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Abnormal sodium(Na+) and water handling by the kidney may be the cause of hypertension in rats of the Milan hypertensive strain (MHS). In addition, the plasma cell membrane Ca-ATPase at Vmax is lower in MHS than in normotensive controls (MNS). The isolated kidney preparation was used to explore the role of extracellular free calcium (Ca2+) concentrations (1.25, 1.00 and 0.75 mmol/l) in tubular Na+ transport of pre-hypertensive MHS rats.At the Ca2+ concentration of 1.0 mmol/l, the following parameters were significantly higher (P<0.01) in MHS: glomerular filtration rate (GFR) and urinary volume (UV), + 104.8 and +147.2%, respectively; urinary Na+ excretion (UNa+), +318.0%; tubular Na+ reabsorption (TNa+), +91.0% and oxygen consumption Q O2, +42.9%.Raising the Ca2+ concentration to 1.25 mmol/l increased UV (+167.0%) and UNa+ ( + 231.0%) in MHS without substantially affecting MNS. The difference between the two strains was therefore considerably larger for these parameters, but disappeared for TNa+ and Q O2. The overall kidney function of MHS was poor as compared with renal function at Ca2+ 1.0 mmol/l. The differences between the two strains virtually la+ disappeared at the lowest Ca2+ concentration (0.75 mmol/l); only GFR and TN. remained slightly greater in MHS mainly because of the poor viability of MNS kidneys in this experimental condition. It thus appears that the lower activity of Ca2+-ATPase of MHS compared with MNS plasma cell membranes influences the differences in Na+ and water handling in the two strains.