Drugs online research references
Circ Res. 1983 Feb;52(2 Pt 2):I115-9.
Inhibition of platelet aggregation by diltiazem. Comparison with verapamil and nifedipine and inhibitory potencies of diltiazem metabolites.
Kiyomoto A, Sasaki Y, Odawara A, Morita T.
The inhibitory effects of three calcium blockers, diltiazem (d-form), verapamil, and nifedipine, on ADP- and collagen-induced platelet aggregation of human and rabbit platelets were compared. The potency of diltiazem was greater than those of verapamil and nifedipine in human platelet-rich plasma. A similar order of the inhibitory potencies was observed in rabbit platelet-rich plasma, but this order was reversed when washed platelets were aggregated in buffered saline. Antiaggregatory potencies of metabolites on diltiazem and their optical isomers were examined in human platelet-rich plasma. All the metabolites except deacetyl-N-demethyl diltiazem showed greater activity than diltiazem in ADP- or collagen-induced platelet aggregation. The potencies of the l-isomers of the deacetyl-N-demethyl metabolites were greater than those of the d-isomers. On the other hand, the inhibitory effect of the d-isomer of deacetyl-O-demethyl diltiazem was greater than that of the l-form at lower concentrations, whereas the relationship was opposite at higher concentrations. There was no marked difference in antiaggregatory potency between the d- and l-forms of diltiazem and N-demethyl diltiazem.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6831645&dopt=Abstract
Cardiovasc Res. 1999 Jun;42(3):752-60.
Nifedipine improves endothelial function in hypercholesterolemia, independently of an effect on blood pressure or plasma lipids.
Verhaar MC, Honing ML, van Dam T, Zwart M, Koomans HA, Kastelein JJ, Rabelink TJ.
Department of Nephrology and Hypertension, University Hospital, Utrecht, Netherlands.
OBJECTIVE: Dihydropyridine calcium antagonists have been shown to retard atherogenesis in animal models and to prevent the development of early angiographic lesions in human coronary arteries. Endothelial dysfunction is an early event in the pathogenesis of cardiovascular disease. We investigated whether nifedipine could improve endothelial function in hypercholesterolemia, independently of changes in blood pressure or plasma lipids. METHODS: First, we compared in vivo forearm vascular responses to the endothelium-dependent and independent vasodilators serotonin (5-HT) and sodium nitroprusside (SNP) in 11 patients with familial hypercholesterolemia before and after 6-weeks treatment with nifedipine GITS (60 mg, OD) and in 12 matched controls. In a subgroup of six control subjects forearm vascular function was also assessed before and after 6-weeks nifedipine GITS treatment. In vitro, we subsequently explored possible mechanisms underlying the effect of nifedipine on endothelial function. We investigated the effects of nifedipine on both NO production by recombinant endothelial NO synthase (eNOS) and endothelial cells, using 3H-arginine conversion, as well as on superoxide generation by endothelial cell lysates, using lucigenin enhanced chemiluminescence. RESULTS: In hypercholesterolemia 5-HT-induced vasodilation was impaired (47 +/- 9% increase in forearm bloodflow vs. 99 +/- 8% in controls). Treatment with nifedipine completely restored 5-HT-induced vasodilation (113 +/- 13%), whereas it did not influence basal forearm vasomotion or SNP-induced vasodilation. Nifedipine did not alter forearm vascular responses in control subjects and did not alter blood pressure or plasma lipids. In vitro, we found no direct effect of nifedipine on NO production by recombinant eNOS or endothelial cells. However, we did observe a reduction in endothelial superoxide generation. CONCLUSIONS: Our data show that nifedipine improves endothelial function in hypercholesterolemia. It is suggested from our in vitro experiments that this effect is due to reduced NO degradation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10533616&dopt=Abstract
Biochim Biophys Acta. 1990 Jan 23;1051(1):14-20.
Elevation of bovine endothelial cell angiotensin converting enzyme by cationophores and inhibition by ouabain.
Dasarathy Y, Fanburg BL.
Department of Medicine, New England Medical Center, Boston, MA 02111.
We recently reported that calcium ionophore A23187 causes a several-fold elevation of angiotensin converting enzyme (ACE) activity of bovine pulmonary artery endothelial cells in culture and that this elevation is dependent upon extracellular calcium. Now we have observed that monensin, a sodium ionophore, also elevates the ACE activity of these cells. This elevation in ACE was not inhibited by 0.2 mM EGTA or the calcium channel inhibitor nifedipine, and monensin did not alter intracellular calcium as measured by fluorimetric assessment of fura-2/AM-loaded cells. When confluent endothelial cells were incubated with monensin or A23187 in the presence of 10-20 nM ouabain, a specific inhibitor of Na+/K(+)-ATPase, the elevation in ACE produced by both of the ionophores was totally eliminated. Concentrations of ouabain greater than 10 nM also inhibited baseline levels of ACE activity. Ca2+ measurements of fura-2/AM-loaded cells showed that ouabain had no effect on the influx of Ca2+ produced by A23187. The elevation of ACE seemed to require new protein synthesis, since 0.1 micrograms/ml cycloheximide inhibited the elevation produced by monensin and A23187. Other sodium transport inhibitors such as amiloride or bumetanide had no effect on ACE elevation caused by monensin. These results suggest that ACE levels of bovine endothelial cells in culture are under cation regulation and may be modulated by ouabain-sensitive Na+/K(+)-ATPase.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2153415&dopt=Abstract
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