Disease relevance of BUTOXAMINE HYDROCHLORIDE

• Butoxamine alone depressed the granulocyte labeling index and granulocyte-monocyte colony-forming Cell (GM-CFC) suicide rate at a dose of 3 micrograms/g body weight [1].
• Rabbits treated with dl-propranolol (4 or 8 mg/kg i.p.) or butoxamine (15 or 30 mg/kg i.p.) produced significantly less ESF in response to hypoxia than did saline-treated control animals [2].
• Aerosol administration of the beta antagonists, propranolol (beta 1 and beta 2), atenolol (beta 1), and butoxamine (beta 2) decreased dynamic compliance (Cdyn) and increased pulmonary resistance (RL) in the principal ponies during airway obstruction, but were without effect when the ponies were in clinical remission [3].
• Butoxamine provided some protection against the arrhythmia within a narrow dose range (53 to 79 mg/kg) [4].
• The results showed that drugs with beta 2-adrenoceptor agonist activity and l-ephedrine caused hyperthermia in rats and this effect was selectively inhibited by pretreatment of animals with propranolol (a mixed beta-adrenoceptor antagonist) or butoxamine (a selective beta 2-adrenoceptor antagonist) [5].

Psychiatry related information on BUTOXAMINE HYDROCHLORIDE

• Pretreatment with the beta-adrenergic antagonist, butoxamine, reduced the effects of social confrontation by approximately 50%, and adrenal demedullation almost abolished it without significantly affecting the social interaction [6].

High impact information on BUTOXAMINE HYDROCHLORIDE

• These findings suggest that butoxamine may have a potential use in protecting hematopoiesis during intensive chemotherapy for cancer [1].
• Butoxamine administered 8 hr before an injection of ara-C modified the proportion of GM-CFC in S phase as compared with the number found after ara-C alone [1].
• This response was abolished by iv butoxamine (five pigs) and intracoronary N(omega)-nitro-l-arginine methyl ester (five pigs), even after reversing the increase in arterial pressure and coronary vascular resistance caused by the two blocking agents with iv infusion of papaverine [7].
• This inhibitory effect was mediated via the beta1-adrenoceptor, since it was blocked by atenolol (beta1-adrenoceptor antagonist) but not butoxamine (beta2-adrenoceptor antagonist) [8].
• 6. Propranolol (2 X 10(-5) M) inhibited this stimulatory effect of isoprenaline in vitro but (+)-propranolol (2 X 10(-5) M), practolol and butoxamine (both at 10(-4) M) had no effect on the response [9].

Chemical compound and disease context of BUTOXAMINE HYDROCHLORIDE

• Based on the proposed selectivity of butoxamine for beta2 adrenergic receptors and of practolol for beta1 adrenergic receptors, it is suggested that ESF production in rabbits exposed to hypoxia may involve the activation of beta2 adrenergic receptors [2].

Biological context of BUTOXAMINE HYDROCHLORIDE

• The inhibition curves obtained with procaterol and butoxamine, with apparent Kd values of 3.1 X 10(-9) M and 4.9 X 10(-9) M, further evidence that the high-affinity binding sites correspond to a homogeneous beta 2-receptor subtype [10].
• Atenolol, a beta 1-receptor antagonist, inhibited SCS-induced vasodilation only in the skin, whereas the beta 2-receptor antagonist butoxamine selectively depressed the muscle response [11].
• Metoprolol and butoxamine had no effect on the 8-OH-DPAT-induced increase in defecation, thereby excluding an influence of beta-adrenoceptors [12].
• Therefore, it is suggested that alpha-adrenergic stimulation is involved in the mechanism of diuresis by practolol, a beta1-blocker, and that dopaminergic stimulation is involved in the diuresis caused by butoxamine, a beta2-blocker [13].
• In the same pigs, after hemodynamic variables had returned to the baseline values, blockade of beta2-adrenergic receptors with butoxamine caused an increase in aortic blood pressure and an increase in renal and mesenteric resistance [14].

Anatomical context of BUTOXAMINE HYDROCHLORIDE

• Treatment with butoxamine, a beta-2 antagonist, inhibited the relaxation of dog mesenteric arteries to a greater extent than that of monkey and dog coronary arteries [15].
• Butoxamine was a simple competitive antagonist of responses to all agonists with a 10 to 16 times greater potency in rat uterus than in guinea-pig left atria [16].
• [3H]Dihydroalprenolol (DHA) binding of membranes of adult pancreas differed from that of pancreas of young rats, and the DHA binding in the presence of atenolol or butoxamine also was different in the two age groups [17].
• The apparent dissociation constant for butoxamine was also independent of mast cell purity [18].
• The relative numbers of beta 1- and beta 2-adrenoreceptors as a percentage of the total population of beta-adrenoceptors were estimated to be 18.6% and 81.4%, respectively, from analyses of Hofstee plots of the effects of the beta-agonists on the melanophores in the presence of butoxamine or metoprolol [19].

Associations of BUTOXAMINE HYDROCHLORIDE with other chemical compounds

• The enhancing effect of clenbuterol was unaffected by pretreatment with the beta 1-adrenoceptor antagonist metoprolol but was totally antagonised by the beta 2-adrenoceptor antagonist ICI 118,551 and to a lesser extent by butoxamine [20].
• On the other hand, with submandibular gland, [Na] and [K] of nerve-elicited saliva in the presence of phentolamine were generally higher than levels of sympathetically evoked saliva in the presence of phentolamine and butoxamine [21].
• The beta 2-blocker butoxamine and the beta 1-blocker pamatolol did not influence insulin secretion [22].
• On the other hand, dog coronary arteries responded to dopamine with a relaxation that was abolished by metoprolol, but not influenced by SCH23390 or butoxamine, a beta 2 antagonist [23].
• CGP 12177 caused graded relaxation of the guinea pig taenia caecum, and this response was not influenced by 10(-6) M phentolamine, 3 x 10(-4) M atenolol, 10(-4) M butoxamine or 10(-6) M propranolol [24].

Gene context of BUTOXAMINE HYDROCHLORIDE

• All responses by these stimulations were antagonized by the selective beta 2-adrenergic receptor (AR) antagonist, butoxamine, but not by alpha 1-, alpha 2- and beta 1-AR antagonists [25].
• The selective beta2-adrenoceptor antagonist butoxamine (10 microM) slightly reduced the cardiac response to 50 microg, but not to 100 microg of venom [26].
• Butoxamine, a somewhat selective beta 2-adrenergic antagonist drug, also produced a significant inhibition of the effects of PGE2 on CFU-E in murine marrow cultures [27].
• In the presence of butoxamine, a selective beta 2-adrenoceptor inhibitor, but not metoprolol, a selective beta 1-adrenoceptor inhibitor, SNP still inhibited isoproterenol-relaxation [28].
• In contrast, beta-2 receptor blockade with butoxamine (20 micrograms/kg/min) did not alter the renin secretion response to renal nerve stimulation [29].

Analytical, diagnostic and therapeutic context of BUTOXAMINE HYDROCHLORIDE

• Oral administration of butoxamine produced similar effects [30].
• In contrast, the early component was only partially reduced by adrenalectomy or butoxamine treatment [31].
• Autoradiography showed that inhibition of 3H-TdR incorporation by butoxamine was slightly more pronounced on neutrophil precursors than on red cell precursors (neutrophil series LI..53 and erythroblasts .67 compared to control bone marrow cells at 10(-5) M concentration) [32].

References