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At least 199 records · Page 11Linked to original sources
PubMed1990

Sympathetic nervous system mediates central corticotropin-releasing factor induced suppression of natural killer cytotoxicity.

Corticotropin-releasing factor (CRF) acts within the brain to elicit changes in neuroendocrine, autonomic and behavioral activity similar to those observed after stress. A reduction of cellular immune function as measured by splenic natural killer cell activity has also been described following the central administration of CRF. In this study we evaluated the role of the sympathetic nervous system in mediating CRF-induced suppression of natural killer (NK) cytotoxicity. Synthetic rat CRF (1.0 microgram) microinjected into the lateral ventricle increased noradrenergic function and reduced NK activity in the rat spleen. Pretreatment of the animals by chemical sympathectomy (6-hydroxy-dopamine, 100 mg/kg i.p. daily over 10 days) produced a greater than 95% reduction of splenic norepinephrine concentration and abolished completely both the CRF-induced increase in plasma catecholamine levels and the reduction in splenic NK activity. In addition, beta adrenergic receptor blockade (either propranolol, 10 mg/kg i.p., or butoxamine, 25 mg/kg i.p. 30 min before i.c.v. infusion) antagonized the CRF-induced reduction in NK activity. Measurement of circulating levels of adrenocorticotrophic hormone and corticosterone demonstrated that activation of the pituitary adrenal axis by CRF was dissociated from changes in NK activity. These findings suggest that the sympathetic nervous system mediates the suppression of splenic NK cytotoxicity after i.c.v. CRF.

Animals↗
PubMed1990

Beta adrenoceptor subtype in isolated human, monkey and dog epicardial coronary arteries.

Isolated human, Japanese monkey and dog epicardial coronary arteries and dog renal and mesenteric arteries treated with phentolamine responded to isoproterenol with a concentration-related relaxation. The KB values of metoprolol, a beta-1 antagonist, in the coronary arteries from different mammals did not differ, but were appreciably smaller than those in the dog renal and mesenteric arteries. 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. Terbutaline, a beta-2 agonist, produced a greater relaxation in monkey mesenteric and dog renal and mesenteric arteries than in human, monkey and dog coronary arteries. Norepinephrine relaxed the monkey and dog coronary arteries dose-dependently via mainly beta-1 adrenoceptors, but elicited a contraction or a minute relaxation in dog mesenteric arteries even when treated with high concentrations of phentolamine. Contractile responses to electrical stimulation of adrenergic nerves in monkey coronary arteries were potentiated by treatment with metoprolol and propranolol, whereas the contractions in dog mesenteric arteries were unaffected. It is concluded that the amine-induced relaxation of human and monkey epicardial coronary arteries is mediated mainly by beta-1 adrenoceptor subtype, as is the response of dog coronary arteries. Involvement of beta-1 subtype in coronary artery relaxations would be a mechanism underlying potentiation by beta antagonists of the contraction caused by norepinephrine released from adrenergic nerves in primates.

Animals↗
PubMed1978

Inhibition of thermogenic drinking by beta-adrenergic antagonists.

The thirst induced by transfer of rats from air at 5 degrees C to air at 25 degrees C (thermogenic drink) was inhibited by d,1-, but not d-propranolol (6 mg/kg body weight) administered 0.5 h prior to removal from cold. The thermogenic drink was not inhibited by a similar administration of the beta1-adrenergic antagonist, practolol (50 and 150 mg/kg body weight), but was inhibited by the beta2-adrenergic antagonist, butoxamine (35 mg/kg body weight). The results are consistent with the suggestion that beta2-adrenergic receptors play a role in mediation of the thermogenic drink in rats.

Adrenergic beta-Antagonists↗
PubMed1988

Altered vascular beta adrenoceptor-mediated relaxation in deoxycorticosterone-salt hypertensive rats.

Beta adrenoceptor-mediated relaxation was studied on femoral and mesenteric arteries and thoracic aorta from deoxycorticosterone-salt hypertensive and age-matched normotensive rats. Maximum relaxations to isoproterenol (ISO), fenoterol and norepinephrine were less in hypertensive than in normotensive tissues. Mean negative log EC50 values of ISO and norepinephrine, but not fenoterol, were smaller in femoral and mesenteric strips from hypertensive rats than those from oil-water-treated rats. In thoracic aortas from hypertensive rats, the mean negative log EC50 values of ISO and fenoterol decreased, whereas those of norepinephrine increased as compared with those in oil-water-treated rats. In oil-salt- and deoxycorticosterone-water-treated rats, hypertension did not develop nor were the responses to ISO reduced. Relative potencies of the beta adrenoceptor agonists and Schild plot data for atenolol and butoxamine indicate that femoral arteries of normotensive and hypertensive rats possess beta-1 adrenoceptors mediating relaxation. It also is suggested that the mesenteric artery and thoracic aorta of both normotensive and hypertensive rats predominantly possess beta-2 adrenoceptors mediating relaxation. The present results suggest that an elevation in blood pressure is associated with the reduction of beta-1 adrenoceptor-mediated relaxation in femoral arteries and of beta-2 adrenoceptor-mediated relaxation in mesenteric arteries.

Animals↗
PubMed1988

Functional beta 2-adrenoceptors in right atria isolated from footshock-stressed rats.

The participation of beta 2-adrenoceptors in the chronotropic response was evaluated in right atria isolated from rats submitted to daily footshock stress for three days. Footshock increased both the sensitivity to salbutamol and the pA2 of butoxamine. These results provide additional support for the proposal that repeated footshock stress increases the function of rat atrial postjunctional beta 2-adrenoceptors.

Albuterol↗
PubMed1985

Autoregulation of endogenous epinephrine release via presynaptic adrenoceptors in the rat hypothalamic slice.

High-K+ (30 mM)-evoked release of endogenous epinephrine in hypothalamic slices from three rats in the presence of tetrodotoxin, 3 X 10(-7) M, was measured by high-performance liquid chromatography with an electrochemical detector. Spontaneous and evoked release of epinephrine was markedly reduced, when rats were pretreated with 2,3-dichloro-alpha-methylbenzylamine, an inhibitor of phenylethanolamine N-methyltransferase, the enzyme catalyzing the formation of epinephrine from norepinephrine, 80 mg/kg i.p., before decapitation. The amount of epinephrine released during the resting state was lower by a factor of approximately 2 orders than that of norepinephrine and dopamine but was consistently higher than the limit of the sensitivity of this assay system, 0.1 to 0.3 pmol. The evoked release of epinephrine was Ca++ dependent. Isoproterenol, 10(-8) M to 10(-7) M, dose dependently increased this parameter. I-Propranolol, 3 X 10(-8) M, shifted the dose-effect curve of isoproterenol to the right. Atenolol, 10(-6) M, and butoxamine, 3 X 10(-8) M, beta-1 and beta-2 antagonists, respectively, antagonized the action of isoproterenol, 3 X 10(-8) M. Tazolol, 3 X 10(-7) and 10(-6) M, a beta-1 agonist, and salbutamol, 10(-8) and 3 X 10(-8) M, a beta-2 agonist, dose dependently increased the evoked release of epinephrine. I-Propranolol, 3 X 10(-7) M and 3 X 10(-6) M alone, dose dependently decreased this parameter, but the d-isomer produced no effect. Clonidine, 10(-8) and 10(-7) M, an alpha-2 agonist, dose dependently decreased the parameter, and this decrease was antagonized by yohimbine, 10(-6) M, an alpha-2 antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1986

Beta adrenoceptor modulation of the generation of murine cytotoxic T lymphocytes in vitro.

The effects of stimulating beta adrenoceptors on lymphocytes during the generation of cell-mediated immunity were examined. In an in vitro system for the generation of murine cell-mediated cytotoxicity, addition of isoproterenol (10(-7) M), epinephrine (10(-6) M) or norepinephrine (10(-4) M) enhanced the number of lytic units generated compared to control cultures. This increase was blocked by dl-propranolol (5 X 10(-6) M). I-Propranolol (10(-11) to 10(-7) M) blocked the isoproterenol-induced increase in lytic units per culture, but d-propranolol (10(-11) to 10(-7) M) did not. Terbutaline (10(-5) M), a relatively selective beta-2 agonist, similarly augmented the generation of cell-mediated cytotoxicity, with the increase again blocked by propranolol. Butoxamine (5 X 10(-6) M), a beta-2 antagonist, but not atenolol (5 X 10(-6) M), a beta-1 antagonist, blocked the epinephrine-induced increase in cell-mediated cytotoxicity. Addition of phentolamine (5 X 10(-6) M) had no effect on the epinephrine-induced increase in lytic units per culture. However, in the presence of phentolamine, norepinephrine increased lytic units per culture to a greater degree than that seen with norepinephrine alone, suggesting a balance between positive beta effects and inhibitory alpha effects upon simultaneous alpha and beta stimulation. These data provide further evidence for an immunoenhancing role of beta receptor stimulation during the generation of immune responses.

Adrenergic alpha-Antagonists↗
PubMed1987

Interaction of beta adrenergic agonists and antagonists with brain beta adrenergic receptors in vivo.

There is interest in knowing whether beta adrenergic antagonists or agonists, when administered systemically, can enter the brain to interact with central beta adrenergic receptors. To study this, the reduction in the radioactive content in the brain of rats after administration of (-)-[125I]iodopindolol (IPIN) by systemically administered beta agonists or antagonists was measured. Previous studies show that after the i.v. administration of IPIN the binding in vivo to various areas of the central nervous system has the characteristics expected of binding to beta adrenergic receptors. Of the antagonists tested, pindolol and butylpindolol showed potent interactions with beta receptors in both cortex and cerebellum whereas atenolol and practolol did not interact at doses up to 30 mg/kg. CGP-12177 showed moderate potency in inhibiting IPIN binding in vivo. We have shown previously that propranolol and alprenolol inhibit IPIN binding with high potency in cortex and cerebellum. At high doses, butoxamine, a beta-2 antagonist, reduced the binding of IPIN in the cerebellum but not in the cortex. Of the agonists tested, clenbuterol and prenalterol caused a significant dose-dependent reduction of the binding of IPIN, with clenbuterol being more potent. Isoproterenol, salbutamol, salmefamol and dobutamine had no effect. With the exception of CGP-12177, the affinity of the drugs for central beta adrenergic receptors measured in vitro was correlated significantly with their ability to inhibit IPIN binding in vivo whereas their degree of lipophilicity was not correlated significantly with potency in vivo. The inhibition of IPIN binding in vivo from brain areas can be used to evaluate whether drugs penetrate into brain and interact with central beta adrenergic receptors.

Adrenergic beta-Agonists↗
PubMed1983

Role of cyclic AMP in adrenergically-induced tracheal muscle relaxation.

Studies were performed on the isolated bovine tracheal muscle preparation to assess the possible role of adenosine 3',5'-cyclic monophosphate (cyclic AMP) in adrenergically-induced smooth muscle relaxation. Isoproterenol, epinephrine, terbutaline and soterenol were found to relax the tracheal muscle and to increase its cyclic AMP content. The two events generally paralleled one another when analyzed in terms of dose-response and time-response relationships. Propranolol antagonized the relaxation and the increase in cyclic AMP produced by isoproterenol. However, other findings suggested that there may not be a cause and effect relationship between the biochemical and mechanical responses. Thus, salbutamol and carbuterol failed to increase muscle cyclic AMP even in concentrations which produced maximum relaxation. Additionally, butoxamine and H35/25 antagonized the biochemical response but had additive effects (instead of antagonistic effects) on the mechanical response to isoproterenol. Furthermore, it was observed that low concentrations of H35/25 produced tracheal muscle relaxation associated with an increase in tissue cyclic AMP; however, use of a high concentration of H35/25 paradoxically resulted in autoblockade of the increase in cyclic AMP but not the smooth muscle relaxation.

Adrenergic alpha-Agonists↗
PubMed1984

[Characterization of beta-2 adrenergic receptors in the human uterine artery].

The actions of the hexoprenaline, salbutamol and terbutaline on adrenalin-induced effects in the human artery were studied in vitro. The human uterine artery has a two-part response to adrenalin: The first, rapid (phasic component), and the second, slow and sustained (tonic component). Both beta-2 stimulators relax the tonic component and reduced the amplitude of the phasic component. The depressor effect of the responses to adrenalin is reduced in the presence of butoxamine and intensified in the presence of caffeine. These results suggest the existence on the human uterine artery of beta-2 adrenergic receptors acting as mediators of smooth muscle relaxation, and suggest also that the mechanism of this relaxation is most likely cAMP dependent.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Beta-adrenoceptor selectivity of dobutamine: in vivo and in vitro studies.

We compared the beta-adrenoceptor stimulant actions of dobutamine and (-)-isoprenaline in isolated tissue preparations (atria, trachea, and uterus) from the guinea pig and in chloralose-anaesthetized, vagotomized cats (arterial blood pressure, heart rate, hindlimb perfusion pressure, and soleus muscle contractility). The results obtained in these experiments indicate that, on a dose basis, dobutamine shows little selectivity in producing alpha-, beta 1-, and beta 2-adrenoceptor-mediated effects. In phentolamine-treated cats, reductions in arterial pressure and total peripheral resistance produced by infusions of dobutamine were little affected by the beta 2-adrenoceptor-selective antagonist butoxamine, but were antagonized by atenolol. The rise in cardiac output produced by dobutamine involved increases in both heart rate and stroke volume. There was little indication of a selective inotropic action, a feature that confirmed the results obtained in isolated atrial preparations. The increase in cardiac output appeared to involve both alpha- and beta-receptor-mediated actions, because phentolamine reduced the rise in cardiac output by reducing stroke volume.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Pharmacodynamic differentiation of chronotropic and inotropic beta-adrenergic receptors in rabbit heart.

Isolated, perfused rabbit hearts were used to identify substituted phenylethylamines selective for either chronotropic or inotropic stimulation relative to norepinephrine. Heart rate and dF/dtmax were measured; the difference in their normalized values was used as an index of selectivity. p-Octopamine (OA) showed chronotropic preference, while phenylephrine (PE) showed a significant inotropic preference. Their effects were not prevented by reserpine pretreatment, cocaine, butoxamine, or phenoxybenzamine, but were antagonized by propranolol, which suggests that OA and PE exert their selective actions directly at beta 1-receptors. These findings provide further evidence for the existence of separate chronotropic and inotropic beta-adrenergic receptors in the heart.

Animals↗
PubMed1982

Selective stimulation of PGE1-synthesis by soterenol in the isolated rat vas deferens is mediated by alpha adrenoreceptors.

The effects of soterenol on prostaglandin (PG) release by the isolated rat vas deferens were studied. Soterenol increased the amount of PGE1 released into the medium without affecting that of PGE2 or PGF2 alpha. The effect of soterenol was inhibited by phentolamine but not by butoxamine. It is concluded that soterenol elicits the release of PGE1 by the isolated rat vas deferens via stimulation of alpha adrenoreceptors.

Animals↗
PubMed1980

Hormonal effects on cell proliferation in a human erythroleukemia cell line (K562).

We have investigated the hormonal responsiveness of K562 cells using a serum-substituted in vitro clonogenic assay. Dexamethasone inhibited colony formation by the K562 cells, and the inhibitory effect could be reversed by progesterone (10(-6) M). Fluoxymesterone caused a prominent enhancement of K562 colony growth, whereas estriol had no effect. Stimulation by triiodothyronine was maximal at 10(-7) M, and the thyroid effect could be abrogated by the beta 2-adrenergic antagonist butoxamine in equimolar concentrations. Using standard tissue culture conditions, the beta-adrenergic agent isoproterenol, but not the alpha catecholamine phenylephrine, enhanced the proliferation of K562 cells. When K562 cells were grown under hormone-depleted conditions, they developed responsiveness to phenylephrine and were no longer stimulated by isoproterenol. DbcAMP and prostaglandins of the E series also caused K562 colony enhancement. Prostaglandin F2 alpha had no effect on cell proliferation. Insulin was an effective stimulant of colony formation of K562 cells, as were human growth hormone and ovine prolacin. Bovine growth hormone had no effect. Our results are consistent with the identificaiton of K562 as an erythroid line, and they indicate that K562 cells respond to endocrine hormones in a manner analogous to normal erythroid progenitors.

Butoxamine↗
PubMed1995

Hypotensive effect of intracerebroventricular injection of norepinephrine and its modulation by alpha and beta adrenergic blockers in conscious rabbits.

The present study was designed to investigate the role of central adrenoceptors in the hypotensive effect of intracerebroventricular (ICV) injection of norepinephrine (NE) in conscious rabbits. Experiments were carried out on 19 adult rabbits (oryctolagus cuniculus) of either sex. A dose-dependent hypotensive response to ICV injection of NE was observed with no significant change in heart rate. The hypotensive response of NE was blocked 74.2 +/- 0.7% by yohimbine (alpha-2 adrenergic blocker), and 25.0 +/- 0.5% by metoprolol (beta-1 adrenergic blocker). NE response was not affected either by prazosin or butoxamine (alpha-1 and beta-2 adrenergic blockers respectively). The results suggest that the dose-dependent hypotensive response of ICV administered NE is mediated through alpha-2 and beta-1 central adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed1996

Influence of the estrous cycle on the sensitivity to catecholamines in right atria from rats submitted to foot-shock stress.

We investigated the mechanisms of the alterations in sensitivity to catecholamines in right atria from female rats exhibiting regular 4-day estrous cycles after three foot-shock sessions at estrus, metestrus, and diestrus or at diestrus, proestrus, and estrus. Right atria from stressed rats sacrificed at diestrus showed subsensitivity to noradrenaline and adrenaline. After in vitro sympathetic denervation (38 microM 6-hydroxydopamine) plus inhibition of neuronal reuptake (0.1 microM desipramine) subsensitivity to noradrenaline was abolished, but it was again evident when extraneuronal uptake was also inhibited (10 microM phenoxybenzamine and 30 microM corticosterone). The same pretreatment abolished the subsensitivity to adrenaline. After addition of 1 microM butoxamine, a beta 2-adrenoceptor antagonist, the tissues from stressed rats were subsensitive to adrenaline. Right atria from stressed rats sacrificed at estrus did not show any alteration in sensitivity to catecholamines. We conclude that after foot-shock stress, right atria from female rats sacrificed at diestrus showed subsensitivity of the chronotropic response to catecholamines as a result of a conformational alteration of beta 1-adrenoceptors, simultaneously with an increase in beta 2-adrenoceptor-mediated response. The mechanisms seem to be similar to those which underlie stress-induced alterations in catecholamine sensitivity in right atria from male rats. However, during estrus there are some protective factors that prevent the effects of stress on right atria.

Adrenergic beta-Antagonists↗
PubMed1997

Capillary adrenoceptors in rat skeletal muscle.

The purpose of this study was to examine whether functional alpha- and beta-adrenoceptors exist on capillaries of rat skeletal muscle, and further to determine which subtype of these receptors predominates on these capillaries. Using intravital video microscopy, we measured red blood cell velocity (VRBC) responses in capillaries of rat extensor digitorum longus muscle (EDL) following a local application of these agonists: norepinephrine (NE; alpha 1, alpha 2; 10(-7) to 3 x 10(-3) M), phenylephrine (PE; alpha 1; 3 x 10(-4) to 10(-2) M), clonidine (CLO; alpha 2; 3 x 10(-3) to 10(-2) M), UK14304 (alpha 2; 3 x 10(-4) to 10(-2) M), and isoproterenol (IPR; beta 1, beta 2; 10(-7) to 3 x 10(-3) M). Responses to NE (10(-5) M) were also measured after a local pretreatment with prazosin (alpha 1 antagonist; 10(-5) to 10(-3) M) and rauwolscine (alpha 2 antagonist; 3 x 10(-4) to 3 x 10(-2) M), while responses to IPR (10(-5) M) were measured after local atenolol (ATE; beta 1 antagonist; 10(-3) to 10(-2) M) and butoxamine (BUT; beta 2 antagonist; 10(-3) to 10(-2) M) pretreatment. The overall control VRBC was 226 microns/sec. NE, PE, CLO, and UK14304 resulted in concentration-dependent decreases of VRBC (from -12 to -89%) from the control level, while IPR caused concentration-dependent increases (17 to 174%). PE reduced VRBC to a larger degree than CLO and UK14304. NE-induced VRBC responses tended to be attenuated more by prazosin than by rauwolscine. Both ATE (10(-2) M) and BUT (10(-3) and 10(-2) M) alone decreased VRBC. However, only ATE significantly attenuated the IPR-induced VRBC responses. These results suggest that the capillary of rat EDL muscle has alpha- and beta-adrenoceptors. From the two alpha-adrenoceptor subtypes, the capillary may be predominated by the alpha 1-adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed2000

Adrenergic mediation of TNF alpha-stimulated ICAM-1 expression on human brain microvascular endothelial cells.

Adrenergic innervation derived from locus ceruleus has been implicated in regulating BBB permeability and inflammatory responses associated with neurological disorders. This report demonstrates that adrenergic agents attenuate the tumor necrosis factor-alpha (TNF alpha)-induced expression of intercellular adhesion molecule-1 (ICAM-1) on cerebral microvascular endothelial cells (HBMEC) derived from human brains. HBMEC were incubated with isoproterenol (1-10 microM) alone or in the presence of propranolol (10 microM) for 30 min followed by the addition of various concentrations of TNF alpha. ICAM-1 expression on cultured HBMEC was dose-dependently upregulated by TNF alpha. Incubation with isoproterenol significantly reduced levels of ICAM-1 expression indicating the possible involvement of adrenergic agents on ICAM-1 expression. Treatment with propranolol (beta 1/beta 2-adrenergic antagonist) and butoxamine (beta 2-adrenergic antagonist), but not atenolol (beta 1-adrenergic antagonist) reversed this inhibitory effect. Isoproterenol also dose-dependently stimulated cAMP production (assayed by RIA) by HBMEC; propranolol treatment abolished this effect. These data show that the beta 2-adrenergic receptor/cAMP pathway may be partly involved in TNF alpha-stimulated ICAM-1 expression and indicate the possible involvement of adrenergic mediation of capillary function including BBB integrity.

Adrenergic Fibers↗