Disease relevance of Bunazosin

• Bunazosin (3 x 10(-6) M) abolished the facilitatory effect of hypoxia on beta-adrenoceptor mediated abnormal automaticity [1].
• CONCLUSIONS--These results indicate that long term treatment with bunazosin hydrochloride reduces blood pressure and leads to the regression of cardiac hypertrophy in SHR [2].
• Assuming that the site of action is in the central nervous system, bunazosin was injected intracerebroventricularly (i.c.v.). It produced hypotension accompanied by decreases in heart rate and abdominal sympathetic nerve activity [3].
• In the bunazosin group, none developed arrhythmias [4].
• We conclude that with appropriate dose titration, bunazosin retard is well tolerated and preserves renal blood flow when used to treat hypertension in patients with renal insufficiency [5].

High impact information on Bunazosin

• The voltage-dependent block and use-dependent block of the maximal rate of rise (Vmax) of action potentials by bunazosin (10(-5) to 10(-4) M) and yohimbine (10(-6) to 10(-5) M) were studied [1].
• The analysis of the onset and recovery kinetics from the use-dependent block of drugs showed that both bunazosin and yohimbine act as slow kinetic drugs [1].
• Although addition of bunazosin to L-NAME restored systolic blood pressure to the control level, PAC and AT1-R numbers remained significantly higher than those of control level [6].
• Topically instilled bunazosin at 0.01% partly inhibited both of these vasoconstrictions on the ipsilateral side, but not on the contralateral side [7].
• Sodium nitroprusside, but not timolol or bunazosin, also significantly prevented the NMDA-induced reduction of cell numbers in the GCL and IPL thickness [8].

Chemical compound and disease context of Bunazosin

• Effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) were measured in 53 hypertensive patients (26 renally impaired, 27 with normal renal function) before and after treatment with sufficient bunazosin retard or prazosin to control their high blood pressure [5].
• Intravenous administration of four alpha 1-antagonists-prazosin, bunazosin, SM-2470, and YM-617-produced no changes or decreases in heart rate, in spite of the expected reflex tachycardia resulting from their marked hypotensive effect [9].
• Renal effects of 4-week fixed maintenance doses of bunazosin three times daily (2.0 mg t.i.d., n = 8) and propranolol (40 mg t.i.d., n = 8) were evaluated in patients with mild-to-moderate essential hypertension [World Health Organization (WHO) stages I and II] [10].
• METHODS: Patients with primary open angle glaucoma who had received latanoprost (n = 60) or timolol (n = 60) for 6 months or longer were enrolled and prospectively randomized to receive additional administration of bunazosin or placebo [11].
• The goal was to compare the antihypertensive efficacy, tolerability, and in particular postural hypotension of the alpha 1-adrenoreceptor blocker bunazosin with the calcium channel blocker nitrendipine [12].

Biological context of Bunazosin

• Selective suppression by bunazosin of alpha-adrenergic agonist evoked elevation of intraocular pressure in sympathectomized rabbit eyes [13].
• Intravenous (i.v.) injections of bunazosin, an alpha 1-blocker, elicited depressor responses which were accompanied by corresponding decreases in both heart rate and abdominal sympathetic discharge, dose-dependently [3].
• The alpha 2-adrenergic antagonists, yohimbine and rauwolscine, and the alpha 1-adrenergic antagonist, bunazosin, were used to explore the role of alpha-adrenergic receptors in the regulation of the circadian rhythms of intraocular pressure and aqueous flow in New Zealand white rabbits [14].
• Seven alpha 1 adrenoceptor antagonists competed with [3H]bunazosin for the binding sites in the rank order: R-(-)-YM-12617 greater than prazosin greater than SGB-1534 greater than bunazosin greater than terazosin greater than naftopidil greater than urapidil [15].
• On the other hand, in prostaglandin F2 alpha-preconstricted preparations, these agonists produced no vasodilation and revealed weak vasoconstrictions which were readily suppressed by bunazosin, a selective alpha-1 antagonist [16].

Anatomical context of Bunazosin

• Pretreatment with intracoronary bunazosin, an alpha 1 adrenoceptor antagonist (100 micrograms), showed no protective effect on narrowing of the epicardial major coronary artery or blood flow delay [17].
• The myosin isoenzyme pattern of the left ventricle was significantly shifted toward VM-1 in the bunazosin treated SHR, the VM-1 concentration in the treated group being 38% greater than in the untreated group [2].
• There was a similarity in the potency and rank order of seven alpha 1, adrenoceptor antagonists for the inhibition of [3H] bunazosin and [3H]prazosin binding in human prostates [15].
• In the hippocampus, prazosin and bunazosin produced biphasic displacement of [3H]YM617, but not [3H]prazosin binding [18].
• The results suggest that bunazosin protects the myocardium against ischemic damage [19].

Associations of Bunazosin with other chemical compounds

• Treatment involved 3, 6 or 12 mg bunazosin retard tablets or 25, 50 or 100 mg atenolol tablets, administered orally once a day and prescribed according to blood pressure response [20].
• 4. The acetaldehyde-induced vasoconstriction was inhibited by bunazosin, a potent alpha 1-adrenoceptor antagonist [21].
• 4. ACh did not produce any vasoconstriction in the preparations treated either with alpha-adrenoceptor antagonists (10 microM bunazosin and 10 microM midaglizole) or with 30 microM guanethidine [22].
• The effects of bunazosin on the electrical and mechanical responses of smooth muscle cells elicited by exogenously applied noradrenaline (NA) and by perivascular nerve stimulation were studied in the isolated mesenteric artery and vein of the dog [23].
• To investigate insulin insensitivity and its reversibility, we performed an insulin sensitivity test using the steady state plasma glucose (SSPG) method in 10 lean hypertensive subjects with normal glucose tolerance before and after treatment with alpha 1-blocker bunazosin, and 14 age body mass index-adjusted healthy control subjects [24].

Gene context of Bunazosin

• Insulin insensitivity in nonobese, nondiabetic essential hypertension and its improvement by an alpha 1-blocker (bunazosin) [24].
• Serum total cholesterol level decreased and HDL cholesterol increased significantly after treatment with bunazosin [24].
• Bunazosin HCl significantly inhibited the expression of bFGF and TGFbeta1 mRNA in VSMCs from SHRs, but not in cells from WKY rats [25].
• Bunazosin HCl significantly suppressed the response of DNA synthesis to PDGF-AA and EGF, but not to Ang II, in VSMCs from SHRs [25].
• Phentolamine (an alpha blocker) or yohimbine (an alpha 2 blocker) administration completely inhibited the increase of glucagon secretion caused by epinephrine infusion, but neither the administration of bunazosin (an alpha 1 blocker) nor beta blockers inhibited it [26].

Analytical, diagnostic and therapeutic context of Bunazosin

• In group 2 (n = 12), the alpha 1 blocker bunazosin (0.2 mg.kg-1, intravenously) blunted the shortening of the refractory period in the ischaemic zone induced by OMB ligation (p < 0.01), resulting in a reduction in refractory period dispersion between the ischaemic and non-ischaemic (border and normal) zones [27].
• After a single-blind placebo run-in period lasting 4-6 weeks, the patients were treated either with bunazosin retard or with atenolol for a further 16 weeks including an initial dose titration period to achieve blood pressure control [20].
• Forty-three anesthetized dogs were divided into three groups; the occlusion group (n = 7), the reperfusion group (n = 24), and a group treated with the alpha 1-adrenergic blocker, bunazosin (n = 12) [4].
• 5-HT- and KCl-induced constrictions were not modified by a potent alpha 1-adrenoceptor antagonist, bunazosin [28].
• The contractile response evoked by electrical stimulation at 4 Hz was abolished by tetrodotoxin (10(-7) M) and depressed to approximately 10% by bunazosin (10(-6) M), an alpha 1-antagonist [29].

References