Disease relevance of Flivas

• Effect of naftopidil on urethral obstruction in benign prostatic hyperplasia: assessment by urodynamic studies [1].
• Using a rat model of detrusor overactivity caused by cerebral infarction (CI), we undertook the present study to determine whether the effect of an alpha1-blocker, naftopidil, is dependent on the suppression of C-fiber afferents [2].
• We investigated the mechanism for the differential effects of naftopidil and prazosin on the development of postural hypotension, with special attention on their selectivity for the alpha1-adrenoceptor subtype [3].
• The disappearance of involuntary contraction and the greater increase in first-desire volume with naftopidil may be associated with the relief of nocturia [4].
• Reduction of functional hepatic blood flow in chronic liver disease or, as evidenced in one case as a consequence of shunt surgery, is the probable cause of the observed alteration in naftopidil kinetics [5].

High impact information on Flivas

• The alpha(1D) antagonist naftopidil (0.75 to 1.66 mg/kg) was administered intravenously into the external jugular vein [6].
• Single-blind, randomized controlled study of the clinical and urodynamic effects of an alpha-blocker (naftopidil) and phytotherapy (eviprostat) in the treatment of benign prostatic hyperplasia [7].
• Effects of intrathecal injection of tamsulosin and naftopidil, alpha-1A and 1D adrenergic receptor antagonists, on bladder activity in rats [8].
• Thirty-two patients with voiding dysfunction attributable to symptomatic benign prostatic hyperplasia were treated with naftopidil, an alpha 1-blocker, at doses of 25-75 mg/day for 4-6 weeks [1].
• CONCLUSIONS: These results suggest that naftopidil has an inhibitory effect on C-fiber afferents in the lumbosacral spinal cord, improving BC during the storage phase [2].

Chemical compound and disease context of Flivas

• Comparison of tamsulosin and naftopidil for efficacy and safety in the treatment of benign prostatic hyperplasia: a randomized controlled trial [9].
• Newly developed alpha1-adrenoceptor antagonists including naftopidil are free from the "prazosin-like" side effect of orthostatic hypotension and associated symptoms [3].

Biological context of Flivas

• The inhibition of Ca2+ mobilization was not reflected by a concentration-dependent inhibition of platelet aggregation, although 40 microM naftopidil produced statistically significant inhibition (23.3 +/- 11.7%, P < 0.05) [10].
• I.v. administration of naftopidil significantly increased BC in CI rats without an increase in residual volume, but it had no effects on BC in RTX-CI rats [2].
• Both prazosin and urapidil showed similar affinity to [3H]-prazosin binding sites in human tissue, whereas YM617 and naftopidil showed approximately a 12 and two times higher affinity, respectively, to alpha 1-adrenoceptor sites of prostate than aorta [11].
• The pharmacological profiles of the alpha1-adrenoceptor antagonists naftopidil, tamsulosin and prazosin were studied in an anesthetized dog model that allowed the simultaneous assessment of their antagonist potency against phenylephrine-mediated increases in prostatic pressure and mean blood pressure [12].
• Pharmacokinetics of naftopidil, a novel anti-hypertensive drug, in patients with hepatic dysfunction [5].

Anatomical context of Flivas

• Therefore, in addition to the antagonistic action of these agents on the alpha-1 adrenergic receptors of prostatic smooth muscle, both agents (especially naftopidil) may also act on the lumbosacral cord, and thus may improve collecting disorders in patients with benign prostatic hyperplasia [13].
• 3H-prazosin and 3H-clonidine binding to the rat cortex membranes was inhibited by KT-611 with pKi values of 7.69 and 5.75, respectively [14].
• Thus, it is suggested that naftopidil antagonizes alpha 1-adrenoceptors in human prostates in a competitive and reversible manner [15].
• KT-611 also inhibited the sympathetic adrenergic contraction evoked by electrical transmural stimulation in the dog mesenteric artery, and the inhibition was not relieved upon repetitive washing for 1 hour with the drug-free solution [14].
• Naftopidil exerts its antihypertensive action via alpha 1-adrenoceptor blockage and Ca2+ antagonism in vascular smooth muscle [16].

Associations of Flivas with other chemical compounds

• However, naftopidil (40 microM) inhibited serotonin-induced platelet aggregation (23.9%, 95% confidence interval (CI) 10.7 to 37.1%; P < 0.01) and caused a slight shift to the right of the adrenaline dose-response curve with a mean increase in the EC50 value of 0.5 microM (95% CI 0.07 to 0.93 microM; P < 0.05) [17].
• The effects of intrathecal injection of tamsulosin (an alpha-1A adrenergic receptor antagonist) and naftopidil (an alpha-1D adrenergic receptor antagonist) on isovolumetric bladder contraction were investigated in rats under urethane anesthesia [13].
• 2. Prazosin, YM617, naftopidil and urapidil competed with [3H]-prazosin for the binding sites in a dose-dependent manner in the prostate and aorta of humans [11].
• No effect of naftopidil, urapidil and verapamil was observed on the Na+,K(+)-pump activity or on the number of active Na(+)-pump units in human erythrocytes, leukocytes or platelets [18].
• We examined the effects of the alpha(1)-adrenoreceptor blockers naftopidil and doxazosin and the Ca(2+) antagonist nifedipine on platelet function with reference to stimulus-induced thromboxane (TxB(2)) generation and platelet-derived growth factor (PDGF) efflux [19].

Gene context of Flivas

• Naftopidil, a novel antihypertensive compound, possesses 5-HT1A agonistic properties in addition to being an alpha 1-adrenoceptor antagonist [20].
• However, the responses mediated through prejunctional alpha 2-adrenoceptors (rat vas deferens), beta-adrenoceptors (rat atria), muscarinic receptors (guinea pig ileum) and 5-HT2 receptors (dog mesenteric artery) were little affected by KT-611 [14].
• Naftopidil had no effect on collagen-induced PDGF release [19].
• The metabolism of 14C-naftopidil ((R,S)-1-(2-methoxyphenyl)-1-piperazinyl-3- (1-naphthyl-oxy-2-propanol, CAS 57149-07-2) and the pharmacodynamic action of the metabolites was investigated [21].

Analytical, diagnostic and therapeutic context of Flivas

• High-performance liquid chromatography of naftopidil, a novel antihypertensive drug, and two metabolites in human plasma [22].
• Binding properties of naftopidil and alpha 1-adrenoceptor antagonists to alpha-adrenoceptors in prostates from benign prostatic hypertrophy (BPH) were characterized by radioreceptor assays using [3H]prazosin and [3H]rauwolscine [15].
• An alpha 1-adrenergic radiorecptor assay (RRA) was developed to determine receptor-binding material (parent compound and active metabolites) in the plasma of rats following single oral administration of naftopidil (50 mg/kg) [23].
• The effects of naftopidil on the intracellular concentration and transmembrane fluxes of Na+ and K+ in erythrocytes and on the intracellular Na+, K+ and free cytosolic Ca2+ concentration in platelets were studied in twenty-four normal male subjects, using a double-blind study design [24].
• Usefulness of tamsulosin hydrochloride and naftopidil in patients with urinary disturbances caused by benign prostatic hyperplasia: a comparative, randomized, two-drug crossover study [25].

References