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Arch Int Pharmacodyn Ther. 1984 Jan;267(1):80-90.
Preventive and reverse effects of nifedipine on human bronchoconstriction "in vitro".

Horio S, Kohrogi H, Ando M, Sugimoto M, Araki S.

The effects of nifedipine, a calcium channel blocking agent, on human bronchoconstriction induced by acetylcholine and histamine were studied in vitro. Bronchial preparations were obtained from 13 patients undergoing surgery for bronchial carcinoma. Bronchial strips were mounted for continuous isometric tension recording. Acetylcholine and histamine caused bronchoconstrictions, but the constrictive effects were inhibited by 2.9 X 10(-6) M nifedipine. At a concentration of 2.9 X 10(-6) M nifedipine increased by 22-fold the concentration of acetylcholine required to produce a 50% of maximal contraction of bronchial strips, and by 160-fold the concentration of histamine required. Nifedipine also reversed already established bronchoconstrictions by acetylcholine and histamine. The percentage of contraction at 20 min after 2.9 X 10(-6) M nifedipine was 7 +/- 11.1% (mean +/- SEM) and - 21 +/- 20.0% of the control maximal response by 10(-3) M acetylcholine and 10(-3) M histamine, respectively. Thus, nifedipine clearly prevented and reversed pharmacologically-induced bronchoconstriction in humans. These results suggest that it is valuable to administer nifedipine to prevent and treat asthma attack.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6721626&dopt=Abstract




J Am Soc Nephrol. 1994 Dec;5(6):1385-90.
Contrasting short-term effects of nifedipine on glomerular and tubular functions in glomerulonephritic patients.

Hartmann A, Lund K, Holdaas H, Fauchald P, Reisaeter A, Berg KJ.

Medical Department B, National Hospital, Oslo, Norway.

The short-term effects of nifedipine on glomerular hemodynamics, sieving function, and renal tubular function were assessed in 10 patients suffering from biopsy-verified chronic glomerulonephritis. Three weeks of nifedipine treatment after 2 wk of placebo significantly reduced the blood pressure from 153 +/- 6/90 +/- 3 to 139 +/- 6/84 +/- 4 mm Hg (mean +/- SE; P < 0.05). Renal vascular resistance was reduced from 0.54 +/- 0.10 to 0.46 +/- 0.08 mm Hg/mL per minute. However, GFR (44.3 +/- 7 mL/min), effective RPF (265 +/- 37 mL/min), and filtration fraction (0.17 +/- 0.01) remained unchanged. The excretion of albumin of 1,318 +/- 395 micrograms/min was not affected by nifedipine. The glomerular sieving estimated by use of the fractional dextran clearance technique revealed no significant change by nifedipine compared with placebo in the range of 30 to 60 A of hydrodynamic dextran radius. Fractional proximal reabsorption (lithium clearance method) was reduced by nifedipine from 53 +/- 5 to 46 +/- 4% (P < 0.05). Also, the excretion of beta 2-microglobulin and N-acetyl-beta-glucosaminidase increased from 10.98 +/- 4.62 to 11.86 +/- 4.74 mg/24 h (P < 0.05) and from 19.7 +/- 4.2 to 25.3 +/- 7.0 nmol/h per micromoles of creatinine (P = 0.05), respectively. It was concluded that nifedipine treatment acutely represses proximal tubular function but is without significant effect on glomerular sieving and albuminuria in these patients.

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Biochem Pharmacol. 1994 Mar 2;47(5):887-92.
Absence of antioxidant effects of nifedipine and diltiazem on myocardial membrane lipid peroxidation in contrast with those of nisoldipine and propranolol.

Sugawara H, Tobise K, Onodera S.

First Department of Internal Medicine, Asahikawa Medical College, Japan.

Both the production of active oxygen species and cellular damage due to concurrent lipid peroxidation are believed to be important factors in the pathogenesis of cardiovascular diseases and the ageing process. Since cardiovascular drugs are often administered over a long term, it might be advantageous if they reduced lipid peroxidation. There have been conflicting reports concerning the antiperoxidant effect of nifedipine. Therefore, we investigated whether nifedipine could inhibit lipid peroxidation in a nonenzymatic active oxygen-generating system, utilizing rat crude myocardial membranes, and compared its effect with those of propranolol, nisoldipine, and diltiazem. Nifedipine and diltiazem had no inhibitory effects on the lipid peroxidation of myocardial membranes. In contrast, nisoldipine and propranolol had a concentration-dependent antiperoxidant effect, with IC50 values of 28.2 and 50.1 microM, respectively. In addition, nisoldipine appeared to possess dual antiperoxidant mechanisms, involving both preventive and chain-breaking properties.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8135864&dopt=Abstract













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