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Nitric oxide is a vasodilating and blood pressure lowering substance. To investigate whether calcium antagonists or angiotensin-converting enzyme (ACE) inhibitors increase vascular nitric oxide activity, we assessed systemic and renal vascular sensitivity to nitric oxide synthase inhibition in hypertensives on and off medication.
The nitroxyl anion (HNO) is the one-electron reduction product of NO(). This redox variant has been shown to be endogenously produced and to have effects that are pharmacologically distinct from NO(). This study investigates the vasodilator and chronotropic effects of HNO in the rat isolated coronary vasculature.
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Experiments on rats with the use of ultrasonic techniques demonstrated that serotonin causes an initial significant decrease in the blood flow in the channel of the middle cerebral artery followed by a mild increase in the blood supply to the brain. It was shown in in vivo experiments that nimodipine and nifedipine do not prevent the development of serotonin-induced constriction of the vessels of the middle cerebral artery channel. At the same time, the cerebrovascular effects of nimodipine and nifedipine are significantly weakened under the action of serotonin.
Silybin and related flavonolignans form a major part of the Silybum marianum extract, silymarin, which has been used to treat liver diseases for hundreds of years. Although regarded as safe, many of the extract constituents remain thus far untested for their possible effects on liver biotransformation enzymes. Cytochromes P450 (CYP) are very important in this regard. We tested the effect of four flavonolignans: silybin, its hemisynthetic derivative dehydrosilybin, silydianin, and silycristin on three specific CYP activities: bufuralol 1'-hydroxylation (CYP2D6), p-nitrophenol hydroxylation (CYP2E1), and nifedipine oxidation (CYP3A4). All flavonolignans displayed dose-dependent inhibition of these activities with IC(50) values in the micromolar range. The inhibition was competitive or mixed as revealed by double reciprocal plots of kinetic experiments. However, the inhibition is not considered to be relevant for therapy because physiological concentrations of the individual flavonolignans do not exceed 0.5 microM. The data support the use of the extract as a dietary supplement.
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Anti-obesity effects of calcium antagonists such as benidipine and nifedipine have been described in rodent obesity models, but the mode of action of the calcium antagonists as anti-obesity agents has not been established.
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Prophylactic oral nifedipine was not shown to decrease the uterine tachysystole associated with vaginal misoprostol induction at a 50-microg dose.
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Our data demonstrate that nifedipine and pregnenolone sulphate act at different binding sites when activating TRPM3. The latter activates TRPM3 by binding to a chiral and thus proteinaceous binding site, as inferred from the differential effects of the enantiomers. The double bond between position C5 and C6 of pregnenolone sulphate is not strictly necessary for the activation of TRPM3 channels, but a negative charge at position C3 of the steroid is highly important. These results provide a solid basis for understanding mechanistically the rapid chemical activation of TRPM3 channels.
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We reported the physical chemical characterization of a new series of native dextran (B110-1-2). The chemical structure of the polymer was characterized by IR, (1)H and (13)C NMR spectroscopy and compared with that of a commercial native dextran B512-F obtained from Sigma Company. Molecular weights of the product and different commercial dextran fractions of Leuconostoc mesenteroides from 43000 to 170000 average molecular weight (M(w)) were established by the analysis of intrinsic viscosity in aqueous solutions and compared with those obtained by gel permeation chromatography (GPC). The critical overlap concentration around 9g/L was obtained. No interactions of powder mixtures with different commercial excipients (lactose, cetyl alcohol, HPMC) and drugs (propranolol hydrochloride, acetyl salicyclic acid, isosorbide dinitrate, lobenzarit disodium, and nifedipine) were demonstrated by differential scanning calorimetry (DSC) analysis. Tablets obtained by direct compression showed good physical-mechanical and technological properties. Dextran B110-1-2 has similar physical chemical properties as commercial Sigma B512-F. Water uptake, erosion and dissolution profile studies for dextran tablets established that glucose polymer with molecular weight M(w) > or = 2x10(6) is suitable for the development of controlled release solid dosage forms (soluble drugs). Fraction of dextran (M(w) 40000-170000) could be more useful for immediate release tablets.
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This study aimed to compare the effects of two long-acting dihydropyridine calcium channel blockers (CCBs) with different pharmacologic properties, lercanidipine and nifedipine Gastro-Intestinal Therapeutic System (GITS), in the chronic treatment of essential hypertension. After a 4-week placebo run-in period, 60 patients of both sexes were randomly treated with lercanidipine 10 to 20 mg or nifedipine GITS 30 to 60 mg taken orally for 48 weeks, according to a double-blind, parallel group design. For the first 4 weeks of treatment, the lowest dose of each drug was used, followed by higher doses if diastolic blood pressure (BP) was >90 mm Hg. At the end of the placebo period and after 4, 8, 12, 24, and 48 weeks of active treatment BP, heart rate (HR), and plasma norepinephrine (NE) levels were assessed. Lercanidipine and nifedipine GITS similarly reduced BP values after 48 weeks (-21.7/15.9 mm Hg and -20.7/14.6 mm Hg, respectively, both P <.001 v placebo), with no change in HR. Despite the similar lack of effect on HR, the two drugs displayed different influences on plasma NE, which was significantly increased by nifedipine GITS (+56 pg/mL, P <.05 v placebo) but not by lercanidipine. These findings suggest that 1) sympathetic activation occurs during chronic therapy with nifedipine GITS but not with lercanidipine, which might be related to the different pharmacologic characteristics of the two CCBs at the doses evaluated; and 2) nifedipine GITS seems to activate peripheral but not cardiac sympathetic nerves, consistent with differing regulation of cardiac and peripheral sympathetic activity.
Data from the 7 665 participants included in the ACTION (A Coronary disease Trial Investigating Outcome with Nifedipine GITS) trial was used.