Importance of pulsatility in hypertensive carotid artery growth and remodeling
Arteries experience marked variations in blood pressure and flow during the cardiac cycle that can intensify during exercise, in disease, or with aging. Diverse observations increasingly suggest the importance of such pulsatility in arterial homeostasis and adaptations. We used a transverse aortic a...
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| Veröffentlicht in: | Journal of hypertension 2009-10, Vol.27 (10), p.2010-2021 |
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| creator | Eberth, John F Gresham, Vincent C Reddy, Anilkumar K Popovic, Natasa Wilson, Emily Humphrey, Jay D |
| description | Arteries experience marked variations in blood pressure and flow during the cardiac cycle that can intensify during exercise, in disease, or with aging. Diverse observations increasingly suggest the importance of such pulsatility in arterial homeostasis and adaptations. We used a transverse aortic arch banding model to quantify chronic effects of increased pulsatile pressure and flow on wall morphology, composition, and biaxial mechanical properties in paired mouse arteriesthe highly pulsatile right common carotid artery proximal to the band (RCCA-B) and the nearly normal left common carotid artery distal to the band (LCCA-B). Increased pulsatile mechanical stimuli in RCCA-B increased wall thickness compared with LCCA-B, which correlated more strongly with pulse (r* = 0.632; P < 0.01) than mean (r* = 0.020; P = 0.47) or systolic (r* = 0.466; P < 0.05) pressure. Similarly, inner diameter at mean pressure increased in RCCA-B and correlated slightly more strongly with a normalized index of blood velocity pulsatility (r* = 0.915; P < |
| doi_str_mv | 10.1097/HJH.0b013e32832e8dc8 |
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Diverse observations increasingly suggest the importance of such pulsatility in arterial homeostasis and adaptations. We used a transverse aortic arch banding model to quantify chronic effects of increased pulsatile pressure and flow on wall morphology, composition, and biaxial mechanical properties in paired mouse arteriesthe highly pulsatile right common carotid artery proximal to the band (RCCA-B) and the nearly normal left common carotid artery distal to the band (LCCA-B). Increased pulsatile mechanical stimuli in RCCA-B increased wall thickness compared with LCCA-B, which correlated more strongly with pulse (r* = 0.632; P < 0.01) than mean (r* = 0.020; P = 0.47) or systolic (r* = 0.466; P < 0.05) pressure. Similarly, inner diameter at mean pressure increased in RCCA-B and correlated slightly more strongly with a normalized index of blood velocity pulsatility (r* = 0.915; P < <0.001) than mean flow (r* = 0.834; P < 0.001). Increased wall thickness and luminal diameter in RCCA-B resulted from significant increases in cell number per cross-sectional area (P < 0.001) and collagen-to-elastin ratio (P < 0.05) as well as a moderate (1.7-fold) increase in glycosaminoglycan content, which appears to have contributed to the significant decrease (P < 0.001) in the in-vivo axial stretch in RCCA-B compared with LCCA-B. Changes in RCCA-B also associated with a signficant increase in monocyte chemoattractant protein-1 (P < 0.05) whereas LCCA-B did not. Pulsatile pressure and flow are thus important stimuli in the observed three-dimensional arterial adaptations, and there is a need for increased attention to the roles of both axial wall stress and adventitial remodeling.]]></description><identifier>ISSN: 0263-6352</identifier><identifier>EISSN: 1473-5598</identifier><identifier>DOI: 10.1097/HJH.0b013e32832e8dc8</identifier><identifier>PMID: 19584753</identifier><identifier>CODEN: JOHYD3</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins, Inc</publisher><subject>Animals ; Aorta, Thoracic - physiology ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure - physiology ; Cardiology. Vascular system ; Carotid Artery Diseases - pathology ; Carotid Artery Diseases - physiopathology ; Carotid Artery, Common - pathology ; Carotid Artery, Common - physiology ; Chemokine CCL2 - metabolism ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Collagen - metabolism ; Disease Models, Animal ; Elastin - metabolism ; Heart Rate - physiology ; Hypertension - pathology ; Hypertension - physiopathology ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Pulsatile Flow - physiology ; Stress, Mechanical</subject><ispartof>Journal of hypertension, 2009-10, Vol.27 (10), p.2010-2021</ispartof><rights>2009 Lippincott Williams & Wilkins, Inc.</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4824-e93721dca003f18af0f2e66f37a49fbedbf9633c88b0e6a9c1e5f28cb983d1593</citedby><cites>FETCH-LOGICAL-c4824-e93721dca003f18af0f2e66f37a49fbedbf9633c88b0e6a9c1e5f28cb983d1593</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21990341$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19584753$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Eberth, John F</creatorcontrib><creatorcontrib>Gresham, Vincent C</creatorcontrib><creatorcontrib>Reddy, Anilkumar K</creatorcontrib><creatorcontrib>Popovic, Natasa</creatorcontrib><creatorcontrib>Wilson, Emily</creatorcontrib><creatorcontrib>Humphrey, Jay D</creatorcontrib><title>Importance of pulsatility in hypertensive carotid artery growth and remodeling</title><title>Journal of hypertension</title><addtitle>J Hypertens</addtitle><description><![CDATA[Arteries experience marked variations in blood pressure and flow during the cardiac cycle that can intensify during exercise, in disease, or with aging. Diverse observations increasingly suggest the importance of such pulsatility in arterial homeostasis and adaptations. We used a transverse aortic arch banding model to quantify chronic effects of increased pulsatile pressure and flow on wall morphology, composition, and biaxial mechanical properties in paired mouse arteriesthe highly pulsatile right common carotid artery proximal to the band (RCCA-B) and the nearly normal left common carotid artery distal to the band (LCCA-B). Increased pulsatile mechanical stimuli in RCCA-B increased wall thickness compared with LCCA-B, which correlated more strongly with pulse (r* = 0.632; P < 0.01) than mean (r* = 0.020; P = 0.47) or systolic (r* = 0.466; P < 0.05) pressure. Similarly, inner diameter at mean pressure increased in RCCA-B and correlated slightly more strongly with a normalized index of blood velocity pulsatility (r* = 0.915; P < <0.001) than mean flow (r* = 0.834; P < 0.001). Increased wall thickness and luminal diameter in RCCA-B resulted from significant increases in cell number per cross-sectional area (P < 0.001) and collagen-to-elastin ratio (P < 0.05) as well as a moderate (1.7-fold) increase in glycosaminoglycan content, which appears to have contributed to the significant decrease (P < 0.001) in the in-vivo axial stretch in RCCA-B compared with LCCA-B. Changes in RCCA-B also associated with a signficant increase in monocyte chemoattractant protein-1 (P < 0.05) whereas LCCA-B did not. Pulsatile pressure and flow are thus important stimuli in the observed three-dimensional arterial adaptations, and there is a need for increased attention to the roles of both axial wall stress and adventitial remodeling.]]></description><subject>Animals</subject><subject>Aorta, Thoracic - physiology</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure - physiology</subject><subject>Cardiology. Vascular system</subject><subject>Carotid Artery Diseases - pathology</subject><subject>Carotid Artery Diseases - physiopathology</subject><subject>Carotid Artery, Common - pathology</subject><subject>Carotid Artery, Common - physiology</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Collagen - metabolism</subject><subject>Disease Models, Animal</subject><subject>Elastin - metabolism</subject><subject>Heart Rate - physiology</subject><subject>Hypertension - pathology</subject><subject>Hypertension - physiopathology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Pulsatile Flow - physiology</subject><subject>Stress, Mechanical</subject><issn>0263-6352</issn><issn>1473-5598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU1v1DAQhi0EotvCP0AoF8QpxV9J7AsSqoAtquACZ8txxhuDEwfb6Wr_PV51tQUOI2vGz7wzmhehVwRfEyy7d9sv22vcY8KAUcEoiMGIJ2hDeMfqppHiKdpg2rK6ZQ29QJcp_cQYC9mx5-iCyEbwrmEb9PV2WkLMejZQBVstq086O-_yoXJzNR4WiBnm5O6hMjqG7IZKl0o8VLsY9nms9DxUEaYwgHfz7gV6ZrVP8PL0XqEfnz5-v9nWd98-3958uKsNF5TXIFlHyWA0xswSoS22FNrWsk5zaXsYeitbxowQPYZWS0OgsVSYXgo2kEayK_T-QXdZ-wkGA3OO2qsluknHgwraqX9_ZjeqXbhXtBOswUeBtyeBGH6vkLKaXDLgvZ4hrEl1jBNWOF5I_kCaGFKKYM9TCFZHJ1RxQv3vRGl7_feGj02n0xfgzQnQyWhvY_HApTNHiZT4uMR5_j74cvj0y697iGoE7fOoiqeYi47WFGNJjlldgnD2B_SjpSw</recordid><startdate>200910</startdate><enddate>200910</enddate><creator>Eberth, John F</creator><creator>Gresham, Vincent C</creator><creator>Reddy, Anilkumar K</creator><creator>Popovic, Natasa</creator><creator>Wilson, Emily</creator><creator>Humphrey, Jay D</creator><general>Lippincott Williams & Wilkins, Inc</general><general>Lippincott Williams & Wilkins</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>200910</creationdate><title>Importance of pulsatility in hypertensive carotid artery growth and remodeling</title><author>Eberth, John F ; Gresham, Vincent C ; Reddy, Anilkumar K ; Popovic, Natasa ; Wilson, Emily ; Humphrey, Jay D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4824-e93721dca003f18af0f2e66f37a49fbedbf9633c88b0e6a9c1e5f28cb983d1593</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Aorta, Thoracic - physiology</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure - physiology</topic><topic>Cardiology. Vascular system</topic><topic>Carotid Artery Diseases - pathology</topic><topic>Carotid Artery Diseases - physiopathology</topic><topic>Carotid Artery, Common - pathology</topic><topic>Carotid Artery, Common - physiology</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Collagen - metabolism</topic><topic>Disease Models, Animal</topic><topic>Elastin - metabolism</topic><topic>Heart Rate - physiology</topic><topic>Hypertension - pathology</topic><topic>Hypertension - physiopathology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Pulsatile Flow - physiology</topic><topic>Stress, Mechanical</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Eberth, John F</creatorcontrib><creatorcontrib>Gresham, Vincent C</creatorcontrib><creatorcontrib>Reddy, Anilkumar K</creatorcontrib><creatorcontrib>Popovic, Natasa</creatorcontrib><creatorcontrib>Wilson, Emily</creatorcontrib><creatorcontrib>Humphrey, Jay D</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Eberth, John F</au><au>Gresham, Vincent C</au><au>Reddy, Anilkumar K</au><au>Popovic, Natasa</au><au>Wilson, Emily</au><au>Humphrey, Jay D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Importance of pulsatility in hypertensive carotid artery growth and remodeling</atitle><jtitle>Journal of hypertension</jtitle><addtitle>J Hypertens</addtitle><date>2009-10</date><risdate>2009</risdate><volume>27</volume><issue>10</issue><spage>2010</spage><epage>2021</epage><pages>2010-2021</pages><issn>0263-6352</issn><eissn>1473-5598</eissn><coden>JOHYD3</coden><abstract><![CDATA[Arteries experience marked variations in blood pressure and flow during the cardiac cycle that can intensify during exercise, in disease, or with aging. Diverse observations increasingly suggest the importance of such pulsatility in arterial homeostasis and adaptations. We used a transverse aortic arch banding model to quantify chronic effects of increased pulsatile pressure and flow on wall morphology, composition, and biaxial mechanical properties in paired mouse arteriesthe highly pulsatile right common carotid artery proximal to the band (RCCA-B) and the nearly normal left common carotid artery distal to the band (LCCA-B). Increased pulsatile mechanical stimuli in RCCA-B increased wall thickness compared with LCCA-B, which correlated more strongly with pulse (r* = 0.632; P < 0.01) than mean (r* = 0.020; P = 0.47) or systolic (r* = 0.466; P < 0.05) pressure. Similarly, inner diameter at mean pressure increased in RCCA-B and correlated slightly more strongly with a normalized index of blood velocity pulsatility (r* = 0.915; P < <0.001) than mean flow (r* = 0.834; P < 0.001). Increased wall thickness and luminal diameter in RCCA-B resulted from significant increases in cell number per cross-sectional area (P < 0.001) and collagen-to-elastin ratio (P < 0.05) as well as a moderate (1.7-fold) increase in glycosaminoglycan content, which appears to have contributed to the significant decrease (P < 0.001) in the in-vivo axial stretch in RCCA-B compared with LCCA-B. Changes in RCCA-B also associated with a signficant increase in monocyte chemoattractant protein-1 (P < 0.05) whereas LCCA-B did not. Pulsatile pressure and flow are thus important stimuli in the observed three-dimensional arterial adaptations, and there is a need for increased attention to the roles of both axial wall stress and adventitial remodeling.]]></abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>19584753</pmid><doi>10.1097/HJH.0b013e32832e8dc8</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Aorta, Thoracic - physiology Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Pressure - physiology Cardiology. Vascular system Carotid Artery Diseases - pathology Carotid Artery Diseases - physiopathology Carotid Artery, Common - pathology Carotid Artery, Common - physiology Chemokine CCL2 - metabolism Clinical manifestations. Epidemiology. Investigative techniques. Etiology Collagen - metabolism Disease Models, Animal Elastin - metabolism Heart Rate - physiology Hypertension - pathology Hypertension - physiopathology Medical sciences Mice Mice, Inbred C57BL Pulsatile Flow - physiology Stress, Mechanical |
| title | Importance of pulsatility in hypertensive carotid artery growth and remodeling |
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