Neural And Humoral Control Of Regional Vascular Beds Via A1 Adenosine Receptors Located In The Nucleus Of The Solitary Tract

Publication Year:
2010
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Repository URL:
https://digitalcommons.wayne.edu/oa_dissertations/145
Author(s):
Mcclure, Joseph Martin
Tags:
adrenalectomy; adrenergic receptors; iliac vascular conductance; NTS; purinergic receptors; V1 receptor blockade;; Physiology
thesis / dissertation description
Previous studies from our laboratory showed that activation of NTS A1 adenosinereceptors yields variable hemodynamic responses with prevailing pressor and iliacvasoconstrictor responses. These responses are accompanied with differentialactivation of regional sympathetic activity (adrenal>>renal≥lumbar) and inhibition ofbaroreflex mechanisms at the level of the NTS. The variability of the hemodynamicresponses was a result of simultaneous Β-adrenergic vasodilation counteracted withsympathetic and unknown humoral vasoconstriction. Among many potentialvasoconstrictors vasopressin, angiotensin II and circulating norepinephrine wereconsidered. Therefore, blood pressure and iliac vascular responses evoked byselective stimulation of NTS A1 adenosine receptors (CPA 330 pmol/ 50 nl) in intactanesthetized (urethane/chloralose) Sprague Dawley rats were compared with theresponses evoked following the blockade of each potential vasoconstrictor mechanism.I found that vasopressin is the major vasoconstrictor released into the circulation mostlikely 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 evaluationconfirmed that the levels of circulating vasopressin increased over 4-fold in response tostimulation of NTS A1 adenosine receptors.Since NTS A1 adenosine receptors contribute to the pressor component of thestress/hypothalamic defense (HDR) response it was interesting if these receptorscontribute to the redistribution of blood from visceral (mesenteric and renal) to somatic(iliac) vascular beds, which is and integral part of HDR. Therefore, regional vasculareffects of three major vasoactive factors triggered by stimulation of NTS A1 adenosinereceptors (Β-adrenergic vasodilation opposed by sympathetic and vasopressinergicvasoconstriction) were compared; these vasoactive factors differentially affected theregional vascular beds. The Β-adrenergic vasodilation, which dominates in the initialphase of the response, was significantly greater in the iliac than the mesenteric andrenal vasculatures. Significant sympathetic vasoconstriction was observed in the iliacbut not in the mesenteric and renal vascular beds. In contrast, vasopressin exerted amarked, sustained vasoconstriction similar in all vascular beds. This pattern of regionalvascular 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 somaticvasculature.