Disease relevance of nicardipine

• Nicardipine and urinary retention [1].
• The effects of the slow calcium channel blocker nicardipine on the synchrony of left ventricular filling were examined in eight patients with angina pectoris [2].
• With exercise to ischemia, nicardipine preserved the salutary effects on left ventricular function seen at rest and significantly blunted the increase in left ventricular end-diastolic pressure observed in the control setting [3].
• In conclusion, long-term antianginal therapy with propranolol or nicardipine improved several markers of myocardial ischemia in approximately two-thirds of the patients [4].
• Comparative effects of nicardipine, a new calcium antagonist, on size of myocardial infarction after coronary artery occlusion in dogs [5].

Psychiatry related information on nicardipine

• The use of nicardipine for electroconvulsive therapy: a dose-ranging study [6].
• Slow-release nicardipine caused a significant reduction in distension-induced activity (P less than 0.05) but did not alter rectal sensory thresholds [7].
• In the last 15 years, the main efforts were aimed to develop sustained or controlled release formulations of nicardipine to improve patient compliance by reducing the number of doses required each day [8].
• In the patients with irritable bowel syndrome, standard nicardipine caused a significant reduction in distension-induced rectal motor activity (P less than 0.05) and increased the rectal sensory thresholds for desire to defecate and discomfort (P less than 0.02) [7].

High impact information on nicardipine

• Thyroid carcinoma in rats has been associated with treatment with nicardipine and after exposure to several aromatic hydrocarbons.(ABSTRACT TRUNCATED AT 400 WORDS)[9]
• The calcium antagonists nifedipine, nicardipine, and diltiazem did not compete for the same binding site [10].
• The Ca2+ responses to endothelin and thrombin were not affected by nicardipine (1 microM), (+) Bay K 8644, or Ca2+-free solutions [11].
• Nicardipine, a calcium channel blocker, also increased the skin blood flow, but the blood flow increment and blood pressure fall were comparable [12].
• In the Montreal Heart Institute trial, nicardipine did not influence the overall rate of progression and regression; however, nicardipine-treated patients experienced significantly less progression of minimal lesions, defined as stenoses of < or = 20% severity [13].

Chemical compound and disease context of nicardipine

• In the second experiment, rats received 0.05% captopril, 0.02% enalapril, or 0.02% nicardipine in the drinking water for 1 day before and for 48 hours after the induction of renal artery stenosis or sham operation [14].
• Noninvasive assessment of the direct action of oral nifedipine and nicardipine on left ventricular contractile state in patients with systemic hypertension: importance of reflex sympathetic responses [15].
• A placebo-controlled, double-blind multicenter trial was conducted in 123 patients with severe hypertension to examine the efficacy and safety of intravenously administered nicardipine hydrochloride in controlling blood pressure [16].
• The interference by two unrelated calcium entry blockers, nicardipine and verapamil, with the forearm vascular response to graded exogenous norepinephrine was evaluated in two groups (n = 6 each) of patients with uncomplicated hypertension [17].
• The RR reduction of angiographically detected cerebral vasospasm was statistically significant for AT877 (38%; 95% CI, 17 to 54%) and nicardipine (21%; 95% CI, 6 to 34%) but not for nimodipine (9%; 95% CI, -2 to 19%) [18].

Biological context of nicardipine

• This suggested blood pressure reduction may account for the beneficial action of nicardipine [19].
• In humans at rest, intravenous nicardipine administration produced pronounced coronary and systemic vasodilation with improved left ventricular systolic performance and enhanced relaxation accompanied by reflex sympathetic activation [3].
• Effects of nicardipine on regional diastolic left ventricular function in patients with angina pectoris [2].
• Both effects were blocked by L-type Ca2+ channel antagonists (nicardipine, calciseptine) and were occluded by the L-type channel agonist BayK 8644-arguing that the D1 receptor-mediated effects on evoked activity at depolarized membrane potential were mediated by enhancement of L-type Ca2+ currents [20].
• Surprisingly, the two dihydropyridine class calcium channel blockers, nimodipine and nicardipine, also failed to enhance cisplatin's antitumor actions despite the fact that their specificity and kinetics for binding to the dihydropyridine receptor component of the calcium channel favors them (nimodipine and nicardipine) over nifedipine [21].

Anatomical context of nicardipine

• Thus, nicardipine administered before or early after coronary artery occlusion limited infarct size by 37% to 49%, whereas when administration was delayed for 3 hr infarct size was not reduced [5].
• Furthermore, nicardipine had more striking effects on the ischemic myocardium of dogs with small hypoperfused zones than on that of dogs with large hypoperfused zones [5].
• In isolated feline papillary muscle, nicardipine produced a dose-dependent calcium antagonistic effect manifested by depressed indexes of contraction and relaxation [3].
• The effects of calcium antagonists (verapamil, diltiazem, and nicardipine) on beta-adrenergic receptors of cultured cardiac myocytes isolated from neonatal rat ventricle were studied with the hydrophilic ligand [3H]CGP-12177, which identifies cell surface-bound beta-receptors [22].
• Nicardipine prevents calcium loading and "oxygen paradox" in anoxic single rat myocytes by a mechanism independent of calcium channel blockade [23].

Associations of nicardipine with other chemical compounds

• Arterial and coronary sinus blood samples and coronary blood flow measurements were obtained before and after 1 month of oral administration of propranolol or of the calcium antagonist nicardipine [4].
• Inward currents were also completely blocked by the dihydropyridine Ca2+ channel blocker, nicardipine (10 mumol/L), suggesting the presence of predominantly L-type Ca2+ channels in rabbit portal vein cells [24].
• The interaction of AVP with the sympathetic nervous system may be independent of the state of the renin-angiotensin system, since the exaggeration of RSNA by AVP antagonist was qualitatively the same with nicardipine as with captopril [25].
• Totally noninvasive techniques showed a differential effect on left ventricular contractility between nifedipine and nicardipine when alterations in afterload and reflex sympathetic responses were eliminated as confounding variables [15].
• Both plasma renin activity (p less than 0.05) and norepinephrine (p less than 0.005) were significantly increased with nicardipine therapy [26].

Gene context of nicardipine

• The increase in BDNF mRNA expression induced at high K(+) was repressed not only by nicardipine, an antagonist for L-VDCC, but also by dl-amino-5-phosphonovalerate, an antagonist for NMDA-R, which was supported by the effects of antagonists on the Ca(2+) influx [27].
• Intracellular mobilization was linked to increases in IP3 turnover because 1 microM ET-1 increased IP3 content by 48% from its control value (EC50 = 23 nM), whereas Ca2+ influx occurred through a non-L-type Ca2+ channel because preexposure to 1 microM nicardipine did not affect either the height or the duration of a [Ca2+]i transient [28].
• The IC(50) values for the inhibition of CYP2D6 and CYP2C9 for nicardipine were 3 to 9 microM, whereas those for all others ranged from 14 to >150 microM [29].
• Niguldipine, nicardipine, and nitrendipine also demonstrated potent BCRP inhibition, whereas nifedipine had no effect [30].
• Nicardipine strongly inhibited two-pathways of triazolam hydroxylation both catalyzed by CYP3A4 [31].

Analytical, diagnostic and therapeutic context of nicardipine

• Increases in RSNA induced by captopril and nicardipine were larger by central infusion of AVP antagonist than by intravenous infusion [25].
• In this report, we studied the results of the long-term use of nicardipine after liver transplantation [32].
• Nicardipine as antihypertensive therapy in liver transplant recipients: results of long-term use [32].
• Nicardipine increased RBF (P less than .01), GFR (P less than .05), and urinary Na+ excretion (P less than .01) and decreased total renal vascular resistance (P less than .01) in groups A and B, but these parameters remain unchanged in group C. The filtration fraction remained unaltered in all groups [33].
• Short- and long-term efficacy of nicardipine, assessed by placebo-controlled single- and double-blind crossover trials in patients with chronic stable angina [34].

References