Blood flow shear rates in arterioles of spontaneously hypertensive rats atearly and established stages of hypertension

Citation
D. Lominadze et al., Blood flow shear rates in arterioles of spontaneously hypertensive rats atearly and established stages of hypertension, CLIN EXP HY, 23(4), 2001, pp. 317-328
Citations number
39
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
CLINICAL AND EXPERIMENTAL HYPERTENSION
ISSN journal
10641963 → ACNP
Volume
23
Issue
4
Year of publication
2001
Pages
317 - 328
Database
ISI
SICI code
1064-1963(200105)23:4<317:BFSRIA>2.0.ZU;2-D
Abstract
Alterations of blood rheological properties can affect blood flow shear rat es and therefore alter changes in the interactions between blood and vascul ar wall components during the development of hypertension. This study was d one to evaluate alterations of blood flow shear rates in resistance vessels during the development of genetic hypertension in rats. In the current stu dy, measurements were carried out on spontaneously hypertensive rats (SHR) during an early (3 weeks of age) and an established stage (12 weeks of age) of hypertension development. Age matched normotensive Wistar Kyoto (WKY) r ats were used as controls. Intravital television microscopy was used to qua ntitate blood flow shear rates in first-(1A), second-(2A) and third-order ( 3A) arterioles of the cremaster muscle. In the young SHRs mean arterial blo od pressure was not different from age matched WKY rats, but there was a si gnificant increase of shear rate values in all observed (1A, 2A, 3A) arteri oles of SHRs. However, shear rate values were significantly less in arterio les (1A, 2A, 3A) of SHRs with an established hyper tension compared to the 3-week-old SHR group. We conclude that shear rates are elevated in resistan ce vessels prior to an increase in mean arterial pressure during the develo pment of genetic hypertension. These results suggest that a change in blood rheology may cause a change in peripheral vascular resistance and thus con tribute to the pathogenesis of hypertension.