Document Detail


Contribution of fluid shear response in leukocytes to hemodynamic resistance in the spontaneously hypertensive rat.
MedLine Citation:
PMID:  15166092     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Shunichi Fukuda; Takanori Yasu; Nobuhiko Kobayashi; Nahoko Ikeda; Geert W Schmid-Schönbein
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.     Date:  2004-05-27
Journal Detail:
Title:  Circulation research     Volume:  95     ISSN:  1524-4571     ISO Abbreviation:  Circ. Res.     Publication Date:  2004 Jul 
Date Detail:
Created Date:  2004-07-09     Completed Date:  2004-11-30     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  100-8     Citation Subset:  IM    
Affiliation:
Department of Bioengineering, The Whitaker Institute of Biomedical Engineering, University of California San Diego, La Jolla, Calif 92093-0412, USA.
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MeSH Terms
Descriptor/Qualifier:
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:
HL-10881/HL/NHLBI NIH HHS; HL-43026/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Glucocorticoids; 50-02-2/Dexamethasone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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