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PubMed1975

Hypercalcemic effect of catecholamines and its prevention by thyrocalcitonin.

Earlier work by others has shown that the catecholamines, epinephrine and isoproterenol, can raise blood calcium levels in parathyroidectomized but not intact rats, and can restrict the hypocalcemic effect of injected thyrocalcitonin (TCT). The present findings support this earlier work, further showing that such catecholamines can produce hypercalcemia in rats after removal of the thyroid gland by acute thyroparathyroidectomy (TPTX) and indicating that these drugs may raise blood calcium by mobilizing calcium from bone. Rats were fasted overnight, subjected to TPTX and concurrently injected with adrenergic agonist or antagonist drugs alone or in combination. Epinephrine, isoproterenol, and the beta-2 adrenergic agonist, salbutamol, in doses greater than or equal to 1 mg/kg raised blood calcium from low normal levels (approximately 9-10 mg/100 ml) by 1.5 to 2 mg/100 ml (p less than 0.01). Hypercalcemia was apparent by 1 hour after injection and lasted for 1-4 hours. The extent of Ca elevation was dose-related. Pretreatment of rats with the alpha-adrenergic antagonist, phenoxybenzamine, enhanced the effect of epinephrine while pretreatment with the beta-antagonist, propranolol, reduced the effect of isoproterenol. The more selective beta-2 antagonist, butoxamine, but not the beta-1 antagonist, practolol, also reduced the hypercalcemic effect of isoproterenol in TPTX rats. These results suggest that catecholamine-induced hypercalcemia in TPTX rats is mediated by beta-2 adrenergic receptors. Related studies using rats prelabeled with 45Ca further suggest that the catecholamines, like parathyroid hormone, may act to raise blood calcium by mobilizing calcium from bone. The fact that these catecholamines could induce marked hypercalcemia in acutely TPTX rats but not in intact rats indicated that endogenous TCT protects the thyroid intact rat against hypercalcemia. The present findings support this idea in showing that isoproterenol and salbutamol raised levels of immunoreactive rat TCT in both thyroid venous and peripheral blood. Catecholamines apparently can promote TCT secretion, either directly or by a small transient increase in blood calcium. This, in turem, acts to combat hypercalcemia in thhroid-intact rats.

Albuterol↗
PubMed2003

Involvement of noradrenergic system within the central nucleus of the amygdala in naloxone-precipitated morphine withdrawal-induced conditioned place aversion in rats.

RATIONALE: We previously reported that the central nucleus of the amygdala (CeA) plays a crucial role in the negative affective, rather than somatic, component of morphine withdrawal. However, numerous studies have reported that the central ascending noradrenergic system is implicated in morphine withdrawal syndrome, although the roles of the noradrenergic system within the CeA in the negative affective component remains less clear. OBJECTIVES: The possible role of the noradrenergic system within the CeA in the negative affective component of morphine withdrawal was investigated. METHODS: The extracellular noradrenaline level within the CeA during naloxone-precipitated morphine withdrawal was measured using an in vivo microdialysis experiment on unanesthetized and freely moving rats. The effects of microinjection of beta-adrenoceptor antagonists into the bilateral CeA on the naloxone-precipitated morphine withdrawal-induced conditioned place aversion (CPA) and somatic signs were examined. RESULTS: The extracellular noradrenaline level within the CeA was transiently elevated during morphine withdrawal. Intra-CeA injections of beta-adrenoceptor antagonists propranolol (30 nmol per side) and timolol (10 nmol per side) significantly attenuated the morphine withdrawal-induced CPA. Similarly, beta(1)-antagonist atenolol (30 nmol per side) or beta(2)-antagonist butoxamine (30 nmol per side) significantly attenuated the CPA. In contrast, they did not affect morphine withdrawal-induced somatic signs, except for propranolol. CONCLUSION: These results suggest that the activation of the noradrenergic system within the CeA contributes to naloxone-precipitated morphine withdrawal-induced CPA, rather than somatic signs, through beta(1)- and beta(2)-adrenoceptors.

Adrenergic beta-Antagonists↗
PubMed1998

Haemodynamic effects of the intravenous administration of growth hormone in anaesthetized pigs.

Administration of growth hormone in humans has been reported variably to affect arterial blood pressure and ventricular contractility. The present study was undertaken in anaesthetized pigs to establish whether increases in the blood levels of growth hormone primarily affect haemodynamic variables and to determine the mechanisms involved. In pigs anaesthetized with pentobarbitone sodium, left circumflex or anterior descending coronary blood flow was measured with an electromagnetic flowmeter. In a first group of 23 pigs, growth hormone administration (0.05 IU kg-1 i.v.) increased aortic blood pressure and reduced coronary blood flow when heart rate and aortic blood pressure were held constant. These responses were augmented by graded increases in plasma levels of growth hormone. The mechanisms of the above responses were studied in a second group of 29 pigs and involved beta2-adrenergic receptors since they were abolished by propranolol or butoxamine but not by atropine, phentolamine or atenolol. The present study showed that administration of growth hormone in anaesthetized pigs primarily increased aortic blood pressure and vasoconstricted the coronary circulation. The mechanisms of these responses involved beta2-adrenoceptor effects.

Adjuvants, Anesthesia↗
PubMed1989

Introduction of cyclic AMP phosphodiesterase into rat submandibular acini prevents isoproterenol-stimulated cyclic AMP rise without affecting mucin secretion.

Cyclic AMP phosphodiesterase has been incorporated into isolated rat submandibular acini by hypotonic swelling. This resulted in complete inhibition of the cyclic AMP rise stimulated by isoproterenol (10 microM), but had no effect on the stimulation of mucin secretion. Acini swollen in the absence of cyclic AMP phosphodiesterase showed similar cyclic AMP and mucin secretion responses to those of unswollen acini. The dissociation between cyclic AMP rise and mucin secretion was not due to stimulation of different beta-receptor subtypes since both responses to isoproterenol were inhibited by the beta 1 antagonist atenolol, but not by the beta 2 antagonist, butoxamine. The results are the first to directly demonstrate that a maximally effective concentration of isoproterenol can increase mucin secretion in the absence of a detectable increase in cyclic AMP.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1979

Adrenoceptors involved in the contractile activity of islated pregnant rat uterus.

Cumulative log dose-response curves of soterenol, isoproterenol, phenylephrine and norepinephrine on isolated pregnant rat uterus at different days of gestation, were investigated. Soterenol produced a sustained inhibition of spontaneous motility during the whole pregnancy and this effect was blocked by butoxamine. The affinity of myometrium for the beta 2-adrenoceptor agonist was parallel to the concentration of progesterone in plasma during pregnancy. Isoproterenol, norepinephrine and phenylephrine caused dual, alpha- and beta-mediated responses, their relative dominance varied with the concentration and the days of pregnancy, alpha-Adrenoceptor effects of the amines coincided with increased plasma concentrations of estrogens, whereas beta ones were in parallel with the increment of plasma progesterone. It is concluded that: (a) there exist in the pregnant rat uterus beta 2-receptor-mediated responses influenced by the length of gestation; and (b) the concentration-pregnancy-dependent biphasic actions of isoproterenol, norepinephrine or phenylephrine suggest that their variable hormone-modulated ability interacts with both alpha- and beta-adrenoceptive uterine sites.

Animals↗
PubMed1981

Effects of selective and non-selective beta-adrenergic agents on insulin secretion in vivo.

The effects of various beta-adrenergic agents on insulin secretion were investigated in vivo in mice. The non-selective beta-stimulator isopropylnoradrenaline and the selective beta 2-stimulator terbutaline both stimulated insulin secretion markedly, with the same efficacy and in a dose-dependent manner. The peak levels of plasma insulin after these two beta-agonists were achieved at a later time point (5-6 min) than after stimulation with glucose or carbachol (1.5-2.5 min). At very high dose levels the beta 2-stimulator isopropylaminothiazoloxypropanol slightly increased plasma insulin concentrations. The non-selective beta-blocker propranolol and the beta 2-selective blocker ICI 188,551 inhibited terbutaline-induced insulin release markedly and at comparable low dose levels, whereas the selective beta 1-blocker metoprolol exerted this effect only at a high dose level. At higher dose levels these three blockers moderately depressed the insulin response to glucose suggesting a partial dependence on intact beta-adrenoceptors for the effect of glucose. The beta 2-blocker butoxamine and the beta 1-blocker pamatolol did not influence insulin secretion. In conclusion, beta-adrenoceptor stimulation enhanced insulin secretion in vivo, but the beta-adrenoceptors regulating insulin secretion do not fit well into the conventional subdivision of beta 1 and beta 2, though they apparently are mainly of the beta 2-type.

Adrenergic beta-Agonists↗
PubMed1983

Effect of fenoterol on immunological release of leukotrienes and histamine from human lung in vitro: selective antagonism by beta-adrenoceptor antagonists.

The inhibitory effects of fenoterol, a beta 2-adrenoceptor agonist, on the release of SRS-A leukotrienes and histamine from chopped human lung tissue were measured and selective beta-adrenoceptor antagonists used to investigate the nature of the receptors involved. Fenoterol 0.01-1.0 microM inhibited the antigen-induced release of SRS-A and histamine, but not the release induced by the calcium ionophore A23187. Propranolol 0.1 and 1.0 microM and butoxamine 10 and 100 microM significantly antagonized the effects of fenoterol 0.1 microM on SRS-A and histamine at concentrations which affect (beta 2-adrenoceptors, while atenolol 0.1 to 10 microM showed no antagonism at concentrations which affect beta 1-adrenoceptors. These results suggest that adrenoceptors in human lung which modulate the immunological release of SRS-A leukotrienes are of the beta 2-subtype as for histamine release.

Adrenergic beta-Antagonists↗
PubMed1984

Beta-adrenergic inhibitory effect of alloimmune antibody on isolated oviductal tract of mice.

The effects of IgG purified from BALB/c anti CF1 sera on the spontaneous contractions of isolated oviductal tract from CF1 mice were explored. Cumulative dose-response curves were constructed for the effect of immune IgG on nice oviductal tracts from proestrus, estrus, metestrus and diestrus, comparing them with those obtained with norepinephrine. Both the adrenergic agonist and the immune IgG produced a sustained inhibition of spontaneous motility during the whole sex cycle. Normal IgG was virtually devoid of activity. The sensitivity of CF1 mouse oviducts to the inhibitory actions of immune IgG and norepinephrine varied depending on the hormonal stage, i.e. it was higher in natural diestrus than in metestrus; it became smaller in proestrus and was minimal during estrus. The mechanism triggered involved a beta-adrenergic reaction that could be blocked by 10(-7) M (-)-propranolol and 10(-6) M butoxamine and potentiated by chemical sympathectomy of the mice with 6-hydroxydopamine. It is concluded that: (a) alloimmune antibody reacts with isolated oviductal tract of mice inducing functional changes; (b) this action could be associated with an activation of postsynaptic beta-adrenergic sites of the plasma membrane and (c) the different effectiveness of the immune IgG observed during the sex cycle appears to depend on the affinity of beta-adrenoreceptors to react with it.

Animals↗
PubMed1985

Studies on beta-adrenoceptors of purified mast cells from guinea-pig lung.

Ovalbumin-induced histamine release from passively sensitized monodispersed cells (2-4% mast cells) or purified mast cells (50-78%) from guinea-pig lung was inhibited by isoproterenol and sulfonterol and their relative potencies or maximum responses were similar in both cases. The apparent dissociation constant for butoxamine was also independent of mast cell purity. The results indicate that beta-adrenoceptors mediating histamine release inhibition from lung are localized to mast cells and act independently of other cell types.

Animals↗
PubMed1991

Attenuation of insulin-induced drinking by beta-adrenoceptor antagonists.

Insulin-induced drinking (IID) in male Wistar rats, evoked by administering 5 U/kg of crystalline porcine insulin i.p., was significantly decreased by propranolol (0.1 and 0.5 mg/kg s.c.) after 1 and 2 h. The blood glucose of rats treated with a much higher dose of propranolol (10 mg/kg body weight) and insulin did not differ from that of rats treated solely with insulin after 30 and 120 min. Atenolol (0.5 mg/kg s.c.) caused a reduction in IID after 1 and 2h. Butoxamine (1 mg/kg s.c.) also reduced IID after 1 and 2h, and at 0.5 mg/kg after 1h. The alpha-blocker, phenoxybenzamine (10 mg/kg s.c.), had the opposite effect, stimulating IID after 2h. There is no direct evidence that insulin activated the sympathetic system at the doses used in these experiments. Nevertheless, the results reported here seem to be compatible with the involvement of the sympathetic system in IID, possible through the renin-angiotensin system.

Animals↗
PubMed1984

Adrenaline involvement in the presynaptic beta-adrenoceptor-mediated mechanism of dopamine release from slices of the rat hypothalamus.

Slices of rat hypothalamus were superfused and endogenous release of dopamine (DA) was measured by high performance liquid chromatography combined with electrochemical detection. The K+ (20 mM)-evoked release in the presence of tetrodotoxin was Ca2+-dependent. The evoked release was facilitated by a beta-agonist, isoproterenol and this effect was completely abolished by a beta-antagonist, 1-propranolol. Isoproterenol also concentration-dependently facilitated the electrically (at 5Hz) evoked release of DA. The pretreatment with 1-propranolol, beta 1-antagonist, atenolol and beta 2-antagonist, butoxamine shifted the concentration-effect curve of isoproterenol to the right. On the other hand, beta 1-agonist, tazolol, beta 2-agonist, salbutamol and low concentration (10(-9) M) of adrenaline also facilitated the release. 1-Propranolol alone reduced the electrically (at 2 Hz) evoked release, and this effect was completely abolished when the adrenaline content in the brain was drastically reduced by use of a potent PNMT inhibitor, DCMB. These findings suggest that in the rat hypothalamus adrenaline released from adrenaline-containing nerve terminals probably modulates DA release via presynaptic beta 1- and beta 2-adrenoceptors on DA nerve terminals.

Action Potentials↗
PubMed1992

Mediation of contraction and relaxation by alpha- and beta-adrenoceptors in the ureterovesical junction of the sheep.

The effects of alpha- and beta-adrenoceptor agonists and antagonists were studied in the sheep ureterovesical junction. Non-specific adrenergic agonists such as adrenaline and noradrenaline induced contraction in the sheep ureterovesical junction, suggesting a predominance of alpha-over beta-adrenoceptors in this functional unity. An inhibition of the noradrenaline-induced contraction was observed after prior blocking with prazosin (10(-7) M) and yohimbine (10(-7) M), the effect of prazosin being more potent than that of yohimbine. The effect of phenylephrine on alpha 1-adrenoceptors was more potent than that of B-HT 920 on alpha 2-adrenoceptors. Isoproterenol caused a concentration-dependent relaxation that was inhibited by propranolol (10(-6) M), pafenolol (10(-5) M) and butoxamine (10(-5) M). These results suggest that ureterovesical junction contraction is mediated by both alpha 1 and alpha 2-adrenoceptors, alpha 1 predominating over alpha 2. Relaxation is mediated by beta-adrenoceptors of the beta 1 and beta 2 subtypes.

Adrenergic alpha-Agonists↗
PubMed1983

Binding of [3H]-dihydroalprenolol and [3H]-acetobutolol to human blood platelets is not related to occupancy of beta-adrenoceptors.

Binding of [3H]-dihydroalprenolol to human platelet lysates is inhibited by (+/-)-propranolol and (+/-)-butoxamine, but less effectively by (+/-) practolol. (-)-Isoprenaline causes no significant inhibition of binding where stimulation of adenylate cyclase can be shown. Binding of [3H]-acetobutolol is also inhibited by (+/-)-propranolol. "Specific" binding of [3H]-dihydroalprenolol and [3H]-acetobutolol defined by (+/-) propranolol shows a non-classical saturation curve. 50% maximal binding is observed in the range 15-25 mM. The extent of "specific" binding is 2-fold greater for [3H]-dihydroalprenolol. Similar and rapid rates of binding of [3H]-dihydroalprenolol are observed at 4 degrees C and 20 degrees C. No stereoselectivity is observed for inhibition of [3H]-dihydroalprenolol binding by (+) and (-)-propranolol. Binding of [3H]-dihydroalprenolol and [3H]-acetobutolol may relate to the lipophilic character of these radioligands and does not represent interaction with beta-adrenoceptors.

Acebutolol↗
PubMed1992

Prostaglandin E2 synthesis elicited by adrenergic stimuli in guinea pig trachea is mediated primarily via activation of beta 2 adrenergic receptors.

Prostaglandin (PG) E2 synthesis elicited by adrenergic agonists in the guinea pig trachea has been shown to be mediated via activation of beta-adrenergic receptors. The purpose of this study was to examine arachidonic acid (AA) metabolism and to characterize the subtype of beta receptor involved in PG synthesis. [14C]AA was incubated with guinea pig tracheal rings, and the radiolabelled products were extracted from the medium. Thin layer chromatographic analysis and radioimmunoassay of the extract showed that [14C]AA was incorporated into guinea pig tracheal rings and metabolized mainly into radiolabeled and immunoreactive PGE2 (iPGE2) and smaller amounts into PGF2 alpha. Trace amounts of PGD2, TxB2 and 6-keto-PGF1 alpha but not LTB4 or LTC4 were detected by enzyme immunoassay. Incubation of guinea pig tracheal rings for 10 min with isoproterenol or salbutamol resulted in a significant increase in PGE2 synthesis (optimum concentration 0.1 microM for both compounds). In contrast, dobutamine, BRL 37344, BRL 28410, norepinephrine, phenylephrine, and xylazine (up to 1 microM) did not significantly increase PGE2 production. Isoproterenol-induced iPGE2 production was inhibited by the selective beta 2 receptor antagonist butoxamine (0.1-1.0 microM) and somewhat reduced by the beta 1 receptor antagonist practolol (1 microM). The increase in PGE2 synthesis was diminished with increasing concentrations of isoproterenol (0.5-5.0 microM) or salbutamol (0.5-1.0 microM); but it was reversed by pretreatment of tracheal rings with the protein synthesis inhibitors cycloheximide (0.9 microM) and actinomycin D (2 microM) but not by phenylisopropyl adenosine (0.1-1.0 microM), an inhibitor of adenylyl cyclase. These data suggest that isoproterenol-induced iPGE2 synthesis is primarily via activation of a beta 2 adrenergic receptor. Failure to enhance iPGE2 synthesis by a high concentration of isoproterenol is likely to be due to an induction of new inhibitory protein synthesis.

Albuterol↗
PubMed1993

Effects of escapable and inescapable foot-shock on rat atrial beta-adrenoceptors.

The chronotropic responsiveness to norepinephrine (NE) and isoproterenol (ISO) was determined in right atria isolated from rats submitted to repeated escapable or inescapable foot-shock. Significant postjunctional supersensitivity to ISO, but not to NE, was observed in both groups. No significant change in the pA2 value of metoprolol (a selective beta 1-adrenoceptor antagonist) was detected. However, a decrease of the maximum response to soterenol, a partial agonist at beta 1-adrenoceptors, occurred only after inescapable foot-shock. The enhanced sensitivity to ISO was abolished by butoxamine (a selective beta 2-adrenoceptor antagonist) and accompanied by a marked increase in the pA2 value of this antagonist. We conclude that the ability to control the shock prevented the down-regulation of the pacemaker beta 1-adrenoceptors but not the increased participation of beta 2-adrenoceptors in the response of the rat sinoatrial node to catecholamines after repeated foot-shock.

Animals↗
PubMed1990

Propranolol inhibits cyclic AMP accumulation and amylase secretion in parotid acinar cells stimulated by isobutylmethylxanthine and forskolin.

Propranolol inhibited cyclic AMP (cAMP) accumulation stimulated by 3-isobutyl-1-methylxanthine (IBMX) or forskolin in rat parotid acinar cells. The inhibition by propranolol was highly potent; 10(-7) M propranolol was sufficient for the maximum inhibition (approx. 50% at 5 min). The inhibitory effect was observed in both intact and saponin-permeabilized parotid cells, but the effect was more prominent in permeabilized cells than in intact cells. Other beta-blockers, like alprenolol and atenolol, were as effective as propranolol, but butoxamine (beta 2-selective) was slightly less effective. The inhibition by propranolol was similarly detected in the cells prepared from pertussis-toxin-pretreated rats, suggesting that inhibitory guanine nucleotide regulatory protein (Gi) is not involved in the inhibitory mechanism. Propranolol also inhibited the exocytosis of amylase stimulated by IBMX or forskolin. In the presence of propranolol and IBMX, the responsiveness of saponin-permeabilized cells to exogenous cAMP was markedly increased, indicating that propranolol neither promotes the degradation of cAMP nor prevents the inhibitory effect of IBMX on cAMP phosphodiesterase.

1-Methyl-3-isobutylxanthine↗
PubMed1984

Anti-anaphylactic action in the mouse of thyrotropin-releasing hormone (TRH) is mediated through beta 1-adrenoceptive effectors.

Intravenous or intracerebroventricular administration of thyrotropin-releasing hormone (TRH) significantly improved survival in immunized mice subjected to fatal anaphylaxis by intravenous challenge with an antigen. This protective action of TRH was blocked by pretreatment with the beta-adrenergic antagonist propranolol (5 mg/kg), or by prior administration of the cardioselective beta 1-antagonist, metoprolol (5 mg/kg), but not by pretreatment with the beta 2-selective antagonist, butoxamine (5 mg/kg). It is suggested, based on the present and previous findings that the anti-anaphylactic effect of TRH in the mouse is mediated through activation of beta 1-adrenoceptive effectors, secondary to central stimulation of sympathomedullary release of catecholamines.

Adrenal Medulla↗
PubMed1994

Beta 1-adrenergic mechanism is involved in stress-induced increase in arousal.

It has been shown that 1 h restraint shortens pentobarbital (PbNa)-induced sleeping time and that brain corticotropin-releasing hormone (CRH) is involved in the mechanism by which restraint shortens. PbNa-induced sleeping time. The present study was designed to further examine the mechanism of the antagonistic effect of 1 h restraint on PbNa in rats. Intracerebroventricular (i.c.v.) administration of propranolol and metoprolol, but not butoxamine reversed the shortening of PbNa-induced sleeping time by 1 h restraint. The i.c.v. administration of phentolamine blocked the shortening of PbNa-induced sleeping time by restraint, while the same dose of phentolamine prolonged the sleeping time in unrestrained rats. Atropine did not affect the PbNa-induced sleeping time in restrained rats. These results suggest that in addition to CRH, the brain beta 1-adrenergic system is involved in the restraint stress-induced increase in arousal.

Animals↗