Summary
Abnormal activation of blood platelets may be a contributory factor in the accelerated
vascular disease which occurs in hypertension. We investigated the effects of lowering
blood pressure in 12 patients with mild hypertension on several aspects of platelet
function, initially in a placebo-controlled, double-blind, crossover study with nisoldipine,
and subsequently in the same patients comparing nisoldipine with the patients’ usual
anti-hypertensive therapy. Values were compared with those from an age, sex-matched
control population. Seven hypertensive patients with renal failure were also studied.
Administration of nisoldipine reduced ex vivo “spontaneous” aggregation of blood platelets
significantly, and a similar significant effect was seen when blood pressure was lowered
by the patients usual anti-hypertensive therapy. “Spontaneous” aggregation occurring
in the control population was similar to that in the treated hypertensives. Blood
platelet count, and aggregation in response to ADP and adrenalin were unaffected by
treatment. Median plasma beta thromboglobulin levels were significantly higher in
the untreated hypertensive patients (43 ng ml-1) than in the controls (30 ng ml-1), and there was a trend to reduced values for beta thromboglobulin on treatment of
the hypertension. These results indicate that blood platelet activity is enhanced
in hypertension and that function returns towards normal when blood pressure is lowered
by treatment.
Keywords
“Spontaneous” platelet aggregation - Blood pressure - Beta-thromboglobulin - Nisoldipine
