| Contribution of fluid shear response in leukocytes to hemodynamic resistance in the spontaneously hypertensive rat. | |
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MedLine Citation:
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PMID: 15166092 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The mechanisms for elevation of peripheral vascular resistance in spontaneously hypertensive rats (SHR), a glucocorticoid-dependent form of hypertension, are unresolved. An increase in hemodynamic resistance caused by circulating blood may be a factor. Physiological fluid shear stress induces a variety of responses in circulating leukocytes, including pseudopod retraction. Due to high rigidity, leukocytes with pseudopods have greater difficulty to pass through capillaries. Because SHR have more circulating leukocytes with pseudopods, we hypothesize that inhibition of the leukocyte shear response by glucocorticoids in SHR impairs normal leukocyte passage through capillaries and causes enhanced resistance in capillary channels. Fluid shear leads to retraction of pseudopods in normal leukocytes, whereas shear induces pseudopod projection in SHR and dexamethasone-treated Wistar rats. The high incidence of circulating leukocytes with pseudopods results in slower cell passage through capillaries under normal blood flow and during reduced flow enhanced capillary plugging both in vivo and in vitro. SHR blood requires higher pressure (90.0+/-8.2 mm Hg) than Wistar Kyoto rat (WKY, 69.6+/-6.5 mm Hg; P<0.0001) or adrenalectomized SHR (73.5+/-2.1 mm Hg; P=0.0009) at the same flow rate in the resting hemodynamically isolated skeletal muscle microcirculation. Intravenous injection of blood from SHR, but not WKY, causes blood pressure increase in normal rats, which depends on pseudopod formation. We conclude that in addition to enhanced vascular tone, pseudopod formation with lack of normal fluid shear response may serve as mechanisms for an elevated hemodynamic resistance in SHR. |
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Authors:
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Shunichi Fukuda; Takanori Yasu; Nobuhiko Kobayashi; Nahoko Ikeda; Geert W Schmid-Schönbein |
Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. Date: 2004-05-27 |
Journal Detail:
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Title: Circulation research Volume: 95 ISSN: 1524-4571 ISO Abbreviation: Circ. Res. Publication Date: 2004 Jul |
Date Detail:
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Created Date: 2004-07-09 Completed Date: 2004-11-30 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0047103 Medline TA: Circ Res Country: United States |
Other Details:
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Languages: eng Pagination: 100-8 Citation Subset: IM |
Affiliation:
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Department of Bioengineering, The Whitaker Institute of Biomedical Engineering, University of California San Diego, La Jolla, Calif 92093-0412, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Pressure Capillaries / cytology Dexamethasone / pharmacology Glucocorticoids / pharmacology Hypertension / physiopathology* Leukocytes / drug effects, physiology*, ultrastructure Male Mechanotransduction, Cellular* Microcirculation / cytology Muscle, Skeletal / blood supply Pseudopodia / ultrastructure Rats Rats, Inbred SHR Rats, Inbred WKY Rats, Wistar Vascular Resistance* |
| Grant Support | |
ID/Acronym/Agency:
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HL-10881/HL/NHLBI NIH HHS; HL-43026/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Glucocorticoids; 50-02-2/Dexamethasone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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