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Platelet noradrenaline release in patients with familial hypercholesterolaemia
Author(s) -
SMITH C. C. T.,
WILSON A. P.,
PRICHARD B. N. C.,
BETTERIDGE D. J.
Publication year - 1989
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1989.tb00225.x
Subject(s) - platelet , medicine , thrombin , endocrinology , stimulation , catecholamine , chemistry
. We have examined resting and thrombin (0.3 units ml ‐1 ) induced release of noradrenaline by washed platelets from 15 normal subjects and eight patients with heterozygous familial hypercholesterolaemia. Platelets from both normal and hypercholesterolaemic subjects showed irreversible aggregation with 0.3 units ml ‐1 thrombin. Extents of aggregation were 76.3% and 90.8% respectively, platelets from hypercholesterolaemic patients being significantly more sensitive ( P < 0.002). Under resting conditions platelet noradrenaline release was 136% greater ( P <0.02) in hypercholesterolaemic patients than in normal subjects. Thrombin‐stimulated release of noradrenaline was also higher (73%, P <0.05) in hypercholesterolaemics than in normals. The differences between resting and thrombin‐stimulated release were greater for hypercholesterolaemic patients than normal subjects ( P <0.05). Under resting conditions total platelet noradrenaline levels (sum of supernatant and platelet pellet concentrations) were similar in preparations from the two groups. However, following thrombin stimulation total noradrenaline concentrations were substantially greater (86%) in platelets from hypercholesterolaemics than normals ( P <0.02). In hypercholesterolaemic patients thrombin stimulation was associated with an 101% increase (over resting levels) in total platelet noradrenaline ( P <0.01), no increases being observed with normal subjects. We suggest that platelet membranes may be more permeable in patients with familial hypercholesterolaemia leading to increased non‐specific release of catecholamines. Platelets from patients with familial hypercholesterolaemia may also be more responsive to stimulation with respect to catecholamine release. The results obtained on calculation of total platelet noradrenaline levels may indicate that abnormalities of platelet dense granules occur in familial hypercholesterolaemia. In this context the relative proportions of free and conjugated catecholamine may be of relevance. The importance of lipoprotein‐platelet interactions has been emphasized as regards the development of atherosclerosis. Platelet thrombus formation is also of undoubted importance in myocardial infarction. The platelet abnormalities described in this paper may contribute to the increased risk of premature vascular disease in patients with familial hypercholesterolaemia.