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
vasculature.
","abstract_html":"<p>Previous studies from our laboratory showed that activation of NTS A<sub>1</sub> adenosine</p> <p>receptors yields variable hemodynamic responses with prevailing pressor and iliac</p> <p>vasoconstrictor responses. These responses are accompanied with differential</p> <p>activation of regional sympathetic activity (adrenal>>renal≥lumbar) and inhibition of</p> <p>baroreflex mechanisms at the level of the NTS. The variability of the hemodynamic</p> <p>responses was a result of simultaneous Β-adrenergic vasodilation counteracted with</p> <p>sympathetic and unknown humoral vasoconstriction. Among many potential</p> <p>vasoconstrictors vasopressin, angiotensin II and circulating norepinephrine were</p> <p>considered. Therefore, blood pressure and iliac vascular responses evoked by</p> <p>selective stimulation of NTS A<sub>1</sub> adenosine receptors (CPA 330 pmol/ 50 nl) in intact</p> <p>anesthetized (urethane/chloralose) Sprague Dawley rats were compared with the</p> <p>responses evoked following the blockade of each potential vasoconstrictor mechanism.</p> <p>I found that vasopressin is the major vasoconstrictor released into the circulation most</p> <p>likely as a result of A<sub>1</sub>-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</p> <p>confirmed that the levels of circulating vasopressin increased over 4-fold in response to</p> <p>stimulation of NTS A<sub>1</sub> adenosine receptors.</p> <p>Since NTS A<sub>1</sub> adenosine receptors contribute to the pressor component of the</p> <p>stress/hypothalamic defense (HDR) response it was interesting if these receptors</p> <p>contribute to the redistribution of blood from visceral (mesenteric and renal) to somatic</p> <p>(iliac) vascular beds, which is and integral part of HDR. Therefore, regional vascular</p> <p>effects of three major vasoactive factors triggered by stimulation of NTS A1 adenosine</p> <p>receptors (Β-adrenergic vasodilation opposed by sympathetic and vasopressinergic</p> <p>vasoconstriction) were compared; these vasoactive factors differentially affected the</p> <p>regional vascular beds. The Β-adrenergic vasodilation, which dominates in the initial</p> <p>phase of the response, was significantly greater in the iliac than the mesenteric and</p> <p>renal vasculatures. Significant sympathetic vasoconstriction was observed in the iliac</p> <p>but not in the mesenteric and renal vascular beds. In contrast, vasopressin exerted a</p> <p>marked, sustained vasoconstriction similar in all vascular beds. This pattern of regional</p> <p>vascular responses suggests that activation of A<sub>1</sub> adenosine receptors in the NTS has minor, if any, effect on the redistribution of blood from the visceral to the somatic</p> <p>vasculature.</p>","abstract_has_math":false,"creators":["Mcclure, Joseph Martin"],"institution":null,"degree_name":"Ph.D.","degree_level":"Open Access Dissertation","degree_discipline":"Physiology","degree_department":null,"school":null,"contributors":["Tadeusz J. Scislo"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2010,"date_issued":"2010-01-01T08:00:00Z","date_published":"2010-01-01T08:00:00Z","updated_at":"2026-07-24T05:58:42Z","subjects":["adrenalectomy","adrenergic receptors","iliac vascular conductance","NTS","purinergic receptors","V1 receptor blockade;","Physiology"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://digitalcommons.wayne.edu/oa_dissertations/145","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Tadeusz J. Scislo"]},{"key":"dc:creator","label":"Author","values":["Mcclure, Joseph Martin"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2010-11-08T08:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Physiology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Open Access Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["adrenalectomy","adrenergic receptors","iliac vascular conductance","NTS","purinergic receptors","V1 receptor blockade;","Physiology"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://digitalcommons.wayne.edu/oa_dissertations/145"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["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
vasculature.
"]},{"key":"dc:title","label":"Title","values":["Neural And Humoral Control Of Regional Vascular Beds Via A1 Adenosine Receptors Located In The Nucleus Of The Solitary Tract"]}]}],"canonical_facts":{"dc:contributor":["Tadeusz J. Scislo"],"dc:creator":["Mcclure, Joseph Martin"],"dc:date.available":["2010-11-08T08:00:00Z"],"dc:description.abstract":["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
vasculature.
"],"dc:identifier":["https://digitalcommons.wayne.edu/oa_dissertations/145"],"dc:subject":["adrenalectomy","adrenergic receptors","iliac vascular conductance","NTS","purinergic receptors","V1 receptor blockade;","Physiology"],"dc:title":["Neural And Humoral Control Of Regional Vascular Beds Via A1 Adenosine Receptors Located In The Nucleus Of The Solitary Tract"],"thesis:degree_discipline":["Physiology"],"thesis:degree_level":["Open Access Dissertation"],"thesis:degree_name":["Ph.D."]},"updated_at":"2026-07-24T05:58:42Z"}