EFFECT OF PROSTACYCLIN ON PLATELET INTRACELLULAR FREE CALCIUM-CONCENTRATION OF HYPERTENSIVE AND NORMOTENSIVE HUMANS

Platelet intracellular free calcium concentration ([Ca2+]i) has been r eported to be increased in essential hypertensive patients (EHT) as co mpared with normotensive controls (NT). Prostacyclin (PGI2), which inf luences cellular Ca2+, has been reported to be reduced in EHT. This st udy tested the hypothesis that the resting level of platelet [Ca2+]i i n humans is influenced by PGI2. We also investigated the role of PGI2 in regulating platelet [Ca2+]i of 28 EHT subjects compared to 28 NT co ntrols. Platelet [Ca2+]i was measured using the fluorescent Ca2+ probe fura-2 under control conditions and a 10-min preincubation with PGI2. Simultaneous measurement of platelet cyclic-adenosine 3':5'-monophosp hate (cAMP) was performed by radioimmunoassay. The resting level of pl atelet [Ca2+]i was significantly higher in EHT than in NT (32.7 +/- 1. 4 v 28.3 +/- 0.9 nmol/L; P <.01). PGI2 from 30 nM to 1 mumol/L lowered the resting level of platelet [Ca2+]i in a dose-dependent manner (EHT - 22.2 +/- 2.4, NT - 22.9 +/- 2.3%, 1 mumol/L PGI2); however, no sign ificant difference in platelet [Ca2+]i was observed between NT and EHT . While prostacyclin induced a transient rise in platelet cAMP, the ma gnitude of PGI2-induced cAMP level was similar between the two groups. These results do not support the hypothesis that endogenous PGI2 acti vity contributes to the increased level of platelet [Ca2+]i in EHT, al though PGI2 incubation lowered the resting level of platelet [Ca2+]i.