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Histamine receptors and substance P ...
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Wong, Brett James.
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Histamine receptors and substance P in cutaneous active vasodilation and thermal hyperemia in humans.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Histamine receptors and substance P in cutaneous active vasodilation and thermal hyperemia in humans./
作者:
Wong, Brett James.
面頁冊數:
207 p.
附註:
Source: Dissertation Abstracts International, Volume: 66-09, Section: B, page: 4571.
Contained By:
Dissertation Abstracts International66-09B.
標題:
Biology, Animal Physiology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3190556
ISBN:
9780542334825
Histamine receptors and substance P in cutaneous active vasodilation and thermal hyperemia in humans.
Wong, Brett James.
Histamine receptors and substance P in cutaneous active vasodilation and thermal hyperemia in humans.
- 207 p.
Source: Dissertation Abstracts International, Volume: 66-09, Section: B, page: 4571.
Thesis (Ph.D.)--University of Oregon, 2005.
The ability to increase skin blood flow in response to an increase in core temperature or local skin temperature represents important thermoregulatory and protective functions of the cutaneous vasculature in humans. However, the mechanism(s) underlying these changes in skin blood flow are unclear. The purpose of this dissertation was to investigate the role of histamine receptors and substance P in cutaneous active vasodilation and thermal hyperemia. In Chapter IV, the contribution of histamine receptors to active vasodilation was investigated. The results demonstrate the H 1, but not H2, isoform of the histamine receptor contributes to active vasodilation. In Chapter V, we investigated the contribution of histamine receptors to thermal hyperemia. These results suggest a minimal role for H1 receptors and no role for H2 receptors in thermal hyperemia. In Chapter VI, studies were carried out to investigate mechanisms of substance P-induced vasodilation. The results demonstrated a nitric oxide (NO) component to substance P-induced vasodilation but no histamine receptor component. Importantly, the results from this study provide evidence the neurokinin-1 (NK1) receptors, to which substance P binds to with high affinity, become desensitized to two consecutive microdialysis infusions of substance P. These results provided the experimental model for the studies described in Chapters VII and VIII. The project in Chapter VII examined the contribution of substance P and NK1 receptors to active vasodilation. The results from this study suggest substance P and NK1 receptors contribute to active vasodilation. The fifth project (Chapter VIII) was designed to investigate substance P and NK1 receptors in thermal hyperemia. The results suggest substance P and NK1 receptors contribute to thermal hyperemia. The purpose of Chapter IX was to determine if the concentration of histamine in the skin increases during whole body heating and can thus account for the observed H1 receptor activation component of active vasodilation. There was no significant difference in histamine concentration between baseline samples and whole body heating samples. Thus, it appears histamine per se does not contribute to active vasodilation and cannot account for the observed H1 receptor activation component. This dissertation contains both my previously published and my co-authored materials.
ISBN: 9780542334825Subjects--Topical Terms:
1017835
Biology, Animal Physiology.
Histamine receptors and substance P in cutaneous active vasodilation and thermal hyperemia in humans.
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Source: Dissertation Abstracts International, Volume: 66-09, Section: B, page: 4571.
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The ability to increase skin blood flow in response to an increase in core temperature or local skin temperature represents important thermoregulatory and protective functions of the cutaneous vasculature in humans. However, the mechanism(s) underlying these changes in skin blood flow are unclear. The purpose of this dissertation was to investigate the role of histamine receptors and substance P in cutaneous active vasodilation and thermal hyperemia. In Chapter IV, the contribution of histamine receptors to active vasodilation was investigated. The results demonstrate the H 1, but not H2, isoform of the histamine receptor contributes to active vasodilation. In Chapter V, we investigated the contribution of histamine receptors to thermal hyperemia. These results suggest a minimal role for H1 receptors and no role for H2 receptors in thermal hyperemia. In Chapter VI, studies were carried out to investigate mechanisms of substance P-induced vasodilation. The results demonstrated a nitric oxide (NO) component to substance P-induced vasodilation but no histamine receptor component. Importantly, the results from this study provide evidence the neurokinin-1 (NK1) receptors, to which substance P binds to with high affinity, become desensitized to two consecutive microdialysis infusions of substance P. These results provided the experimental model for the studies described in Chapters VII and VIII. The project in Chapter VII examined the contribution of substance P and NK1 receptors to active vasodilation. The results from this study suggest substance P and NK1 receptors contribute to active vasodilation. The fifth project (Chapter VIII) was designed to investigate substance P and NK1 receptors in thermal hyperemia. The results suggest substance P and NK1 receptors contribute to thermal hyperemia. The purpose of Chapter IX was to determine if the concentration of histamine in the skin increases during whole body heating and can thus account for the observed H1 receptor activation component of active vasodilation. There was no significant difference in histamine concentration between baseline samples and whole body heating samples. Thus, it appears histamine per se does not contribute to active vasodilation and cannot account for the observed H1 receptor activation component. This dissertation contains both my previously published and my co-authored materials.
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