Dietary potassium is known to cause reduction in blood pressure in several models of
hypertension in human and animal studies but its haematological effects are not known. Here, experiments are designed to study the haematological effects of
potassium adaptation (achieved by administering 0.75% KCl
solution in
drinking water for five weeks) in Wistar rats. The animals are divided into four groups comprising controls,
potassium-adapted, renal hypertensive, and renal hypertensive with later adaptation to
potassium. Packed cell volume (PCV) and platelet count (PC), whole blood and plasma viscosities, and platelet aggregation in the presence of
sodium nitroprusside,
levcromakalim, and
glibenclamide, are studied. Results showed comparable PCV and PC in all groups. While relative whole blood viscosity was significantly higher (P<0.05) in the hypertensive group, relative plasma viscosity was similar in all groups. Adaptation significantly reduced (P<0.05) the tendency of platelets to aggregate to
collagen.
Sodium nitroprusside significantly reduced (P<0.05) the pro-aggregatory effects of
collagen only in the control group. Neither of the
potassium-channel modulators (
levcromakalim,
glibenclamide) caused any significant alteration in platelet response to
collagen at the concentrations studied. Although these results suggest that
potassium adaptation may not affect haemorheology, the reduced ability of platelets to aggregate--by mechanisms not clearly understood--has implications for reduced
thromboembolism and the attendant cardiovascular sequelae.