Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans

1  Geriatric Research, Education, and Clinical Center, Department of Veterans Affairs, South Texas Veterans Health Care System, Audie L. Murphy Memorial Veterans Hospital Division, and Divisions of 2  Geriatrics and Gerontology and 3  Nephrology, Department of Medicine, University of Texas Health Sc...

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Veröffentlicht in:Journal of applied physiology (1985) 2002-10, Vol.93 (4), p.1215-1221
Hauptverfasser: Kellogg, D. L., Jr, Liu, Y, McAllister, K, Friel, C, Pergola, P. E
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container_end_page 1221
container_issue 4
container_start_page 1215
container_title Journal of applied physiology (1985)
container_volume 93
creator Kellogg, D. L., Jr
Liu, Y
McAllister, K
Friel, C
Pergola, P. E
description 1  Geriatric Research, Education, and Clinical Center, Department of Veterans Affairs, South Texas Veterans Health Care System, Audie L. Murphy Memorial Veterans Hospital Division, and Divisions of 2  Geriatrics and Gerontology and 3  Nephrology, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229 To test the hypothesis that bradykinin effects cutaneous active vasodilation during hyperthermia, we examined whether the increase in skin blood flow (SkBF) during heat stress was affected by blockade of bradykinin B 2 receptors with the receptor antagonist HOE-140. Two adjacent sites on the forearm were instrumented with intradermal microdialysis probes for local delivery of drugs in eight healthy subjects. HOE-140 was dissolved in Ringer solution (40 µM) and perfused at one site, whereas the second site was perfused with Ringer alone. SkBF was monitored by laser-Doppler flowmetry (LDF) at both sites. Mean arterial pressure (MAP) was monitored from a finger, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Water-perfused suits were used to control body temperature and evoke hyperthermia. After hyperthermia, both microdialysis sites were perfused with 28 mM nitroprusside to effect maximal vasodilation. During hyperthermia, CVC increased at HOE-140 (69 ± 2% maximal CVC, P  
doi_str_mv 10.1152/japplphysiol.01142.2001
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L., Jr ; Liu, Y ; McAllister, K ; Friel, C ; Pergola, P. E</creator><creatorcontrib>Kellogg, D. L., Jr ; Liu, Y ; McAllister, K ; Friel, C ; Pergola, P. E</creatorcontrib><description>1  Geriatric Research, Education, and Clinical Center, Department of Veterans Affairs, South Texas Veterans Health Care System, Audie L. Murphy Memorial Veterans Hospital Division, and Divisions of 2  Geriatrics and Gerontology and 3  Nephrology, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229 To test the hypothesis that bradykinin effects cutaneous active vasodilation during hyperthermia, we examined whether the increase in skin blood flow (SkBF) during heat stress was affected by blockade of bradykinin B 2 receptors with the receptor antagonist HOE-140. Two adjacent sites on the forearm were instrumented with intradermal microdialysis probes for local delivery of drugs in eight healthy subjects. HOE-140 was dissolved in Ringer solution (40 µM) and perfused at one site, whereas the second site was perfused with Ringer alone. SkBF was monitored by laser-Doppler flowmetry (LDF) at both sites. Mean arterial pressure (MAP) was monitored from a finger, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Water-perfused suits were used to control body temperature and evoke hyperthermia. After hyperthermia, both microdialysis sites were perfused with 28 mM nitroprusside to effect maximal vasodilation. During hyperthermia, CVC increased at HOE-140 (69 ± 2% maximal CVC, P  &lt; 0.01) and untreated sites (65 ± 2% maximal CVC, P  &lt; 0.01). These responses did not differ between sites ( P  &gt; 0.05). 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Psychology ; Heat ; Hot Temperature ; Humans ; Laser-Doppler Flowmetry ; Male ; Microdialysis ; Peptides ; Receptor, Bradykinin B2 ; Skin ; Skin - blood supply ; Stress, Physiological - physiopathology ; Thermoregulation. Hibernation. Estivation. 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E</creatorcontrib><title>Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans</title><title>Journal of applied physiology (1985)</title><addtitle>J Appl Physiol (1985)</addtitle><description>1  Geriatric Research, Education, and Clinical Center, Department of Veterans Affairs, South Texas Veterans Health Care System, Audie L. Murphy Memorial Veterans Hospital Division, and Divisions of 2  Geriatrics and Gerontology and 3  Nephrology, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229 To test the hypothesis that bradykinin effects cutaneous active vasodilation during hyperthermia, we examined whether the increase in skin blood flow (SkBF) during heat stress was affected by blockade of bradykinin B 2 receptors with the receptor antagonist HOE-140. Two adjacent sites on the forearm were instrumented with intradermal microdialysis probes for local delivery of drugs in eight healthy subjects. HOE-140 was dissolved in Ringer solution (40 µM) and perfused at one site, whereas the second site was perfused with Ringer alone. SkBF was monitored by laser-Doppler flowmetry (LDF) at both sites. Mean arterial pressure (MAP) was monitored from a finger, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Water-perfused suits were used to control body temperature and evoke hyperthermia. After hyperthermia, both microdialysis sites were perfused with 28 mM nitroprusside to effect maximal vasodilation. During hyperthermia, CVC increased at HOE-140 (69 ± 2% maximal CVC, P  &lt; 0.01) and untreated sites (65 ± 2% maximal CVC, P  &lt; 0.01). These responses did not differ between sites ( P  &gt; 0.05). Because the bradykinin B 2 -receptor antagonist HOE-140 did not alter SkBF responses to heat stress, we conclude that bradykinin does not mediate cutaneous active vasodilation. microdialysis; laser-Doppler flowmetry</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Body fluids</subject><subject>Bradykinin - analogs &amp; derivatives</subject><subject>Bradykinin - metabolism</subject><subject>Bradykinin - pharmacology</subject><subject>Bradykinin Receptor Antagonists</subject><subject>Endocrine system</subject><subject>Female</subject><subject>Forearm</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heat</subject><subject>Hot Temperature</subject><subject>Humans</subject><subject>Laser-Doppler Flowmetry</subject><subject>Male</subject><subject>Microdialysis</subject><subject>Peptides</subject><subject>Receptor, Bradykinin B2</subject><subject>Skin</subject><subject>Skin - blood supply</subject><subject>Stress, Physiological - physiopathology</subject><subject>Thermoregulation. Hibernation. Estivation. Ecophysiology and environmental effects</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilation - physiology</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><issn>8750-7587</issn><issn>1522-1601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kF2L1DAUhoMo7jj6F7QIijcdc_LRTC7XxVVhwZvV25Ck6TRjp6lJujr_3oxTXBG8Cpw873sOD0IvAG8AOHm719M0TP0x-TBsMAAjG4IxPECr8ktqaDA8RKut4LgWfCsu0JOU9gVgjMNjdAGEUI5BrNDXd1G3x29-9GPVBpeqMeTq4Fqvs6vsnPXowpwqbbO_c9WdTqH1g84-FHyOftxVvdO5Sjm6lKpS0s8HPaan6FGnh-SeLe8afbl-f3v1sb75_OHT1eVNbRljuSay4x1vwTCugZgGOsGZgS3n0krLttgYZ8GYMjCMCNJKThspbNtors2W0jV6fe6dYvg-u5TVwSfrhuF8txIEMOGsKeDLf8B9mONYblOEEOCUSlEgcYZsDClF16kp-oOORwVYnbyrv72r397VyXtJPl_qZ1Ps3ecW0QV4tQA6WT10UY_Wp3uOSsqIlIV7c-Z6v-t_-OjUsi3sjqftSlLFSm25eI3Y_9HreRhu3c98yvyJqKnt6C9zEbDc</recordid><startdate>20021001</startdate><enddate>20021001</enddate><creator>Kellogg, D. L., Jr</creator><creator>Liu, Y</creator><creator>McAllister, K</creator><creator>Friel, C</creator><creator>Pergola, P. E</creator><general>Am Physiological Soc</general><general>American Physiological Society</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20021001</creationdate><title>Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans</title><author>Kellogg, D. L., Jr ; Liu, Y ; McAllister, K ; Friel, C ; Pergola, P. E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-29f5f5d1b45a12b61f754b18559c9c480bbec1bb855b4272d953697cd6a5ab833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Body fluids</topic><topic>Bradykinin - analogs &amp; derivatives</topic><topic>Bradykinin - metabolism</topic><topic>Bradykinin - pharmacology</topic><topic>Bradykinin Receptor Antagonists</topic><topic>Endocrine system</topic><topic>Female</topic><topic>Forearm</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Heat</topic><topic>Hot Temperature</topic><topic>Humans</topic><topic>Laser-Doppler Flowmetry</topic><topic>Male</topic><topic>Microdialysis</topic><topic>Peptides</topic><topic>Receptor, Bradykinin B2</topic><topic>Skin</topic><topic>Skin - blood supply</topic><topic>Stress, Physiological - physiopathology</topic><topic>Thermoregulation. Hibernation. Estivation. Ecophysiology and environmental effects</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilation - physiology</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kellogg, D. L., Jr</creatorcontrib><creatorcontrib>Liu, Y</creatorcontrib><creatorcontrib>McAllister, K</creatorcontrib><creatorcontrib>Friel, C</creatorcontrib><creatorcontrib>Pergola, P. 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E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans</atitle><jtitle>Journal of applied physiology (1985)</jtitle><addtitle>J Appl Physiol (1985)</addtitle><date>2002-10-01</date><risdate>2002</risdate><volume>93</volume><issue>4</issue><spage>1215</spage><epage>1221</epage><pages>1215-1221</pages><issn>8750-7587</issn><eissn>1522-1601</eissn><coden>JAPHEV</coden><abstract>1  Geriatric Research, Education, and Clinical Center, Department of Veterans Affairs, South Texas Veterans Health Care System, Audie L. Murphy Memorial Veterans Hospital Division, and Divisions of 2  Geriatrics and Gerontology and 3  Nephrology, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229 To test the hypothesis that bradykinin effects cutaneous active vasodilation during hyperthermia, we examined whether the increase in skin blood flow (SkBF) during heat stress was affected by blockade of bradykinin B 2 receptors with the receptor antagonist HOE-140. Two adjacent sites on the forearm were instrumented with intradermal microdialysis probes for local delivery of drugs in eight healthy subjects. HOE-140 was dissolved in Ringer solution (40 µM) and perfused at one site, whereas the second site was perfused with Ringer alone. SkBF was monitored by laser-Doppler flowmetry (LDF) at both sites. Mean arterial pressure (MAP) was monitored from a finger, and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Water-perfused suits were used to control body temperature and evoke hyperthermia. After hyperthermia, both microdialysis sites were perfused with 28 mM nitroprusside to effect maximal vasodilation. During hyperthermia, CVC increased at HOE-140 (69 ± 2% maximal CVC, P  &lt; 0.01) and untreated sites (65 ± 2% maximal CVC, P  &lt; 0.01). These responses did not differ between sites ( P  &gt; 0.05). Because the bradykinin B 2 -receptor antagonist HOE-140 did not alter SkBF responses to heat stress, we conclude that bradykinin does not mediate cutaneous active vasodilation. microdialysis; laser-Doppler flowmetry</abstract><cop>Bethesda, MD</cop><pub>Am Physiological Soc</pub><pmid>12235017</pmid><doi>10.1152/japplphysiol.01142.2001</doi><tpages>7</tpages></addata></record>
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source MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Adult
Biological and medical sciences
Body fluids
Bradykinin - analogs & derivatives
Bradykinin - metabolism
Bradykinin - pharmacology
Bradykinin Receptor Antagonists
Endocrine system
Female
Forearm
Fundamental and applied biological sciences. Psychology
Heat
Hot Temperature
Humans
Laser-Doppler Flowmetry
Male
Microdialysis
Peptides
Receptor, Bradykinin B2
Skin
Skin - blood supply
Stress, Physiological - physiopathology
Thermoregulation. Hibernation. Estivation. Ecophysiology and environmental effects
Vasodilation - drug effects
Vasodilation - physiology
Vertebrates: anatomy and physiology, studies on body, several organs or systems
title Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans
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