Relationship of blood viscosity and blood pressure in normotensive and spontaneously hypertensive rats

Increased viscosity of whole blood can make a significant contribution to an increase in total peripheral resistance, disruption of systemic hemodynamics and microcirculation disorders in arterial hypertension. However, changes in blood viscosity (BV) also lead to changes in shear stress on the endothelium, which can affect vascular tone. There have been no studies of the relationship between changes in BV and blood pressure in animals under conditions of arterial hypertension. The purpose of the work was to study the correlation between blood viscosity and blood pressure in normotensive Wistar rats and spontaneously hypertensive rats (SHR) under normal conditions, as well as under conditions of decreased and increased blood viscosity. Reduction/increase of BV was carried out using isovolumic hemodilution/hemoconcentration. Mean arterial pressure (MAP) was recorded using the MP150 system (Biopac Systems, Inc, USA). BV was measured on a Brookfield DV–II+Pro rotational viscometer (Brookfield Engineering Labs Inc., USA) at a shear rate of 450 s-1. In normotensive rats there were no statistically significant correlations between the initial values of BV and MAP. After isovolumic hemodilution or hemoconcentration in normotensive rats, statistically significant correlations between BV and MAP were also not found. In SHR, compared with Wistar rats, a significant positive statistical relationship of moderate strength was observed between the initial values of BV and MAP (R = 0.643, p 0.05). In SHR, the identified statistically significant correlations of moderate strength between the values of BV and MAP remained, both after hemodilution (R = 0.530, p 0.05) and after hemoconcentration (R = 0.689, p 0.05). Analysis of correlations shows that in SHR, unlike Wistar rats, changes in blood pressure passively follow changes in blood viscosity, which is probably due to the failure of the mechanisms of endothelium-dependent vasodilation in hypertension.