Modulation of platelet Ca2+ homeostasis by hypertensive plasma factor(s) derived from patients with early-stage renal disease.

Abstract

To determine whether blood-borne factors in hypertension accompanying early-stage kidney disease might be responsible for altered cellular calcium homeostasis, we measured changes in cytosolic calcium before and after incubating platelets in plasma ultrafiltrates from normotensive and hypertensive renal patients. With the use of the chelating agent quin 2, we found the free-calcium concentrations in platelets to be higher in the hypertensive than in the normotensive group. When both groups of participants were combined, a direct correlation was found between arterial pressure and cytosolic calcium. The cytosolic calcium concentration in platelets of normotensive renal patients increased after incubation with plasma from patients with untreated renal hypertension, but it was unchanged after incubation with plasma from normotensive subjects. These data indicate that the total cell burden of calcium is increased in platelets of hypertensive patients with early-stage renal disease, and that plasma from these patients contains a substance that is capable of increasing the cytosolic calcium concentration in platelets. If the plasma factor (or factors) acts not only on platelets, but also on vascular smooth muscle cells, it may contribute to the increased peripheral vascular resistance associated with hypertension of renal origin.