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Eur J Pharmacol. 1993 Feb 15;244(3):269-75.
Dihydropyridine Ca2+ channel antagonists inhibit the salvage pathway for DNA synthesis in human vascular smooth muscle cells.

Agrotis A, Little PJ, Saltis J, Bobik A.

Baker Medical Research Institute, Alfred Baker Medical Unit, Alfred Hospital, Prahran, Victoria, Australia.

We examined the mechanisms by which Ca2+ channel antagonists inhibit the growth of smooth muscle cells by determining their effect on epidermal growth factor (EGF)-stimulated (i) induction of the early signalling gene, c-fos, (ii) incorporation of [3H]thymidine into cells as a measure of DNA synthesis, and (iii) increase in cell number. Verapamil, diltiazem, and the dihydropyridines felodipine, MDL 72892 A-15 (MDL) and nisoldipine had no effect on EGF-stimulated c-fos mRNA induction. Furthermore, only small inhibitory effects were observed on EGF-stimulated increases in cell number; felodipine, MDL, and nisoldipine at 0.3 microM inhibited EGF-stimulated cell proliferation by 9, 11, and 15%, respectively. In contrast, the dihydropyridine Ca2+ channel antagonists were found to be potent inhibitors of [3H]thymidine incorporation suggesting that they inhibit DNA synthesis. However, further examination revealed that the potent effects of dihydropyridine Ca2+ channel antagonists on [3H]thymidine incorporation were due not to an effect on incorporation of [3H]thymidine into DNA, but to a marked inhibitory effect on the cellular uptake of [3H]thymidine. Thus, we conclude that the small antiproliferative effects of the dihydropyridine antagonists are predominantly due to their ability to inhibit the activity of the salvage pathway for thymidylate synthesis in human vascular smooth muscle cells.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8458401&dopt=Abstract

Jpn Heart J. 1977 Jan;18(1):120-31.
Cardiohemodynamic effects of SK&F 24260, D 600, diltiazem, dilazep, and trimetazidine in the dog.

Imai Y, Himori N, Taira N.

The cardiohemodynamic effects of a hypotensive agent, SK&F 24260, and coronary vasodilators, diltiazem, dilazep, and trimetazidine, and D 600 were studied in anesthetized open-chest dogs. The systemic blood pressure, cardiac output (pulmonary arterial flow), venous return (sum of the inferior and superior caval flow) right atrial pressure and heart rate were measured. All 5 drugs decreased the systemic blood pressure and heart rate and increased the right atrial pressure. The venous return and the cardiac output were reduced by higher doses of all the 5 drugs. However, SK&F 24260 in a wide range of doses greatly and diltiazem slightly but clearly increased the venous return and cardiac output. It appears that SK&F 24260 afects predominantly blood vessels whereas the other drugs affect rather the heart to produce a negative inotropic action.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=846043&dopt=Abstract

Circ Res. 1993 Jun;72(6):1218-28.
Mechanisms of oxygen-induced contraction of ductus arteriosus isolated from the fetal rabbit.

Nakanishi T, Gu H, Hagiwara N, Momma K.

Department of Pediatric Cardiology, Heart Institute, Tokyo Women's Medical College, Japan.

The present study was designed to investigate the effect of O2 on intracellular Ca concentration ([Ca]i) in the ductus arteriosus and the mechanisms for O2-induced ductal contraction. The force of isometric contraction of the ring of the ductus arteriosus isolated from fetal rabbits at 30 days of gestation (term, 31 days) was measured. The ductus arteriosus was loaded with fura 2, a calcium-sensitive dye, and [Ca]i was determined from the ratio of fluorescence intensity at 340 and 380 nm excitation wavelengths. The ductus arteriosus was initially superfused with hypoxic control solutions and contraction was induced by application of oxygenated solutions. The O2-induced contraction of the ductus arteriosus was associated with increases in [Ca]i and was eliminated in the absence of extracellular calcium. An increase in [K]o from 5 to 50 mM, which causes membrane depolarization, induced ductal contraction. The calcium channel blockers verapamil, diltiazem, and nickel caused a similar inhibition of O2-induced contraction as well as KCl-induced contraction. The role of intracellular calcium stores in O2-induced ductal contraction was examined using ryanodine, an inhibitor of calcium uptake and release from the sarcoplasmic reticulum. The inhibition of O2-induced contraction by ryanodine was minimal. Infusion of glibenclamide, an inhibitor for opening the ATP-sensitive potassium channel, caused contraction of the ductus arteriosus in the hypoxic solution. Cromakalim, an opener of ATP-sensitive potassium channels, completely relaxed the contraction induced by O2. These data suggest that O2 increases [Ca]i and causes contraction in the ductus arteriosus. Application of O2 may change from anaerobic to aerobic metabolism and depolarize membrane potential by closing the ATP-sensitive potassium channel, which in turn increases calcium influx via the voltage-dependent calcium channel. Mechanisms other than the ATP-sensitive potassium channel may also be involved in the O2-induced contraction and remain to be studied.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8495551&dopt=Abstract

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