Disease relevance of Nivadil

• The mechanism of the antianginal actions of nilvadipine was investigated in 11 patients with effort angina pectoris [1].
• Compared with chest pain during control exercise testing, pain at peak exercise disappeared or abated and the ST segment at peak exercise also showed less significant depression after administration of nilvadipine [1].
• Thus, nilvadipine might prevent cerebral vascular disorders at doses routinely used for essential hypertension [2].
• We investigated the effects of nilvadipine, a calcium antagonist, on cerebral ischemia in rats [3].
• By densitometric quantification of the electrophoretically separated soluble proteins, mean +/- SEM MAP2 content in the hippocampus (14.4 +/- 1.8 micrograms/mg protein) was depleted (5.4 +/- 0.5 micrograms/mg, p less than 0.01) 4 days after ischemia; this depletion was significantly inhibited by 1 or 10 mg nilvadipine/kg/day [4].

Psychiatry related information on Nivadil

• The total scores of the Brief Psychiatric Rating Scale decreased significantly when the patients were on nilvadipine compared with placebo [5].
• We investigated the effects of the Ca(2+) antagonist nilvadipine on the dopaminergic system and motor activity in aged mice, in comparison with an other Ca(2+) antagonist, amlodipine [6].
• The total binding affinity (nK) between LDL and verapamil enantiomers was increased by 3.3-, 4.6-, 7.0-, and 19-fold after 0.5, 1, 2, and 12 h oxidation, respectively, whereas the nK value between nilvadipine and LDLwas increased by 1.3-, 1.4-, 1.4-, and 1.7-fold in the same reaction times, respectively [7].
• The BP decreased in the HCT/T group (n = 124) compared to the nilvadipine group to a similar degree (p = 0.91, n.s.) from 160/103 +/- 17/8 mm Hg by -17/-13 +/- 18/11 mm Hg [8].
• Nilvadipine may have a neuroprotective effect and could be a useful pharmacotherapeutic agent for cerebrovascular dementia [9].

High impact information on Nivadil

• At rest and at peak exercise, mean blood pressure, pulmonary artery wedge pressure and systemic vascular resistance decreased significantly, whereas heart rate and cardiac index increased significantly after nilvadipine [1].
• Coronary sinus flow at peak exercise increased significantly and total coronary vascular resistance at rest and at peak exercise decreased significantly after nilvadipine [1].
• Systolic blood pressure decreased significantly in the high-dose nilvadipine-treated group but not in the low-dose nilvadipine-treated group [2].
• Attenuated neuropathology by nilvadipine after middle cerebral artery occlusion in rats [3].
• The effects of systemic administration of 1 microg/kg per hour nilvadipine (a calcium antagonist), 300 microg/kg Nomega-nitro-l-arginine (l-NAME, a nonselective NOS inhibitor), and 5 mg/kg indomethacin or sympathetic nerve amputation on the changes in NB after reduction of IOP were studied [10].

Chemical compound and disease context of Nivadil

• To examine the pathologic molecular mechanism of CAR, and to elucidate an effective therapy for CAR, the function and morphology of CAR were compared with those of phototoxic retinal damage, another form of photoreceptor dysfunction, and the effect of nilvadipine, a Ca(2+) antagonist, on the retinal degenerations was studied, using these models [11].
• Effects of calcium channel entry blockers, nifedipine and nilvadipine, on colonic motor activity [12].
• The effects of five dihydropyridine slow channel calcium blocking agents, nifedipine, nitrendipine, FR 34235, niludipine and nisoldipine were compared to those of the peripheral vasodilator hydralazine on the reflex bradycardia and tachycardia after abrupt increases and decreases in arterial pressure in conscious dogs [13].
• The purpose of the present study was to compare the effects of a new calcium channel blocker, FR 34235, on the distribution of blood flow between subendocardium and subepicardium (endo/epi) distal to a proximal flow-limiting coronary artery stenosis, with those of nifedipine and diltiazem in anesthetized dogs [14].
• Beneficial effects of the dihydropyridine calcium antagonist, FR 34235, in a chronic coronary occlusion model [15].

Biological context of Nivadil

• The inhibitory effects of delapril were more prominent than those of nilvadipine, although both drugs reduced right ventricular pressure to the same extent [16].
• Nisoldipine, FR 34235 and nifedipine produced the greatest coronary vasodilation whereas niludipine, nitrendipine and hydralazine were less effective [17].
• The chemotaxis, irrespective of the attractants used, was strongly inhibited by nilvadipine, a potent calcium antagonist, and the IC50 values were around 1 x 10(-10) M [18].
• Smooth muscle cell migration induced by inflammatory cell products and its inhibition by a potent calcium antagonist, nilvadipine [18].
• Multiple-dose pharmacokinetics of nilvadipine in healthy volunteers [19].

Anatomical context of Nivadil

• CONCLUSIONS: These data suggest that nilvadipine is beneficial for the preservation of photoreceptor cells in RCS rats and can be used to treat some patients with RP [20].
• Effects of nilvadipine, a calcium antagonist, on rabbit ocular circulation and optic nerve head circulation in NTG subjects [21].
• CONCLUSIONS: Nilvadipine increased blood velocity and, probably, blood flow in the ONH, choroid, and retina of rabbits [21].
• Antiatherogenic activity of FR34235 (Nilvadipine), a new potent calcium antagonist. Effect on cuff-induced intimal thickening of rabbit carotid artery [22].
• These results suggest that inflammatory cells such as macrophages and polymorphonuclear leukocytes (PMN) have an important role in the migration of SMC into the intima during atherogenesis, and that nilvadipine might be useful for preventing and treating atherosclerosis [18].

Associations of Nivadil with other chemical compounds

• The effects of systemic administration of 1 micro g/kg per hour nilvadipine (a calcium antagonist), 30 mg/kg N(omega)-nitro-L-arginine (L-NAME), or 5 mg/kg indomethacin, or those of sympathetic nerve amputation on the time course of the changes in NB were studied [23].
• By optimizing chromatographic conditions such as column temperature and flow rate, the baseline separation of nilvadipine enantiomers was attained with a short analysis time and with a column efficiency comparable to commercially available chiral stationary phases based on a protein, such as ovomucoid or alpha1-acid glycoprotein [24].
• We determined the effect of nilvadipine, a dihydropyridine-type calcium channel blocker, in preventing glutamate neurotoxicity in purified retinal ganglion cells (RGCs) [25].
• It is suggested that some types of Ca(2+) channel blockers, such as nilvadipine and nicardipine, are able to preserve photoreceptor cells in rd mouse and can potentially be used to treat some RP patients [26].
• In addition, the application of nilvadipine significantly reduced glutamate-induced apoptosis (P<0.001) [25].

Gene context of Nivadil

• On the other hand, no inhibition of CYP2B6-mediated 7-benzyloxyresorufin O-debenzylation, CYP2D6-mediated bufuralol 1'-hydroxylation, or CYP2E1-mediated chlorzoxazone 6-hydroxylation by nilvadipine at 40 microM concentration was observed [27].
• The clinical course and laboratory findings suggest that carbamazepine decreased the plasma concentration and hence the antihypertensive effect of nilvadipine probably via CYP3A induction [28].
• 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 [29].
• The effects of nilvadipine, a dihydropyridine calcium antagonist, on cytochrome P450 (CYP) activities in human hepatic microsomes were investigated [27].
• Studies using immunohistochemistry, RT-PCR, and Western blot analysis revealed significant enhancement of rhodopsin kinase and alphaA-crystallin expression and suppression of caspase 1 and 2 expression in the retina of nilvadipine-treated rats [20].

Analytical, diagnostic and therapeutic context of Nivadil

• We investigated the efficacy of nilvadipine, a calcium channel inhibitor, for psychiatric symptoms and tardive dyskinesia in 30 patients with chronic schizophrenia in a placebo-controlled double-blind crossover study [5].
• Twenty-four hours after the occlusion, the percentage infarct volumes in nilvadipine-treated animals in groups 1-3 (21 +/- 11%, 24 +/- 11%, and 26 +/- 7%, respectively) were smaller than those in the respective control groups (36 +/- 5%, 35 +/- 3%, and 35 +/- 3%; P < 0.05) [30].
• Nilvadipine restored cortical perfusion levels in Tg APPsw to values similar to those observed in control littermates without notably affecting the CBF of control mice [31].
• The versatility of the HPFA method using a diol-silica column was demonstrated by developing a novel on-line HPFA-chiral HPLC system for a simple and easy determination of the unbound concentration of nilvadipine (NV) enantiomers [32].
• In addition, we performed DNA microarray analysis both in nilvadipine treated and control retinas to understand their drug effects at molecular levels [26].

References