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

<p>Previous studies from our laboratory showed that activation of NTS A₁ 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 A₁ 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 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</p> <p>confirmed that the levels of circulating vasopressin increased over 4-fold in response to</p> <p>stimulation of NTS A₁ adenosine receptors.</p> <p>Since NTS A₁ 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 A₁ 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>

Name thesis:degree_name

Ph.D.

Level thesis:degree_level

Open Access Dissertation

Discipline thesis:degree_discipline

Physiology

Year dc:date.available

2010

Author dc:creator

• Mcclure, Joseph Martin

Contributors dc:contributor

• Tadeusz J. Scislo

• adrenalectomy
• adrenergic receptors
• iliac vascular conductance
• NTS
• purinergic receptors
• V1 receptor blockade;
• Physiology

Repository record dc:identifier

https://digitalcommons.wayne.edu/oa_dissertations/145

OAI identifier oai:identifier

oai:digitalcommons.wayne.edu:oa_dissertations-1144