Previous studies from our laboratory showed that activation of NTS A 1 adenosine receptors yields variable hemodynamic responses with prevailing pressor and iliac vasoconstrictor responses. These responses are accompanied with differential activation of regional sympathetic activity (adrenal>>renal≥lumbar) and inhibition of baroreflex mechanisms at the level of the NTS. The variability of the hemodynamic responses was a result of simultaneous β2-adrenergic vasodilation counteracted with sympathetic and unknown humoral vasoconstriction. Among many potential vasoconstrictors vasopressin, angiotensin II and circulating norepinephrine were considered. Therefore, blood pressure and iliac vascular responses evoked by selective stimulation of NTS A1 adenosine receptors (CPA 330 pmol/50 nl) in intact anesthetized (urethane/chloralose) Sprague Dawley rats were compared with the responses evoked following the blockade of each potential vasoconstrictor mechanism. I found that vasopressin is the major vasoconstrictor released into the circulation most likely as a result of A11-adenosine-receptor-mediated inhibition of baroreflex mechanism and disinhibition of tonic restraint of vasopressin release. Angiotensin II and circulating norepinephrine had virtually no contribution to the responses. The direct evaluation confirmed that the levels of circulating vasopressin increased over 4-fold in response to stimulation of NTS A1 adenosine receptors.
Since NTS A1 adenosine receptors contribute to the pressor component of the stress/hypothalamic defense (HDR) response it was interesting if these receptors contribute to the redistribution of blood from visceral (mesenteric and renal) to somatic (iliac) vascular beds, which is and integral part of HDR. Therefore, regional vascular effects of three major vasoactive factors triggered by stimulation of NTS A1 adenosine receptors (β2-adrenergic vasodilation opposed by sympathetic and vasopressinergic vasoconstriction) were compared; these vasoactive factors differentially affected the regional vascular beds. The β2-adrenergic vasodilation, which dominates in the initial phase of the response, was significantly greater in the iliac than the mesenteric and renal vasculatures. Significant sympathetic vasoconstriction was observed in the iliac but not in the mesenteric and renal vascular beds. In contrast, vasopressin exerted a marked, sustained vasoconstriction similar in all vascular beds. This pattern of regional vascular responses suggests that activation of A1 adenosine receptors in the NTS has minor, if any, effect on the redistribution of blood from the visceral to the somatic vasculature.
|Advisor:||Scislo, Tadeusz J.|
|Commitee:||Goshgarian, Harry, O'Leary, Donal S., Rossi, Noreen F.|
|School:||Wayne State University|
|School Location:||United States -- Michigan|
|Source:||DAI-B 71/12, Dissertation Abstracts International|
|Keywords:||Adrenalectomy, Adrenergic receptors, Iliac vascular conductance, Nts, Purinergic receptors, Solitary tract, V1 receptor blockade|
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