Effects of nilvadipine on cytokine-levels and soluble factors in collagen disease complicated with essential hypertension.
We examined some immunological parameters, particularly cytokines and soluble factors in collagen diseases complicated with essential hypertension. We also investigated the effects of Nilvadipine on immunological parameters after treatment with this drug for six months. The frequency of helper/inducer T cells (CD4+ CD8- cells, CD4+ CD45RA- cells) decreased in the peripheral blood on a 6 month treatment with nilvadipine. There was a significant decrease of suppressor/inducer T cells (CD4+ 45RA+ cells), and an insignificant decrease of activated T cells (CD3+ HLA-DR+ cells) and memory T cells (CD45RA- CD45RO+ cells) after treatment. Before treatment with Nilvadipine, interleukin-1beta, tumor necrosis factor-a, and interleukin-6 levels increased higher in the patients than in healthy volunteers. However, interleukin-1beta and interleukin-6 concentrations tended to decrease after treatment with Nilvadipine. Besides, tumor necrosis factor-alpha decreased significantly after treatment. The soluble interleukin-2 receptor concentrations also showed a decreased tendency after treatment, although high concentrations were found in the patients before treatment. In contrast, soluble human leukocyte antigen-1 and soluble thrombomodulin levels showed no significant change after treatment. These results suggest that Nilvadipine inhibits the generation of cytokines derived from activated T lymphocytes. Nilvadipine, calcium antagonist, may be useful for inhibition of vascular complication in collagen diseases.
Kagawa
H
H
The First Department of Internal Medicine, Kansai Medical University, Moriguchi, Osaka, Japan.
Nomura
S
S
Ozaki
Y
Y
Nagahama
M
M
Fukuhara
S
S
D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000187:drug effects; D016516:CD4-CD8 Ratio; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D003095:Collagen Diseases / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000276:immunology; D016207:Cytokines / Q000097:blood* / Q000187:drug effects; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D015798:HLA-DR1 Antigen / Q000187:drug effects / Q000276:immunology; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000209:etiology* / Q000276:immunology; D007375:Interleukin-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D017493:Leukocyte Common Antigens / Q000187:drug effects / Q000276:immunology; D008213:Lymphocyte Activation / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D009543:Nifedipine / Q000031:analogs & derivatives* / Q000494:pharmacology; D015375:Receptors, Interleukin-2 / Q000097:blood / Q000187:drug effects; D012189:Retrospective Studies; D016176:T-Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D006377:T-Lymphocytes, Helper-Inducer / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects / Q000378:metabolism
D002121:Calcium Channel Blockers; D016207:Cytokines; D015798:HLA-DR1 Antigen; D007375:Interleukin-1; D015850:Interleukin-6; D015375:Receptors, Interleukin-2; D014409:Tumor Necrosis Factor-alpha; C035100:nilvadipine; D017493:Leukocyte Common Antigens; D009543:Nifedipine