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Open Access Dissertation

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First Advisor

Tadeusz J. Scislo


Previous studies from our laboratory showed that activation of NTS A1 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 Β-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 A1-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 (Β-adrenergic vasodilation opposed by sympathetic and vasopressinergic

vasoconstriction) were compared; these vasoactive factors differentially affected the

regional vascular beds. The Β-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


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