title: Long-term treatment with nifedipine modulates procoagulant marker and C-C chemokine in hypertensive patients with type 2 diabetes mellitus.
abstract: 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.
authors.affiliation: First Department of Internal Medicine, Kansai Medical University, 10-15 Fumizono-cho, Moriguchi, Osaka 570-8507, Japan. shosaku-n@mbp.ocn.ne.jp
authors.forename: Shosaku
authors.initials: S
authors.lastname: Nomura
authors.forename: Akira
authors.initials: A
authors.lastname: Shouzu
authors.forename: Seitarou
authors.initials: S
authors.lastname: Omoto
authors.forename: Mitsushige
authors.initials: M
authors.lastname: Nishikawa
authors.forename: Toshiji
authors.initials: T
authors.lastname: Iwasaka
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000097:blood; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000097:blood; D019742:Chemokines, CC / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000150:complications* / Q000188:drug therapy* / Q000503:physiopathology; D019402:Macrophage Inflammatory Proteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D009543:Nifedipine / Q000627:therapeutic use*; D019007:P-Selectin / Q000097:blood; D015539:Platelet Activation / Q000187:drug effects*; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D015415:Biomarkers; C111835:CCL2 protein, human; D002121:Calcium Channel Blockers; D018932:Chemokine CCL2; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D019742:Chemokines, CC; D019402:Macrophage Inflammatory Proteins; D019007:P-Selectin; D019010:Vascular Cell Adhesion Molecule-1; D009543:Nifedipine