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1.
Influence of polymeric effectors on binding of 3H-dihydroalprenolol to beta-adrenergic receptor of rat brain 总被引:1,自引:0,他引:1
The significance of anionic and cationic charges of glycocalyx, phospholipid or protein, etc. on the cell surface of the rat brain was examined for beta-adrenoceptors using the radioligand binding assay method. Thus, this experiment was designed to assess the effects of polymeric effectors, DNA, heparin, polymyxin B, histone, gelatin, colominic acid and bovine serum albumin (BSA), on the affinity of beta-adrenoceptors. The rat brain was used and the beta-adrenoceptor binding assay was carried out using 3H-dihydroalprenolol as a radioligand. Polymyxin B, DNA and heparin significantly caused a reduction in the maximum number of beta-adrenoceptors (Bmax), but only small changes were observed with histone, gelatin, BSA and colominic acid. Only DNA induced a decrease in the value of the dissociation constant (Kd) of beta-adrenoceptors. These results suggest that anionic or cationic charges in the environment of the receptor sites could have a crucial role in drug-receptor interaction. 相似文献
2.
P J Little J H Campbell H Skews A Bobik 《Clinical and experimental pharmacology & physiology》1984,11(5):503-511
The effects of short term (1 h) as well as prolonged (16 h) activation of beta-adrenoceptors by isoprenaline on the functioning of the beta-adrenoceptor linked adenylate cyclase system of rabbit aortic smooth muscle cells in the contractile phenotype in primary culture was examined. Smooth muscle cells responded to 50 mumol/l isoprenaline with a rapid increase in intracellular cAMP. Continued exposure of these cells to this concentration of isoprenaline results in a rapid time dependent reduction in maximum beta-adrenoceptor responsiveness. In vitro analyses of adenylate cyclase activities, phosphodiesterase activity and 125I-iodocyanopindolol specific (beta-adrenoceptor) binding sites suggest that the decrease in the cells' ability to increase intracellular cAMP may be due to a reduction in beta-adrenoceptor binding sites. The loss in cell receptor responsiveness and membrane receptor concentration was only very slowly reversible. These results suggest that following prolonged exposure of vascular smooth muscle cells to beta-adrenoceptor agonists, beta-adrenoceptors are rapidly internalized and degraded. This mechanism may account for the haemodynamic tolerance observed to chronic therapy with beta-adrenoceptor agonists. 相似文献
3.
The inotropic effects of isoproterenol (ISO), as well as the beta-adrenoceptors population, were measured in cardiac tissues from normal and short-term (3 days) diabetic rats. ISO increased the tension of both normal and diabetic ventricles, but the efficacy (Emax) of the concentration-response curve was greater on ventricles from diabetic rats than in those from the normal control. This phenomenon was accompanied by a decrease in the number of beta-adrenoceptor sites (Bmax) during diabetes. Insulin-treated diabetic hearts partially reversed the phenomenon. Propanolol blocked, in a competitive manner, the positive inotropic action of ISO in both types of ventricles. Inhibition of the synthesis and receptors of thromboxane (TX) reduced the hyperreactivity to ISO and increased the number of beta-adrenoceptors during diabetes, producing Bmax values almost similar to those of the normal heart. Additionally, the diabetic heart generated and released a greater amount of TXB2 than the normal heart, even in the presence or absence of ISO. The stimulatory effect of ISO upon TXB2 release was altered by the specific beta-adrenergic blockade and by verapamil. In addition, the drugs able to induce a sustained increase of endogenous cAMP also inhibited the release of TXB2 by diabetic ventricles. Exogenous TXB2 exerted the same type of hyperreactivity in diabetic ventricles. This phenomenon was accompanied by an inhibition of Na+ + K+-ATPase activity. These results suggest that beta-adrenergic inotropic stimulation is secondary to receptor-mediated hydrolysis of arachidonic acid with subsequent release of thromboxanes, which, in turn, may be responsible for both the superreactivity and the decrease in the number of beta-adrenoceptors during diabetes. The abnormal reactivity to beta-agonists also could be associated with alterations of the diabetic cardiac Na+ + K+-ATPase activity induced by TXB2 whose production is increased during diabetes. 相似文献
4.
Regulation of beta-adrenoceptor number and subtype in 3T3-L1 preadipocytes by sodium butyrate 总被引:1,自引:0,他引:1
In mouse 3T3-L1 preadipocytes, the glucocorticoid dexamethasone has been shown to promote a switch in beta-adrenoceptor subtype expression from beta 1 to beta 2 and to increase the total number of beta-adrenoceptors. The present study demonstrates that sodium butyrate also modulates beta-adrenoceptor expression in these cells. Incubation of preadipocytes with 2-10 mM butyrate for 24-48 h promoted a dose- and time-dependent switch in beta-adrenoceptor subtype from a near equal mixture of beta 1 and beta 2 to greater than 85% beta 2 and caused an approximate doubling of the receptor number. beta-Adrenoceptors were assayed in membranes prepared from 3T3-L1 cells using the radiolabeled antagonist [125I]iodocyanopindolol and the beta 2-selective antagonist ICI 118.551. Other short chain acids were not as effective as butyrate in promoting changes in beta-adrenoceptor expression. Cycloheximide (1.0 microgram/ml) inhibited the effects of butyrate on both beta-adrenoceptor subtype and number. Alterations in beta-adrenoceptor phenotype promoted by either butyrate or dexamethasone were functionally correlated with cAMP accumulation in these cells. Comparison of the effects of butyrate and dexamethasone on beta-adrenoceptor expression suggests that these two agents regulate beta-adrenoceptors by different mechanisms. 相似文献
5.
Haemophilus influenzae induced loss of lung beta-adrenoceptor binding sites and modulation by changes in peripheral catecholaminergic input 总被引:1,自引:0,他引:1
Vaccination of guinea pigs with killed suspensions of Haemophilus influenzae, a bacterium often found in the deeper respiratory airways of asthmatic bronchitics, results in a number of effects suggesting an impairment of beta-adrenoceptor function. A [3H]dihydroalprenolol binding assay was used to determine the number of beta-adrenoceptors (Bmax) following H. influenzae vaccination. The Bmax declined significantly by 29% from 1240 +/- 80 to 880 +/- 70 fmol/mg protein, while the binding affinity of the sites was not changed. Specific binding in the presence of 1.8 nM [3H]DHA to tracheal longitudinal smooth muscle was also significantly lower in H. influenzae-vaccinated animals as compared to controls. Furthermore modulation of peripheral sympathetic input to lung beta-adrenoceptors was evaluated in our model. Pretreatment with Ro4-4602, an inhibitor of dopa-decarboxylase, increased the number of beta-adrenoceptors and prevented the H. influenzae-induced loss of beta-adrenoceptors. On the other hand repeated doses of the antidepressant desipramine mimicked the effect of H. influenzae vaccination i.e. a loss of beta-adrenoceptors. Desipramine and H. influenzae vaccination were not synergistic in their effects. The effects of H. influenzae and modulation of catecholaminergic input on guinea pig lung beta-adrenoceptors were compared with tracheal strip relaxation by isoproterenol, following similar treatments assessed in a superfusion model. Changes in lung beta-adrenoceptor number were almost identical with changes in tracheal strip relaxation. These results suggest that compensatory regulation adapts the number of respiratory beta-adrenoceptors to changes in sympathetic input. A similar mechanism may underlie the loss of beta-adrenoceptors following H. influenzae vaccination. 相似文献
6.
Bordallo C Cantabrana B Velasco L Secades L Meana C Méndez M Bordallo J Sánchez M 《European journal of pharmacology》2008,598(1-3):68-74
Endogenous polyamines mediate acute metabolic effects and cardiac hypertrophy associated to beta-adrenoceptor stimulation. The aim of this study is to characterize the role of polyamines on beta-adrenoceptor system mediated responses. To this end, the functional interaction of polyamine modifying drugs on isoproterenol-elicited cardiotonic effect, in isolated left atria of male Wistar rats, and their effects on [(3)H]dihydroalprenolol (DHA) binding on beta-adrenoceptors and on adenylyl cyclase activity of membrane heart were studied. Polyamines interact with beta-adrenoceptors in rat heart, as shown by the displacement of [(3)H]DHA binding. Furthermore, putrescine (but not spermidine or spermine) increased adenylyl cyclase activity, elicited a positive inotropism and increased intracellular cAMP. The putrescine effect on adenylyl cyclase was not antagonized by the beta-adrenoceptors blockers, alprenolol and ICI-118,551, and facilitated the isoproterenol effect. Neither alprenolol, atenolol nor ICI-118,551 antagonized putrescine-elicited positive inotropism. However, the effect was abolished in preparations with desensitized beta-adrenoceptors. alpha-Difluoromethylornithine, an inhibitor of ornithine decarboxylase, antagonized the effect of isoproterenol on inotropism and cAMP increase. In addition, putrescine might elicit effects by mechanisms independent of beta-adrenoceptor system, since in left atria with functional desensitized receptors an interaction with ouabain-elicited cardiotonic effect was observed. These results suggest that putrescine may act as a low affinity agonist on beta-adrenoceptors and modulate acute responses mediated by beta-adrenoceptors. These findings may be of importance in the physiology and in diseases involving cardiac beta-adrenoceptors. 相似文献
7.
Time course and extent of alpha 1-adrenoceptor density changes in rat heart after beta-adrenoceptor blockade. 总被引:3,自引:3,他引:0
1. It has been suggested that impaired beta-adrenoceptor stimulation is a condition under which the functional role of cardiac alpha 1-adrenoceptors is enhanced. We therefore investigated the extent and time course of changes in alpha 1-adrenoceptor characteristics after chronic treatment with the beta-adrenoceptor blocker propranolol in rat heart. For comparison beta-adrenoceptors were also studied. The mechanism of the changes in adrenoceptor density was investigated with cycloheximide, an inhibitor of protein synthesis. The functional significance of an increased alpha 1-adrenoceptor density was tested by measuring isometric force of contraction in the presence of phenylephrine or isoprenaline in right ventricular papillary muscles. 2. Rats were treated with propranolol (9.9 mg kg-1 daily) or 0.9% NaCl, applied with osmotic minipumps for 1, 2, 3 or 7 days. Propranolol treatment resulted in a maximally 28% increase of alpha 1-adrenoceptor density after 3 days (NaCl 95.9 +/- 3.5 vs. propranolol 123.0 +/- 1.6 fmol mg-1 protein, n = 6, P less than 0.01). This up regulation reached significant levels after 2 days of treatment and was reversible after cessation of treatment within two days. KD-values were the same for NaCl- and propranolol-treated rats. Changes of Bmax and KD in beta-adrenoceptor binding assays did not reach significant levels. 3. Cycloheximide (1.5 mg kg-1 i.p. daily for 3 days) inhibited the propranolol-induced increase in Bmax of alpha 1-adrenoceptors completely. In addition, cycloheximide also decreased the density of alpha 1- and beta-adrenoceptors also under control conditions.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
8.
The possible relationship between methoxyverapamil (D600) as a calcium-channel blocker and the beta-adrenoceptors was investigated on heart cells grown in culture, using [3H]CGP-12177 as a radioligand. Treatment with D600 (20 micrograms/mL) for 24 hr caused a decrease of 30% in the [3H]CGP-12177 binding sites. Scatchard analysis showed that the Bmax is similar in control and D600-treated cells, but the Kd in D600-treated cells increases. The effect of D600 on the isoproterenol-induced adenylate cyclase activation was examined and it was found that the D600 prevented the increase in cAMP obtained by isoproterenol treatment. These results indicate that the action of D600 on the beta-adrenoceptors is a competitive inhibition of the [3H]CGP-12177 binding sites. We investigated the effect of Ca2+ in the growth medium on the level of beta-adrenoceptors. Heart cells grown for 24 hr in Ca(2+)-free medium showed a decrease of 36% in the [3H]CGP-12177 binding sites without changing the dissociation constant. This decrease is probably a result of reduction in synthesis of the receptors. The level of receptors returned to control values following replenishment with normal growth medium. These results show that calcium is essential for the development of the beta-adrenoceptors in heart cells in vitro. 相似文献
9.
Inflammatory mediators and beta-adrenoceptor function 总被引:2,自引:0,他引:2
J A Raaijmakers C Beneker E C van Geffen T M Meisters P Pover 《Agents and actions》1989,26(1-2):45-47
In this study the, in vitro, influence of arachidonic acid metabolites on human beta-adrenoceptors was investigated. Incubation of normal human pulmonary membranes with PAF, LTB4 and LTC4 affected pulmonary beta-adrenoceptor properties, as was shown in radioligand binding studies. The same mediators were able to induce a decreased lymphocyte cAMP synthesis. It is concluded that beta-adrenoceptor deficiencies, that can be demonstrated in peripheral lung tissue of COLD patients, may result from pathological processes such as inflammation. 相似文献
10.
The influence of thyroid hormone deficiency on beta-adrenoceptors in the rat cerebral cortex was investigated using the 3H-dihydroalprenolol binding assay. The maximal number of binding sites (Bmax) and the dissociation constants (KD) were determined in the brain tissue from euthyroid animals and from rats made hypothyroid by feeding 6-propyl-2-thiouracil. Hypothyroidism resulted in a 37% decrease in beta-adrenoceptor density (Bmax). The dissociation constants (KD) of both groups were not significantly different. 相似文献
11.
H L Elliott C R Jones N M Deighton P A Meredith J L Reid 《British journal of clinical pharmacology》1987,23(5):511-521
A comparative study in eight healthy normotensive males of the effects on blood pressure, heart rate and beta-adrenoceptor function following single oral doses of adimolol (600 mg), propranolol (240 mg) and placebo. Both active treatments produced small but significant reductions in blood pressure and heart rate, supine and erect. These effects persisted for up to 7 days after adimolol. The heart rate increases following both dynamic exercise and intravenous isoprenaline were attenuated by both propranolol and adimolol. With adimolol evidence of functional beta-adrenoceptor antagonism was sustained for up to 7 days. Lymphocyte beta-adrenoceptor binding studies showed that both adimolol and propranolol significantly reduced affinity for beta-adrenoceptors. In addition, adimolol significantly reduced receptor number and even by 3 days after dosing Bmax had only returned to half the control value. In a small sub-group of subjects there was no evidence to suggest that adimolol had additional alpha-adrenoceptor antagonist properties. Adimolol was detected in plasma for up to 3 days after dosing. The mean terminal elimination half-life was 14 h, compared to 3 h for propranolol. This study confirms that adimolol has prolonged beta-adrenoceptor antagonist activity with effects persisting for up to 7 days after a single dose. The reduction in beta-adrenoceptor number following adimolol suggests that this prolonged effect may not be solely due to competitive antagonism but may additionally depend upon non-competitive antagonism at beta-adrenoceptors. 相似文献
12.
Yu XC Diao TM Pei JM Zhang WM Wong NS Wong TM 《Journal of cardiovascular pharmacology》2001,38(2):232-239
To explore the signaling mechanisms of the negative modulation of beta-adrenoceptors by kappa-Opioid receptors (kappa-OR) in the heart, the possibility of the interaction at the level of G protein and receptor was determined. Cholera toxin, an activator of the stimulatory G protein (Gs), elevated electrically induced intracellular Ca2+ ([Ca2+]i) transients and induced ribosylation of the alpha-subunit of Gs (Gsalpha) in rat ventricular myocytes. The effects were significantly attenuated by U50,488H, a specific agonist of kappa-OR, and were abolished by nor-binaltorphimine, a selective kappa-OR antagonist. The content of Gsalpha, however, was not affected by U50,488H. Receptor binding experiments showed that neither Bmax nor Kd of the binding of [3H]CGP-12177, a beta-adrenoceptor antagonist, was affected by U50,488H. The current study provides the first evidence that kappa-OR stimulation inhibits the ribosylation of the alpha-subunit of the Gs protein, thus inhibiting the action of cholera toxin on the protein. 相似文献
13.
Subsensitivity of the failing human heart to isoprenaline and milrinone is related to beta-adrenoceptor downregulation 总被引:5,自引:0,他引:5
M B?hm F Diet G Feiler B Kemkes E Kreuzer C Weinhold E Erdmann 《Journal of cardiovascular pharmacology》1988,12(6):726-732
The number of cardiac beta-adrenoceptors and the positive inotropic effect of isoprenaline and milrinone were measured in cardiac membranes and isolated, electrically driven muscle strips from nonfailing donor hearts and from patients with mitral valve disease (NYHA II-III), ischemic heart disease, and dilated cardiomyopathy (NYHA IV). In nonfailing hearts, the number of beta-adrenoceptors were 41.5 fmol/mg protein (mean, n = 3). In ischemic heart disease and NYHA II-III, there was a loss of cardiac beta-adrenoceptors (22.1 fmol/mg protein, mean, n = 3; 23.2 +/- 2.7 fmol/mg protein, n = 30), respectively. In NYHA IV, there was a pronounced reduction of the number of cardiac beta-adrenoceptors to 12.1 +/- 1.5 fmol/mg protein (n = 15). The Kd value did not differ in either group. Correspondingly, the positive inotropic effect of isoprenaline was more pronounced in nonfailing myocardium, reduced in NYHA II-III and ischemic heart disease and almost blunted in NYHA IV. Similar results were observed with the phosphodiesterase inhibitor milrinone. A good correlation of the beta-adrenoceptor density to the maximal positive inotropic effect of isoprenaline and milrinone was observed. Neither the number of cardiac beta-adrenoceptors nor the positive inotropic effect of isoprenaline correlated with the age of the patients. We conclude that the number of cardiac beta-adrenoceptors and the positive inotropic effect of beta-adrenoceptor agonists are reduced in the failing human heart depending on the severity of heart failure. Furthermore, the positive inotropic effect of milrinone is also reduced and related to the reduction of beta-adrenoceptors. The lack of correlation with the age of the patients provides evidence for a predominant role of heart disease rather than aging in the reduction of beta-adrenoceptors and subsensitivity to cyclic AMP-increasing positive inotropic agents in the failing human heart. 相似文献
14.
The time course of resensitization of the down-regulated beta-adrenoceptor system of rat myometrium was studied. The isoprenaline-induced decrease of myometrial cAMP reversed rather rapidly and after 4 and 8 days no significant change of the cAMP level was demonstrated, however, the cAMP level was higher than in the control myometrium after 12 days. The elevated phosphodiesterase activity decreased to 80% of control activity after 4 days, but returned to control activity after 8 days. The decreased number of beta-adrenoceptors increased gradually after discontinuing the treatment and reached the number of the controls after 12 days. Our results suggest that the resensitization of the beta-adrenoceptor-cAMP-system is rather complex, the normalization of the cAMP content and the phosphodiesterase activity is more rapid than the normalization of the beta-adrenoceptor number which is a rather slow process in myometrial tissue. 相似文献
15.
The autonomic receptors in the rat kidney were characterized using the radioligands [3H]prazosin, [3H]clonidine, [3H]dihydroalprenolol (DHA) and [3H]quinuclidinyl benzilate (QNB). The specific binding of [3H]prazosin, [3H]clonidine, [3H]DHA and [3H]QNB to rat kidney membranes was saturable and of high affinity, and showed a pharmacological specificity as well as stereospecificity which characterized renal alpha 1-, alpha 2- and beta-adrenoceptors and muscarinic cholinoceptors, respectively. There was a relatively greater density of alpha-adrenoceptors than beta-adrenoceptors or muscarinic cholinoceptors in the rat kidney. Chemical sympathectomy of rats with 6-hydroxydopamine X HBr (6-OHDA, 50 X 2 mg/kg i.v., 24 h interval) caused a significant increase (21-56%) in the Bmax values for renal [3H]prazosin, [3H]clonidine and [3H]DHA binding at 1 and 2 weeks following the treatment, without a change in the Kd values. 6-OHDA treatment had no significant effect on the Kd and Bmax values for [3H]QNB binding at 1-3 weeks after the treatment. The norepinephrine (NE) concentration was reduced (68-76%) in the 6-OHDA-treated rat kidney. In conclusion, the present study provides biochemical evidence for the possible localization of postsynaptic alpha 1-, alpha 2- and beta-adrenoceptors and muscarinic cholinoceptors in the rat kidney and also for the regulation of these adrenoceptors by the sympathetic nervous system. 相似文献
16.
Prostaglandin E2 synthesis in rabbit splenic fibroblasts was stimulated by noradrenaline but not by isoprenaline. Noradrenaline, isoprenaline and prostaglandin E2 increased intracellular cAMP accumulation. Noradrenaline-, but not isoprenaline-evoked cAMP accumulation was reduced by indomethacin; only combinations of phentolamine or indomethacin with propranolol abolished the noradrenaline effect. We conclude that the noradrenaline-induced increase in cAMP levels of rabbit splenic fibroblasts was due to stimulation of both alpha- and beta-adrenoceptors. The response to alpha-receptor stimulation was possibly mediated by prostaglandin E2. 相似文献
17.
A J Van Oosterhout G Folkerts G A Ten Have F P Nijkamp 《European journal of pharmacology》1988,147(3):421-429
The beta-adrenergic binding sites on splenic lymphocyte membranes of the guinea pig were characterized with the radio-ligand [125I]cyanopindolol and showed a maximal number of binding sites (Bmax) of 125 fmol/mg protein and an affinity (Kd) of 170 pM. The potency of various beta-adrenoceptor antagonists to compete for [125I]cyanopindolol binding suggested that the receptor is of the beta 2 subtype. Endotoxin (1 mg/kg) induced a 35% decrease in the number of beta-adrenergic binding sites on lymphocytes, 4 days after i.p. administration. The reduction in the number of beta-adrenoceptors on the lymphocytes was accompanied by a 30% decrease in the relaxation of isolated guinea pig tracheal spirals to isoprenaline and a 20% reduction in the number of beta-adrenergic binding sites in peripheral lung tissue. The endotoxin-induced deterioration of the beta-adrenergic system in the respiratory airways was completely prevented by splenectomy. It is concluded that the spleen, and or cells or products derived from the spleen, are involved in the changes of the beta-adrenergic system in the respiratory airways and lymphocytes. 相似文献
18.
Binding characteristics of 3H-dihydroalprenolol to beta-adrenergic receptors of rat brain: influence of lectins 总被引:1,自引:0,他引:1
The significance of the carbohydrate moieties of the beta-adrenergic receptor molecule in the rat brain was examined using the radioligand binding assay method. Thus, this experiment was designed to assess the effects of lectins, concanavalin A (Con A), Phaseolus vulgaris agglutinin (PHA), and wheat germ agglutinin (WGA) on the affinity of the beta-adrenoceptor. The rat brain was used and the beta-adrenoceptor binding assay was carried out using 3H-dihydroalprenolol as a ligand. Con A and PHA significantly caused an increase in the values of the density of beta-adrenoceptor (Bmax) and a reduction in the values of the dissociation constant (Kd), but significant changes were not observed with WGA. These results strongly suggest that the carbohydrate moieties of the cell surface containing the beta-adrenoceptor molecule may have a crucial role in the drug-receptor interaction, and they imply that the beta-adrenoceptor molecule is a glycoprotein which contains N-linked carbohydrate chains. 相似文献
19.
用放射配体结合分析法分别测定了正常组、特布他林组、特布他林十曲尼司特组豚鼠的肺组织β受体最大结合力和解离常数,结果显示:给特布他林后豚鼠肺组织β受体发生明显的向下调节.曲尼司特可预防此向下调节的发生. 相似文献
20.
Respective degree of expression of beta 1-, beta 2- and beta 3-adrenoceptors in human brown and white adipose tissues.
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C. Deng A. Paoloni-Giacobino F. Kuehne O. Boss J. P. Revelli M. Moinat M. A. Cawthorne P. Muzzin J. P. Giacobino 《British journal of pharmacology》1996,118(4):929-934
1. The possible existence of a beta 3-adrenoceptor in human brown and white adipose tissues was investigated by mRNA expression and binding studies. 2. The relative amounts of beta 1-, beta 2- and beta 3-adrenoceptor mRNA, as determined by total RNA Northern blot analysis in newborn brown adipose tissue, were 28, 63 and 9% respectively of the total beta-adrenoceptor mRNA. 3. The beta 1/beta 2-adrenoceptors of human brown adipose tissue plasma membranes were characterized using [3H]-CGP 12177 as a ligand. Their Kd and Bmax values were 1.9 nM and 156 fmol mg-1 of membrane proteins, respectively. The beta 3-adrenoceptor was characterized by use of the new specific radioligand [3H]-SB 206606. The binding of this ligand was stereospecifically displaced by the active R,R- or the inactive S,S-enantiomer of BRL 37344 up to a concentration of about 10 microM. The Kd and Bmax values of the brown adipose tissue membrane beta 3-adrenoceptors were 87 nM and 167 fmol mg-1 of proteins, respectively. A low affinity [3H]-CGP 12177 binding site population was also detected in these membranes. 4. In human omental white adipose tissue, no beta 3-adrenoceptor mRNA could be detected in total RNA Northern blots and the beta 1-and beta 2-adrenoceptor mRNAs represented 9 and 91%, respectively of the total beta-adrenoceptor mRNA, and no specific binding of [3H]-SB 206606 could be measured. 相似文献