Abstract
Background and Aim: Platelets play a role in the microvascular as well as macrovascular complications of diabetic patients with serious implications in the pathogenesis of vascular disease in patients with type 2 diabetes. Hyperglycemia changes platelet functions by impairing calcium homeostasis. So, it is important to study the effect of nifedipine on platelet functions and cardiovascular complications associated with diabetes. Methods: There were 3 groups, i.e. healthy non diabetics (control), type 2 diabetics, and type 2 diabetics with nifedipine therapy (20 in each). For all, the following measurements were done: the cytoplasmic free Ca 2+ concentration, platelet aggregation, lipid profiles, arterial blood pressure and heart rate. Results: Using nifedipine significantly reduced resting and thrombin (0.5 u ⁄ml) phase 2 platelet cytosolic free calcium in the presence of (1 mM) external calcium compared with the diabetic group. Nifedipine showed no significant change in thrombin induced phase 2 platelet cytosolic free calcium in absence of external calcium compared with the diabetic group. There were no significant differences of peak platelet cytosolic free calcium (thrombin 0.5 u⁄ml) induced in the presence of 1 mM external calcium and in the absence of external calcium between all three groups. There was a significant reduction of lipid profiles except HDL in the diabetic group after nifedipine therapy compared with the diabetic group. HDL cholesterol showed significant increase after nifedipine therapy compared with the diabetic group. Conclusion: Nifedipine therapy is useful for patients with diabetes mellitus type 2 from its effects on platelet aggregation, lipid metabolism and cardiovascular functions.
Highlights
The pathophysiology of diabetic micro- and macroangiopathy may be associated with a hypercoaguable state driven by platelet hyperreactivity [1]
There was no significant change of the platelet count in the diabetic group after nifedipine therapy compared with the diabetic group alone
There was a significant reduction of resting and agonist platelet aggregation after nifedipine therapy compared with the diabetic group (Table 2)
Summary
The pathophysiology of diabetic micro- and macroangiopathy may be associated with a hypercoaguable state driven by platelet hyperreactivity [1]. This hyperactivity includes increased platelet adhesion, aggregation, thromboxane production, increased plasma levels of platelet-specific proteins, and increase of platelet turnover [2]. This may lead to increased microembolism in the capillaries and local progression of pre-existing vascular lesions [3]. It is important to study the effect of nifedipine on platelet functions and cardiovascular complications associated with diabetes
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