Platelet Norepinephrine Fluxes In Normotensive Subjects And Essential Hypertensive Patients

Disturbed neuronal metabolism and storage of monoamines has been described in various experimental and human hypertensive diseases. Since blood platelets are considered as valid models of sympathetic neurons, the uptake and release of [³H] norepinephrine (NE) was investigated in platelets isolated from normal subjects and from patients having essential hypertension. In addition, the intracellular metabolism of [³H] -NE was followed by high performance liquid chromatography.

In basal conditions, NE was found to be slowly incorporated into the platelets and approximately 25% of the absorbed radioactivity was recovered as a sulfoconjugate metabolite which is thought to represent the cytoplasmic form of the monoamine. The uptake of NE was inhibited by drugs known to interfere with the platelet serotonin accumulation at the plasma membrane level (chlorimipramine, ouabain) or at the vesicular storage level (tyramine, reserpine). In addition, drugs which impair the intravesicular storage of monoamines leading to their accumulation in the cytoplasm, induced a marked increase in platelet NE metabolism and release.

The uptake of norepinephrine was slightly reduced in platelets from essential hypertensive patients. A marked increase in spontaneous NE release was measured in correlation with increased intracellular NE metabolism. The results are compatible with impaired intravesicular storage of the monoamine leading to increased diffusion through the plasma membrane.