In
type 2 diabetes mellitus, there is increased risk of nephropathy and cardiovascular complications and the incidence of
renal failure increases in advanced stages of the disease.
Nifedipine, a
dihydropyridine-type
calcium antagonist, improves endothelial function in
hypercholesterolemia by enhancing
nitric oxide function, and increases endothelial
nitric oxide bioavailability by antioxidative mechanisms. We administered
nifedipine, 50 mg/day, to the hypertensive patients for 12 months. There were no other changes in any of the patient's pharmacologic regimen during
nifedipine treatment. Clinical and biochemical data obtained before and after
nifedipine administration were compared. All markers were measured by ELISA. The levels of platelet activation markers (CD62P, CD63, PAC-1, and
Annexin V), microparticles (
PDMP and
MDMP),
RANTES and soluble adhesion markers (sP-selectin and sVCAM-1) differed in the control group and the
hypertension group. The levels of these markers were also different in hypertensive patients with and without
type 2 diabetes but were unchanged in patients without diabetes in comparison to the control group. However, the concentrations of MDMPs,
chemokines, and soluble adhesion markers in hypertensive patients without
type 2 diabetes decreased significantly following
nifedipine treatment, although the level of
RANTES was unchanged. Systolic blood pressure correlated with CD62P, CD63,
annexin V, and
RANTES levels, and diastolic blood pressure with CD62P and
annexin V levels. The effect of
nifedipine on platelet activation markers and
C-C chemokines in the present study indicates potential effectiveness of
calcium antagonist
therapy for hypertensive patients with
type 2 diabetes.