephrine), ADX + GX + VX and ADX + GX + VX + ATX. In Int animals, stimulation of NTS A₁ adenosine receptors evoked typical variable responses with prevailing pressor and vasoconstrictor effects. VX reversed the responses to depressor ones. ATX did not significantly alter the responses. ADX + GX accentuated pressor and vasoconstrictor responses, whereas ADX + GX + VX and ADX + GX + VX + ATX virtually abolished the responses. Stimulation of NTS A₁ adenosine receptors increased circulating vasopressin over fourfold (26.4 ± 10.4 vs. 117.0 ± 19 pg/ml). These data strongly suggest that vasopressin is a major vasoconstrictor factor opposing β-adrenergic vasodilation in iliac vascular responses triggered by stimulation of NTS A₁ adenosine receptors, whereas angiotensin II and norepinephrine do not contribute significantly to the vasoconstrictor responses.

purinergic receptors; V₁ receptor blockade; angiotensin II type 1 receptor blockade; ganglionic blockade; adrenalectomy; lumbar sympathectomy; iliac vascular conductance