Increased erythrocyte aggregation in spontaneously hypertensive rats.
Alterations of red blood cell (RBC) aggregation and plasma viscosity are major contributors to the changes in blood rheologic properties that cause an increase in peripheral vascular resistance during the development of hypertension. Although basic research and clinical study have provided considerable understanding of the pathophysiology of hypertension, the objective of this study was to determine whether an increase in RBC aggregability and plasma viscosity precede or accompany the development of high arterial blood pressure. To address this question, RBC aggregation and plasma viscosity were studied in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) at 3 and 12 weeks of age. The plasma concentrations of fibrinogen and fibronectin (FN) were also analyzed in both age groups. RBC aggregability and plasma viscosity were increased in both young and mature SHR compared to age-matched normotensive WKY rats. Mean arterial blood pressure and diastolic pressures were increased in mature hypertensive rats, whereas in young SHR only diastolic pressure was elevated significantly. The concentration of fibrinogen was higher only in the mature hypertensive rats, whereas plasma FN content was greater in both 3- and 12-week-old SHR compared to age-matched WKY. These results show the existence of increased RBC aggregability and plasma hyperviscosity not only during the established phase of hypertension, but also during the early stage of hypertension development, when mean arterial blood pressure is not yet significantly elevated in the genetically hypertensive rat model. These changes may be related to significant increase in the plasma protein FN, which occurs at the same time as the RBC aggregability and plasma viscosity changes. These results may increase attention to changes in the rheologic properties and to the mechanisms involved in these processes in the early stages of hypertension development.
Lominadze
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Center for Applied Microcirculatory Research and Department of Physiology and Biophysics, University of Louisville, Kentucky 40292, USA.
Joshua
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Schuschke
D A
DA
D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001809:Blood Viscosity / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D003971:Diastole; D004903:Erythrocyte Aggregation / Q000502:physiology*; D005340:Fibrinogen / Q000378:metabolism; D006321:Heart / Q000033:anatomy & histology; D006339:Heart Rate / Q000502:physiology; D006400:Hematocrit; D006973:Hypertension / Q000097:blood*; D008297:Male; D009929:Organ Size / Q000502:physiology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013997:Time Factors
D005340:Fibrinogen