Vasopressin is a major vasoconstrictor involved in hindlimb vascular responses to stimulation of adenosine A(1) receptors in the nucleus of the solitary tract.
Our previous study 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 beta-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 A(1) receptor agonist N(6)-cyclopentyladenosine (CPA; 330 pmol in 50 nl) in intact (Int) animals and following: V(1) vasopressin receptor blockade (VX), angiotensin II AT(1) 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 A(1) 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 A(1) adenosine receptors increased circulating vasopressin over fourfold (26.4 + or - 10.4 vs. 117.0 + or - 19 pg/ml). These data strongly suggest that vasopressin is a major vasoconstrictor factor opposing beta-adrenergic vasodilation in iliac vascular responses triggered by stimulation of NTS A(1) adenosine receptors, whereas angiotensin II and norepinephrine do not contribute significantly to the vasoconstrictor responses.
McClure
Joseph M
JM
Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan, USA.
Rossi
Noreen F
NF
Chen
Haiping
H
O'Leary
Donal S
DS
Scislo
Tadeusz J
TJ
D000241:Adenosine / Q000008:administration & dosage / Q000031:analogs & derivatives; D058907:Adenosine A1 Receptor Agonists; D000315:Adrenalectomy; D000804:Angiotensin II / Q000378:metabolism*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000008:administration & dosage; D000818:Animals; D065092:Antidiuretic Hormone Receptor Antagonists; D001127:Arginine Vasopressin / Q000008:administration & dosage / Q000031:analogs & derivatives; D017704:Baroreflex / Q000187:drug effects; D001794:Blood Pressure; D006339:Heart Rate; D006614:Hindlimb; D007083:Iliac Artery / Q000294:innervation*; D019808:Losartan / Q000008:administration & dosage; D008297:Male; D008845:Microinjections; D018482:Muscle, Skeletal / Q000098:blood supply*; D009638:Norepinephrine / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D043682:Receptor, Adenosine A1 / Q000378:metabolism*; D044140:Receptor, Angiotensin, Type 1 / Q000187:drug effects / Q000378:metabolism; D017483:Receptors, Vasopressin / Q000378:metabolism; D012039:Regional Blood Flow; D017552:Solitary Nucleus / Q000187:drug effects / Q000378:metabolism*; D013562:Sympathectomy; D013997:Time Factors; D014661:Vasoconstriction / Q000187:drug effects; D014667:Vasopressins / Q000097:blood / Q000378:metabolism*
D058907:Adenosine A1 Receptor Agonists; D047228:Angiotensin II Type 1 Receptor Blockers; D065092:Antidiuretic Hormone Receptor Antagonists; D043682:Receptor, Adenosine A1; D044140:Receptor, Angiotensin, Type 1; D017483:Receptors, Vasopressin; D014667:Vasopressins; D000804:Angiotensin II; D001127:Arginine Vasopressin; C048599:N(6)-cyclopentyladenosine; C025043:vasopressin, 1-(1-mercaptocyclohexaneacetic acid)-2-(O- methyl-L-tyrosine)-8-L-arginine-; D019808:Losartan; D000241:Adenosine; D009638:Norepinephrine