ABSTRACT
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, cross-over 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.
Subject(s)
Antihypertensive Agents/pharmacology , Platelet Activation/drug effects , Adult , Aged , Double-Blind Method , Drug Evaluation , Female , Humans , Hypertension/blood , Hypertension/drug therapy , Kidney Diseases/blood , Kidney Diseases/complications , Male , Middle Aged , Nisoldipine/pharmacology , Platelet Aggregation/drug effects , Platelet Count/drug effects , Platelet Factor 4/drug effects , beta-Thromboglobulin/drug effectsABSTRACT
Nine patients with overt diabetic nephropathy underwent renal scintigraphy and measurement of platelet survival time using indium-111-labelled platelets after treatment for six weeks with aspirin-dipyridamole (990 mg/225 mg/day) or placebo in a double-blind cross-over study. External scanning of the renal areas at 16 and 40 h post-injection showed no excess activity of indium-111 relative to background. Mean platelet survival was within the published normal range at 9.1 +/- 0.6 days and 7.6 +/- 1.4 days using linear and gamma function analyses respectively. Treatment with aspirin-dipyridamole was without effect. The results suggest that significant platelet deposition in renal blood vessels is not an important factor in the pathogenesis of diabetic nephropathy.
